The patient’s symptoms suggest a lesion in the S1 nerve root, which supplies sensation to the posterolateral aspect of the leg and lateral aspect of the foot. This is supported by the presence of sensory loss, weakness in plantarflexion of the foot, reduced ankle reflex, and a positive sciatic nerve stretch test. The other options, such as Achilles tendon rupture, injury to the common fibular nerve, or L4-L5 nerve root compression, do not fully explain the patient’s symptoms.

Understanding Prolapsed Disc and its Features

A prolapsed disc in the lumbar region can cause leg pain and neurological deficits. The pain is usually more severe in the leg than in the back and worsens when sitting. The features of the prolapsed disc depend on the site of compression. For instance, compression of the L3 nerve root can cause sensory loss over the anterior thigh, weak quadriceps, reduced knee reflex, and a positive femoral stretch test. On the other hand, compression of the L4 nerve root can cause sensory loss in the anterior aspect of the knee, weak quadriceps, reduced knee reflex, and a positive femoral stretch test.

Similarly, compression of the L5 nerve root can cause sensory loss in the dorsum of the foot, weakness in foot and big toe dorsiflexion, intact reflexes, and a positive sciatic nerve stretch test. Lastly, compression of the S1 nerve root can cause sensory loss in the posterolateral aspect of the leg and lateral aspect of the foot, weakness in plantar flexion of the foot, reduced ankle reflex, and a positive sciatic nerve stretch test.

The management of prolapsed disc is similar to that of other musculoskeletal lower back pain, which includes analgesia, physiotherapy, and exercises. However, if the symptoms persist even after 4-6 weeks, referral for an MRI is appropriate. Understanding the features of prolapsed disc can help in early diagnosis and prompt management.

Osteomyelitis is most commonly caused by Staphylococcus aureus in both adults and children. IV drug use is a known risk factor for this condition as it can introduce microorganisms directly into the bloodstream. While Escherichia coli can also cause osteomyelitis, it is more prevalent in children than adults. Mycobacterium tuberculosis can also lead to osteomyelitis, but it is less common than Staphylococcus aureus. Bone introduction typically occurs via the circulatory system from pulmonary tuberculosis. However, antitubercular therapy has reduced the incidence of tuberculosis, making bone introduction less likely than with Staphylococcus aureus, which is part of the normal skin flora. Salmonella enterica is the most common cause of osteomyelitis in individuals with sickle cell disease. As the patient is not known to have sickle cell, Staphylococcus aureus remains the most probable cause.

Understanding Osteomyelitis: Types, Causes, and Treatment

Osteomyelitis is a bone infection that can be classified into two types: haematogenous and non-haematogenous. Haematogenous osteomyelitis is caused by bacteria in the bloodstream and is usually monomicrobial. It is more common in children and can be caused by risk factors such as sickle cell anaemia, intravenous drug use, immunosuppression, and infective endocarditis. On the other hand, non-haematogenous osteomyelitis is caused by the spread of infection from adjacent soft tissues or direct injury to the bone. It is often polymicrobial and more common in adults, with risk factors such as diabetic foot ulcers, pressure sores, diabetes mellitus, and peripheral arterial disease.

Staphylococcus aureus is the most common cause of osteomyelitis, except in patients with sickle-cell anaemia where Salmonella species are more prevalent. To diagnose osteomyelitis, MRI is the imaging modality of choice, with a sensitivity of 90-100%.

The treatment for osteomyelitis involves a course of antibiotics for six weeks. Flucloxacillin is the preferred antibiotic, but clindamycin can be used for patients who are allergic to penicillin. Understanding the types, causes, and treatment of osteomyelitis is crucial in managing this bone infection.

Bisphosphonates, such as alendronate and risedronate, are used to treat osteoporosis by preventing bone resorption through the inhibition of osteoclasts. These drugs are taken up by the osteoclasts, preventing them from adhering to the bone surface and continuing the resorption process.

Denosumab is a monoclonal antibody that works by binding to the receptor activator of nuclear factor kappa-B ligand (RANK-L), which blocks the interaction between RANK-L and RANK, ultimately reducing bone resorption.

Raloxifene is a selective estrogen receptor modulator that has estrogen-like effects on bone, leading to decreased bone resorption and improved bone density.

Romosozumab is a monoclonal antibody that inhibits the action of sclerostin, a regulatory factor in bone metabolism, ultimately leading to increased bone formation.

Bisphosphonates: Uses, Adverse Effects, and Patient Counselling

Bisphosphonates are drugs that mimic the action of pyrophosphate, a molecule that helps prevent bone demineralization. They work by inhibiting osteoclasts, the cells responsible for breaking down bone tissue. Bisphosphonates are commonly used to prevent and treat osteoporosis, hypercalcemia, Paget’s disease, and pain from bone metastases.

However, bisphosphonates can cause adverse effects such as oesophageal reactions, osteonecrosis of the jaw, and an increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate. Patients may also experience an acute phase response, which includes fever, myalgia, and arthralgia following administration. Hypocalcemia may also occur due to reduced calcium efflux from bone, but this is usually clinically unimportant.

To minimize the risk of adverse effects, patients taking oral bisphosphonates should swallow the tablets whole with plenty of water while sitting or standing. They should take the medication on an empty stomach at least 30 minutes before breakfast or another oral medication and remain upright for at least 30 minutes after taking the tablet. Hypocalcemia and vitamin D deficiency should be corrected before starting bisphosphonate treatment. However, calcium supplements should only be prescribed if dietary intake is inadequate when starting bisphosphonate treatment for osteoporosis. Vitamin D supplements are usually given.

The duration of bisphosphonate treatment varies depending on the level of risk. Some experts recommend stopping bisphosphonates after five years if the patient is under 75 years old, has a femoral neck T-score of more than -2.5, and is at low risk according to FRAX/NOGG.

Chlorphenamine is a medication.

Antihistamines for Allergic Rhinitis and Urticaria

Antihistamines, specifically H1 inhibitors, are effective in treating allergic rhinitis and urticaria. Sedating antihistamines like chlorpheniramine have antimuscarinic properties that can cause dry mouth and urinary retention. On the other hand, non-sedating antihistamines like loratadine and cetirizine are less likely to cause drowsiness. However, there is some evidence that cetirizine may still cause some level of drowsiness compared to other non-sedating antihistamines. Overall, antihistamines are a valuable treatment option for those suffering from allergic rhinitis and urticaria.

The ulnar nerve supplies the flexor carpi ulnaris muscle, while all other flexor muscles in the anterior compartment of the forearm are innervated by the median nerve. Therefore, the correct answer is flexor carpi ulnaris.

Upper limb anatomy is a common topic in examinations, and it is important to know certain facts about the nerves and muscles involved. The musculocutaneous nerve is responsible for elbow flexion and supination, and typically only injured as part of a brachial plexus injury. The axillary nerve controls shoulder abduction and can be damaged in cases of humeral neck fracture or dislocation, resulting in a flattened deltoid. The radial nerve is responsible for extension in the forearm, wrist, fingers, and thumb, and can be damaged in cases of humeral midshaft fracture, resulting in wrist drop. The median nerve controls the LOAF muscles and can be damaged in cases of carpal tunnel syndrome or elbow injury. The ulnar nerve controls wrist flexion and can be damaged in cases of medial epicondyle fracture, resulting in a claw hand. The long thoracic nerve controls the serratus anterior and can be damaged during sports or as a complication of mastectomy, resulting in a winged scapula. The brachial plexus can also be damaged, resulting in Erb-Duchenne palsy or Klumpke injury, which can cause the arm to hang by the side and be internally rotated or associated with Horner’s syndrome, respectively.

The extensor carpi radialis longus muscle is innervated by the radial nerve. However, in a patient with a radial nerve palsy due to a midshaft humeral fracture, this muscle may be the only forearm extensor directly supplied by the radial nerve. Therefore, it is the most likely correct answer when considering exercises to strengthen the affected muscle.

The extensor carpi radialis brevis muscle, which originates from the lateral epicondyle of the humerus, is also innervated by a branch of the radial nerve. However, its insertion point is different from that described in the MRI, making it an unlikely answer.

The extensor digitorum brevis muscle, which assists in extending the toes, is not relevant to the patient’s wrist condition.

The extensor digitorum longus muscle, which is involved in foot dorsiflexion and toe extension, is also not relevant to the patient’s wrist condition.

Upper limb anatomy is a common topic in examinations, and it is important to know certain facts about the nerves and muscles involved. The musculocutaneous nerve is responsible for elbow flexion and supination, and typically only injured as part of a brachial plexus injury. The axillary nerve controls shoulder abduction and can be damaged in cases of humeral neck fracture or dislocation, resulting in a flattened deltoid. The radial nerve is responsible for extension in the forearm, wrist, fingers, and thumb, and can be damaged in cases of humeral midshaft fracture, resulting in wrist drop. The median nerve controls the LOAF muscles and can be damaged in cases of carpal tunnel syndrome or elbow injury. The ulnar nerve controls wrist flexion and can be damaged in cases of medial epicondyle fracture, resulting in a claw hand. The long thoracic nerve controls the serratus anterior and can be damaged during sports or as a complication of mastectomy, resulting in a winged scapula. The brachial plexus can also be damaged, resulting in Erb-Duchenne palsy or Klumpke injury, which can cause the arm to hang by the side and be internally rotated or associated with Horner’s syndrome, respectively.

Understanding Erythrocyte Sedimentation Rate (ESR)

The Erythrocyte Sedimentation Rate (ESR) is a test that measures the rate at which red blood cells settle in a tube over a period of time. It is a non-specific marker of inflammation and can be affected by various factors such as the size, shape, and number of red blood cells, as well as the concentration of plasma proteins like fibrinogen, alpha2-globulins, and gamma globulins.

A high ESR can be caused by various conditions such as temporal arteritis, myeloma, connective tissue disorders like systemic lupus erythematosus, malignancies, infections, and other factors like increasing age, female sex, and anaemia. On the other hand, a low ESR can be caused by conditions like polycythaemia, afibrinogenaemia, or hypofibrinogenaemia.

It is important to note that while a high ESR can indicate the presence of an underlying condition, it is not a definitive diagnosis and further testing may be required to determine the cause. Therefore, it is essential to consult a healthcare professional for proper evaluation and management.

The patella, which is the largest sesamoid bone in the body, shares an articular space with the femur and tibia. Sesamoid bones are embedded in tendons and often pass over joints to protect the tendon from damage.

Long bones, such as the femur, humerus, tibia, and fibula, have a body that is longer than it is wide.

Short bones, like the carpals, are as wide as they are long.

Flat bones are plate-like structures that serve to protect vital organs.

Irregular bones, such as the vertebrae and mandible, do not fit into any of the other categories.

Knee Problems in Children and Young Adults

Knee problems are common in children and young adults, and can be caused by a variety of conditions. Chondromalacia patellae is a condition that affects teenage girls and is characterized by softening of the cartilage of the patella. This can cause anterior knee pain when walking up and down stairs or rising from prolonged sitting. However, it usually responds well to physiotherapy.

Osgood-Schlatter disease, also known as tibial apophysitis, is often seen in sporty teenagers. It causes pain, tenderness, and swelling over the tibial tubercle. Osteochondritis dissecans can cause pain after exercise, as well as intermittent swelling and locking. Patellar subluxation can cause medial knee pain due to lateral subluxation of the patella, and the knee may give way. Patellar tendonitis is more common in athletic teenage boys and causes chronic anterior knee pain that worsens after running. It is tender below the patella on examination.

It is important to note that referred pain may come from hip problems such as slipped upper femoral epiphysis. Understanding the key features of these common knee problems can help with early diagnosis and appropriate treatment.

Methotrexate hinders the activity of dihydrofolate reductase, which is a crucial enzyme in folate metabolism. This drug is effective in treating various conditions, such as Crohn’s disease, psoriasis, rheumatoid arthritis, and certain types of cancer, by disrupting DNA synthesis and repair. Although other enzymes are also involved in folate metabolism and homeostasis, methotrexate does not inhibit them. Notably, 5-Fluorouracil inhibits thymidylate synthase, while methionine synthase, methylenetetrahydrofolate reductase, and folylpolyglutamate synthase play different roles in folate metabolism.

Methotrexate is an antimetabolite that hinders the activity of dihydrofolate reductase, an enzyme that is crucial for the synthesis of purines and pyrimidines. It is a significant drug that can effectively control diseases, but its side-effects can be life-threatening. Therefore, careful prescribing and close monitoring are essential. Methotrexate is commonly used to treat inflammatory arthritis, especially rheumatoid arthritis, psoriasis, and acute lymphoblastic leukaemia. However, it can cause adverse effects such as mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis.

Women should avoid pregnancy for at least six months after stopping methotrexate treatment, and men using methotrexate should use effective contraception for at least six months after treatment. Prescribing methotrexate requires familiarity with guidelines relating to its use. It is taken weekly, and FBC, U&E, and LFTs need to be regularly monitored. Folic acid 5 mg once weekly should be co-prescribed, taken more than 24 hours after methotrexate dose. The starting dose of methotrexate is 7.5 mg weekly, and only one strength of methotrexate tablet should be prescribed.

It is important to avoid prescribing trimethoprim or co-trimoxazole concurrently as it increases the risk of marrow aplasia. High-dose aspirin also increases the risk of methotrexate toxicity due to reduced excretion. In case of methotrexate toxicity, the treatment of choice is folinic acid. Overall, methotrexate is a potent drug that requires careful prescribing and monitoring to ensure its effectiveness and safety.

The correct order of contents in the tarsal tunnel, from anterior to posterior, is as follows: tibialis posterior tendon, flexor digitorum longus tendon, posterior tibial artery and vein, tibial nerve, and flexor hallucis longus tendon. Therefore, the correct answer is 3. Answers 1 and 2 are incorrect as they include the tibialis anterior tendon, which is not located in the tarsal tunnel.

The foot has two arches: the longitudinal arch and the transverse arch. The longitudinal arch is higher on the medial side and is supported by the posterior pillar of the calcaneum and the anterior pillar composed of the navicular bone, three cuneiforms, and the medial three metatarsal bones. The transverse arch is located on the anterior part of the tarsus and the posterior part of the metatarsus. The foot has several intertarsal joints, including the sub talar joint, talocalcaneonavicular joint, calcaneocuboid joint, transverse tarsal joint, cuneonavicular joint, intercuneiform joints, and cuneocuboid joint. The foot also has various ligaments, including those of the ankle joint and foot. The foot is innervated by the lateral plantar nerve and medial plantar nerve, and it receives blood supply from the plantar arteries and dorsalis pedis artery. The foot has several muscles, including the abductor hallucis, flexor digitorum brevis, abductor digit minimi, flexor hallucis brevis, adductor hallucis, and extensor digitorum brevis.

Due to the fact that the blood supply to the scaphoid enters from a small non-articular surface near its distal end, there is a risk of non-union with transverse fractures of the scaphoid.

The scaphoid bone has various articular surfaces for different bones in the wrist. It has a concave surface for the head of the capitate and a crescentic surface for the lunate. The proximal end has a wide convex surface for the radius, while the distal end has a tubercle that can be felt. The remaining articular surface faces laterally and is associated with the trapezium and trapezoid bones. The narrow strip between the radial and trapezial surfaces and the tubercle gives rise to the radial collateral carpal ligament. The tubercle also receives part of the flexor retinaculum and is the only part of the scaphoid bone that allows for the entry of blood vessels. However, this area is commonly fractured and can lead to avascular necrosis.

The patient has both osteoarthritis and rheumatoid arthritis, with the latter affecting the smaller joints of the hands and feet. Methotrexate is a commonly used immunosuppressive medication for rheumatoid arthritis, but it can cause hepatotoxicity as a significant side effect.

Although fat emboli are a potential risk after orthopaedic surgery, they usually cause neural and respiratory symptoms rather than liver damage. Additionally, the onset of fat emboli occurs within hours to days after the operation, not three months later.

While calcium channel blockers, ACE inhibitors, and opioid medications have their own side effects, they typically do not affect liver function.

Methotrexate is an antimetabolite that hinders the activity of dihydrofolate reductase, an enzyme that is crucial for the synthesis of purines and pyrimidines. It is a significant drug that can effectively control diseases, but its side-effects can be life-threatening. Therefore, careful prescribing and close monitoring are essential. Methotrexate is commonly used to treat inflammatory arthritis, especially rheumatoid arthritis, psoriasis, and acute lymphoblastic leukaemia. However, it can cause adverse effects such as mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis.

Women should avoid pregnancy for at least six months after stopping methotrexate treatment, and men using methotrexate should use effective contraception for at least six months after treatment. Prescribing methotrexate requires familiarity with guidelines relating to its use. It is taken weekly, and FBC, U&E, and LFTs need to be regularly monitored. Folic acid 5 mg once weekly should be co-prescribed, taken more than 24 hours after methotrexate dose. The starting dose of methotrexate is 7.5 mg weekly, and only one strength of methotrexate tablet should be prescribed.

It is important to avoid prescribing trimethoprim or co-trimoxazole concurrently as it increases the risk of marrow aplasia. High-dose aspirin also increases the risk of methotrexate toxicity due to reduced excretion. In case of methotrexate toxicity, the treatment of choice is folinic acid. Overall, methotrexate is a potent drug that requires careful prescribing and monitoring to ensure its effectiveness and safety.

The nerve that passes through the quadrangular space is the axillary nerve. The dorsal scapular nerve supplies the rhomboids and levator scapulae muscles, while the musculocutaneous nerve innervates the muscles of the anterior compartment of the arm and provides sensory innervation to the lateral surface of the forearm. The radial nerve passes through the triangular interval in the arm and supplies the posterior compartment of the arm. The suprascapular nerve passes through the suprascapular notch and supplies the supraspinatus and infraspinatus muscles. Quadrangular space syndrome involves compression of the axillary nerve and posterior circumflex artery as they pass through the quadrangular space, and can cause shoulder pain and deltoid muscle wasting.

Anatomy of the Axilla

The axilla, also known as the armpit, is a region of the body that contains important structures such as nerves, veins, and lymph nodes. It is bounded medially by the chest wall and serratus anterior, laterally by the humeral head, and anteriorly by the lateral border of the pectoralis major. The floor of the axilla is formed by the subscapularis muscle, while the clavipectoral fascia forms its fascial boundary.

One of the important nerves that passes through the axilla is the long thoracic nerve, which supplies the serratus anterior muscle. The thoracodorsal nerve and trunk, on the other hand, innervate and vascularize the latissimus dorsi muscle. The axillary vein, which is the continuation of the basilic vein, lies at the apex of the axilla and becomes the subclavian vein at the outer border of the first rib. The intercostobrachial nerves, which provide cutaneous sensation to the axillary skin, traverse the axillary lymph nodes and are often divided during axillary surgery.

The axilla is also an important site of lymphatic drainage for the breast. Therefore, any pathology or surgery involving the breast can affect the lymphatic drainage of the axilla and lead to lymphedema. Understanding the anatomy of the axilla is crucial for healthcare professionals who perform procedures in this region, as damage to any of the structures can lead to significant complications.

Frozen shoulder is caused by inflammation of the shoulder capsule, leading to pain and reduced range of movement. Other conditions that can cause shoulder pain include biceps tendonitis, shoulder arthritis, and glenoid labrum tears.

Adhesive capsulitis, also known as frozen shoulder, is a common cause of shoulder pain that is more prevalent in middle-aged women. The exact cause of this condition is not fully understood. It is associated with diabetes mellitus, with up to 20% of diabetics experiencing an episode of frozen shoulder. Symptoms typically develop over a few days and affect external rotation more than internal rotation or abduction. Both active and passive movement are affected, and patients usually experience a painful freezing phase, an adhesive phase, and a recovery phase. Bilateral frozen shoulder occurs in up to 20% of patients, and the episode typically lasts between 6 months and 2 years.

The diagnosis of frozen shoulder is usually made based on clinical presentation, although imaging may be necessary for atypical or persistent symptoms. There is no single intervention that has been proven to improve long-term outcomes. Treatment options include nonsteroidal anti-inflammatory drugs (NSAIDs), physiotherapy, oral corticosteroids, and intra-articular corticosteroids. It is important to note that the management of frozen shoulder should be tailored to the individual patient, and a multidisciplinary approach may be necessary for optimal outcomes.

The Koebner phenomenon is a term used to describe the appearance of skin lesions at the site of injury. Patients with a history of psoriasis and recent skin trauma are at risk of developing this phenomenon, which can also occur in individuals with other skin conditions like warts and vitiligo. Lichen planus is another condition where the Koebner phenomenon is observed. In contrast, the Nikolsky phenomenon is a dermatological phenomenon seen in pemphigus vulgaris, where the epidermis can be moved over the dermis upon palpation. Psoriatic arthritis is a type of arthritis that affects some individuals with psoriasis, causing joint inflammation, pain, stiffness, and swelling.

The Koebner Phenomenon: Skin Lesions at the Site of Injury

The Koebner phenomenon refers to the occurrence of skin lesions at the site of injury. This phenomenon is commonly observed in various skin conditions such as psoriasis, vitiligo, warts, lichen planus, lichen sclerosus, and molluscum contagiosum. In other words, if a person with any of these skin conditions experiences trauma or injury to their skin, they may develop new lesions in the affected area.

This phenomenon is named after Heinrich Koebner, a German dermatologist who first described it in 1876. The exact mechanism behind the Koebner phenomenon is not fully understood, but it is believed to be related to the immune system’s response to injury. In some cases, the injury may trigger an autoimmune response, leading to the development of new lesions.

The Koebner phenomenon can be a frustrating and challenging aspect of managing skin conditions. It is important for individuals with these conditions to take precautions to avoid injury to their skin, such as wearing protective clothing or avoiding activities that may cause trauma. Additionally, prompt treatment of any new lesions that develop can help prevent further spread of the condition.

Understanding Pellagra: Symptoms and Causes

Pellagra is a condition that results from a deficiency of nicotinic acid, also known as niacin. The classic symptoms of pellagra are commonly referred to as the 3 D’s: dermatitis, diarrhoea, and dementia. Dermatitis is characterized by a scaly, brown rash that appears on sun-exposed areas of the skin, often forming a necklace-like pattern around the neck known as Casal’s necklace. Diarrhoea and dementia are also common symptoms of pellagra, with patients experiencing chronic diarrhoea and cognitive impairment, including depression and confusion.

Pellagra can occur as a result of isoniazid therapy, which inhibits the conversion of tryptophan to niacin. This condition is also more common in individuals who consume excessive amounts of alcohol. If left untreated, pellagra can be fatal. Therefore, it is important to recognize the symptoms and seek medical attention promptly. With proper treatment, including niacin supplementation and dietary changes, individuals with pellagra can recover and avoid further complications.

Although Pectineus is a hip flexor, it is not as significant as iliopsoas in this function. Its origin is the pubic bone, and it inserts into the femur. Additionally, it assists in adducting and internally rotating the thigh.

The Psoas Muscle: Origin, Insertion, Innervation, and Action

The psoas muscle is a deep-seated muscle that originates from the transverse processes of the five lumbar vertebrae and the superficial part originates from T12 and the first four lumbar vertebrae. It inserts into the lesser trochanter of the femur and is innervated by the anterior rami of L1 to L3.

The main action of the psoas muscle is flexion and external rotation of the hip. When both sides of the muscle contract, it can raise the trunk from the supine position. The psoas muscle is an important muscle for maintaining proper posture and movement, and it is often targeted in exercises such as lunges and leg lifts.

The forearm has two weight-bearing bones, the scaphoid at the wrist and the radius within the forearm. If someone falls onto outstretched hands, there is a risk of fracturing both of these bones. The shaft of the radius is particularly vulnerable as it carries the weight and takes the full compression of the fall. The ulna is more likely to fracture from stress applied to the side of the arm rather than down its length. The lunate bone at the wrist is not involved in weight-bearing.

Anatomy of the Radius Bone

The radius bone is one of the two long bones in the forearm that extends from the lateral side of the elbow to the thumb side of the wrist. It has two expanded ends, with the distal end being the larger one. The upper end of the radius bone has articular cartilage that covers the medial to lateral side and articulates with the radial notch of the ulna by the annular ligament. The biceps brachii muscle attaches to the tuberosity of the upper end.

The shaft of the radius bone has several muscle attachments. The upper third of the body has the supinator, flexor digitorum superficialis, and flexor pollicis longus muscles. The middle third of the body has the pronator teres muscle, while the lower quarter of the body has the pronator quadratus muscle and the tendon of supinator longus.

The lower end of the radius bone is quadrilateral in shape. The anterior surface is covered by the capsule of the wrist joint, while the medial surface has the head of the ulna. The lateral surface ends in the styloid process, and the posterior surface has three grooves that contain the tendons of extensor carpi radialis longus and brevis, extensor pollicis longus, and extensor indicis. Understanding the anatomy of the radius bone is crucial in diagnosing and treating injuries and conditions that affect this bone.

The muscles located in the deep posterior compartment are:

Muscular Compartments of the Lower Limb

The lower limb is composed of different muscular compartments that perform various actions. The anterior compartment includes the tibialis anterior, extensor digitorum longus, peroneus tertius, and extensor hallucis longus muscles. These muscles are innervated by the deep peroneal nerve and are responsible for dorsiflexing the ankle joint, inverting and evert the foot, and extending the toes.

The peroneal compartment, on the other hand, consists of the peroneus longus and peroneus brevis muscles, which are innervated by the superficial peroneal nerve. These muscles are responsible for eversion of the foot and plantar flexion of the ankle joint.

The superficial posterior compartment includes the gastrocnemius and soleus muscles, which are innervated by the tibial nerve. These muscles are responsible for plantar flexion of the foot and may also flex the knee.

Lastly, the deep posterior compartment includes the flexor digitorum longus, flexor hallucis longus, and tibialis posterior muscles, which are innervated by the tibial nerve. These muscles are responsible for flexing the toes, flexing the great toe, and plantar flexion and inversion of the foot, respectively.

Understanding the muscular compartments of the lower limb is important in diagnosing and treating injuries and conditions that affect these muscles. Proper identification and management of these conditions can help improve mobility and function of the lower limb.

Denosumab has been known to cause hypocalcaemia, which can be identified through the examination finding of facial twitching upon tapping of the face, also known as Chvostek’s sign. This is due to the drug’s ability to inhibit the formation, function, and survival of osteoclasts, which are responsible for releasing calcium into the blood through bone resorption.

On the other hand, lithium is a mood stabilizer that can cause hypercalcaemia by resetting the setpoint for PTH. However, since there is no mention of the patient being on lithium in their medical history, this is unlikely to be the cause of their condition.

Rhabdomyolysis, which can result in hypercalcaemia, is often seen in patients who have experienced falls or prolonged bed rest, particularly in geriatric wards where patients may be less mobile.

Thiazide-like diuretics, such as indapamide, can also cause hypercalcaemia by increasing urinary calcium resorption. However, this usually resolves once the diuretic is discontinued.

Finally, milk-alkali syndrome is a condition characterized by high blood calcium levels caused by excessive intake of calcium and absorbable alkali, often through dietary supplements or antacids taken to prevent osteoporosis.

Denosumab for Osteoporosis: Uses, Side Effects, and Safety Concerns

Denosumab is a human monoclonal antibody that inhibits the development of osteoclasts, the cells that break down bone tissue. It is given as a subcutaneous injection every six months to treat osteoporosis. For patients with bone metastases from solid tumors, a larger dose of 120mg may be given every four weeks to prevent skeletal-related events. While oral bisphosphonates are still the first-line treatment for osteoporosis, denosumab may be used as a next-line drug if certain criteria are met.

The most common side effects of denosumab are dyspnea and diarrhea, occurring in about 1 in 10 patients. Other less common side effects include hypocalcemia and upper respiratory tract infections. However, doctors should be aware of the potential for atypical femoral fractures in patients taking denosumab and should monitor for unusual thigh, hip, or groin pain.

Overall, denosumab is generally well-tolerated and may have an increasing role in the management of osteoporosis, particularly in light of recent safety concerns regarding other next-line drugs. However, as with any medication, doctors should carefully consider the risks and benefits for each individual patient.

Azathioprine is utilized for treating Crohn’s disease in this patient, and it is likely that the drug is metabolized into mercaptopurine, an active compound that acts as a purine analogue and inhibits purine synthesis.

In the purine catabolism pathway, inosine is produced when AMP is deaminated by adenylate (AMP) deaminase to form IMP. Inosine is then formed by hydrolysis of IMP with nucleotidase.

Hypoxanthine is also produced in the purine catabolism pathway through the phosphorylation of inosine. Xanthine is formed when hypoxanthine is oxidized by xanthine oxidase.

The answer purine is incorrect because azathioprine does not convert into purines, but rather it inhibits their synthesis.

Azathioprine is a medication that is converted into mercaptopurine, which is an active compound that inhibits the production of purine. To determine if someone is at risk for azathioprine toxicity, a test for thiopurine methyltransferase (TPMT) may be necessary. Adverse effects of this medication include bone marrow depression, nausea and vomiting, pancreatitis, and an increased risk of non-melanoma skin cancer. If infection or bleeding occurs, a full blood count should be considered. It is important to note that there may be a significant interaction between azathioprine and allopurinol, so lower doses of azathioprine should be used. However, azathioprine is generally considered safe to use during pregnancy.

Antihistamines for Allergic Rhinitis and Urticaria

Antihistamines, specifically H1 inhibitors, are effective in treating allergic rhinitis and urticaria. Sedating antihistamines like chlorpheniramine have antimuscarinic properties that can cause dry mouth and urinary retention. On the other hand, non-sedating antihistamines like loratadine and cetirizine are less likely to cause drowsiness. However, there is some evidence that cetirizine may still cause some level of drowsiness compared to other non-sedating antihistamines. Overall, antihistamines are a valuable treatment option for those suffering from allergic rhinitis and urticaria.

Gout is commonly associated with Lesch-Nyhan syndrome, an inherited enzyme deficiency also known as ‘juvenile gout’. This condition is also characterized by self-injuring behavior, cognitive impairment, and nervous system impairment. However, juvenile idiopathic arthritis and osteoarthritis, which also cause joint pain and swelling, are not strongly linked to gout. On the other hand, pseudogout is associated with hyperparathyroidism.

Predisposing Factors for Gout

Gout is a type of synovitis caused by the accumulation of monosodium urate monohydrate in the synovium. This condition is triggered by chronic hyperuricaemia, which is characterized by uric acid levels exceeding 0.45 mmol/l. There are two main factors that contribute to the development of hyperuricaemia: decreased excretion of uric acid and increased production of uric acid.

Decreased excretion of uric acid can be caused by various factors, including the use of diuretics, chronic kidney disease, and lead toxicity. On the other hand, increased production of uric acid can be triggered by myeloproliferative/lymphoproliferative disorders, cytotoxic drugs, and severe psoriasis.

In rare cases, gout can also be caused by genetic disorders such as Lesch-Nyhan syndrome, which is characterized by hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency. This condition is x-linked recessive, which means it is only seen in boys. Lesch-Nyhan syndrome is associated with gout, renal failure, neurological deficits, learning difficulties, and self-mutilation.

It is worth noting that aspirin in low doses (75-150mg) is not believed to have a significant impact on plasma urate levels. Therefore, the British Society for Rheumatology recommends that it should be continued if necessary for cardiovascular prophylaxis.

If the superior gluteal nerve is damaged, it will cause a Trendelenburg gait.

The Trendelenburg Test: Assessing Gluteal Nerve Function

The Trendelenburg test is a diagnostic tool used to assess the function of the superior gluteal nerve. This nerve is responsible for the contraction of the gluteus medius muscle, which is essential for maintaining balance and stability while standing on one leg.

When the superior gluteal nerve is injured or damaged, the gluteus medius muscle is weakened, resulting in a compensatory shift of the body towards the unaffected side. This shift is characterized by a gravitational shift, which causes the body to be supported on the unaffected limb.

To perform the Trendelenburg test, the patient is asked to stand on one leg while the physician observes the position of the pelvis. In a healthy individual, the gluteus medius muscle contracts as soon as the contralateral leg leaves the floor, preventing the pelvis from dipping towards the unsupported side. However, in a person with paralysis of the superior gluteal nerve, the pelvis on the unsupported side descends, indicating that the gluteus medius on the affected side is weak or non-functional. This is known as a positive Trendelenburg test.

It is important to note that the Trendelenburg test is also used in vascular investigations to determine the presence of saphenofemoral incompetence. In this case, tourniquets are placed around the upper thigh to assess blood flow. However, in the context of assessing gluteal nerve function, the Trendelenburg test is a valuable tool for diagnosing and treating motor deficits and gait abnormalities.

Golimumab is classified as a TNF alpha antagonist, which inhibits the action of tumour necrosis factor. It is prescribed for the treatment of ankylosing spondylitis and is administered subcutaneously every four weeks. Rituximab is an example of a CD20 antagonist, used for the management of rheumatoid arthritis and certain types of blood cancer. CD38 antagonists, such as daratumumab, are being studied in clinical trials and are currently used for the treatment of multiple myeloma. Anakinra is an interleukin-1 inhibitor used for rheumatoid arthritis, while secukinumab is an interleukin-17A inhibitor licensed for the treatment of ankylosing spondylitis under specialist use.

Understanding Tumour Necrosis Factor and its Inhibitors

Tumour necrosis factor (TNF) is a cytokine that plays a crucial role in the immune system. It is mainly secreted by macrophages and has various effects on the immune system, such as activating macrophages and neutrophils, acting as a costimulator for T cell activation, and mediating the body’s response to Gram-negative septicaemia. TNF also has anti-tumour effects and binds to both the p55 and p75 receptor, inducing apoptosis and activating NFkB.

TNF has endothelial effects, including increased expression of selectins and production of platelet activating factor, IL-1, and prostaglandins. It also promotes the proliferation of fibroblasts and their production of protease and collagenase. TNF inhibitors are used to treat inflammatory conditions such as rheumatoid arthritis and Crohn’s disease. Examples of TNF inhibitors include infliximab, etanercept, adalimumab, and golimumab.

Infliximab is also used to treat active Crohn’s disease unresponsive to steroids. However, TNF blockers can have adverse effects such as reactivation of latent tuberculosis and demyelination. Understanding TNF and its inhibitors is crucial in the treatment of various inflammatory conditions.

The deep peroneal nerve is in the front compartment and the tibial nerve is on the inner side. The tibial nerve is located beneath the flexor retinaculum at its end.

Anatomy of the Posterior Tibial Artery

The posterior tibial artery is a major branch of the popliteal artery that terminates by dividing into the medial and lateral plantar arteries. It is accompanied by two veins throughout its length and its position corresponds to a line drawn from the lower angle of the popliteal fossa to a point midway between the medial malleolus and the most prominent part of the heel.

The artery is located anteriorly to the tibialis posterior and flexor digitorum longus muscles, and posteriorly to the surface of the tibia and ankle joint. The posterior tibial nerve is located 2.5 cm distal to its origin. The proximal part of the artery is covered by the gastrocnemius and soleus muscles, while the distal part is covered by skin and fascia. The artery is also covered by the fascia overlying the deep muscular layer.

Understanding the anatomy of the posterior tibial artery is important for medical professionals, as it plays a crucial role in the blood supply to the foot and ankle. Any damage or blockage to this artery can lead to serious complications, such as peripheral artery disease or even amputation.

The hamstring muscle group consists of three muscles: the biceps femoris, which is located on the lateral side, and the semitendinosus and semimembranosus, which are located on the medial side. While less common, it is possible for the gastrocnemius and soleus muscles to also experience a rupture.

The Biceps Femoris Muscle

The biceps femoris is a muscle located in the posterior upper thigh and is part of the hamstring group of muscles. It consists of two heads: the long head and the short head. The long head originates from the ischial tuberosity and inserts into the fibular head. Its actions include knee flexion, lateral rotation of the tibia, and extension of the hip. It is innervated by the tibial division of the sciatic nerve and supplied by the profunda femoris artery, inferior gluteal artery, and the superior muscular branches of the popliteal artery.

On the other hand, the short head originates from the lateral lip of the linea aspera and the lateral supracondylar ridge of the femur. It also inserts into the fibular head and is responsible for knee flexion and lateral rotation of the tibia. It is innervated by the common peroneal division of the sciatic nerve and supplied by the same arteries as the long head.

Understanding the anatomy and function of the biceps femoris muscle is important in the diagnosis and treatment of injuries and conditions affecting the posterior thigh.

Patients who have non-displaced or incomplete fractures of the neck of the femur may be able to bear weight.

Hip fractures are a common occurrence, particularly in elderly women with osteoporosis. The femoral head’s blood supply runs up the neck, making avascular necrosis a risk in displaced fractures. Symptoms include pain and a shortened and externally rotated leg. Patients with non-displaced or incomplete neck of femur fractures may still be able to bear weight. Hip fractures are classified based on their location, either intracapsular or extracapsular. The Garden system is a commonly used classification system that categorizes fractures into four types based on stability and displacement. Blood supply disruption is most common in Types III and IV.

Undisplaced intracapsular fractures can be treated with internal fixation or hemiarthroplasty if the patient is unfit. Displaced fractures require replacement arthroplasty, with total hip replacement being preferred over hemiarthroplasty if the patient was able to walk independently outdoors with no more than a stick, is not cognitively impaired, and is medically fit for anesthesia and the procedure. Extracapsular fractures are managed with a dynamic hip screw for stable intertrochanteric fractures and an intramedullary device for reverse oblique, transverse, or subtrochanteric fractures.

The anterior compartment contains the quadriceps femoris.

Fascial Compartments of the Leg

The leg is divided into compartments by fascial septae, which are thin layers of connective tissue. In the thigh, there are three compartments: the anterior, medial, and posterior compartments. The anterior compartment contains the femoral nerve and artery, as well as the quadriceps femoris muscle group. The medial compartment contains the obturator nerve and artery, as well as the adductor muscles and gracilis muscle. The posterior compartment contains the sciatic nerve and branches of the profunda femoris artery, as well as the hamstrings muscle group.

In the lower leg, there are four compartments: the anterior, posterior (divided into deep and superficial compartments), lateral, and deep posterior compartments. The anterior compartment contains the deep peroneal nerve and anterior tibial artery, as well as the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius muscles. The posterior compartment contains the tibial nerve and posterior tibial artery, as well as the deep and superficial muscles. The lateral compartment contains the superficial peroneal nerve and peroneal artery, as well as the peroneus longus and brevis muscles. The deep posterior compartment contains the tibial nerve and posterior tibial artery, as well as the flexor hallucis longus, flexor digitorum longus, tibialis posterior, and popliteus muscles.

Taking aspirin while on methotrexate treatment can be dangerous as it reduces the excretion of methotrexate, leading to an increased risk of toxicity and bone marrow problems. However, some studies suggest that methotrexate may be helpful in treating severe osteoarthritis and polymyositis. All other options are incorrect.

Methotrexate is an antimetabolite that hinders the activity of dihydrofolate reductase, an enzyme that is crucial for the synthesis of purines and pyrimidines. It is a significant drug that can effectively control diseases, but its side-effects can be life-threatening. Therefore, careful prescribing and close monitoring are essential. Methotrexate is commonly used to treat inflammatory arthritis, especially rheumatoid arthritis, psoriasis, and acute lymphoblastic leukaemia. However, it can cause adverse effects such as mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis.

Women should avoid pregnancy for at least six months after stopping methotrexate treatment, and men using methotrexate should use effective contraception for at least six months after treatment. Prescribing methotrexate requires familiarity with guidelines relating to its use. It is taken weekly, and FBC, U&E, and LFTs need to be regularly monitored. Folic acid 5 mg once weekly should be co-prescribed, taken more than 24 hours after methotrexate dose. The starting dose of methotrexate is 7.5 mg weekly, and only one strength of methotrexate tablet should be prescribed.

It is important to avoid prescribing trimethoprim or co-trimoxazole concurrently as it increases the risk of marrow aplasia. High-dose aspirin also increases the risk of methotrexate toxicity due to reduced excretion. In case of methotrexate toxicity, the treatment of choice is folinic acid. Overall, methotrexate is a potent drug that requires careful prescribing and monitoring to ensure its effectiveness and safety.