<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Torticollis and explain in detail? [/INST] Torticollis, also known as wry neck, is a dystonic condition defined by an abnormal, asymmetrical head or neck position, which may be due to a variety of causes. The term torticollis is derived from the Latin words tortus for twisted and collum for neck.The most common case has no obvious cause, and the pain and difficulty with turning the head usually goes away after a few days, even without treatment in adults.

Signs and symptoms
Torticollis is a fixed or dynamic tilt, rotation, with flexion or extension of the head and/or neck.
The type of torticollis can be described depending on the positions of the head and neck.
laterocollis: the head is tipped toward the shoulder
rotational torticollis: the head rotates along the longitudinal  axis
anterocollis: forward flexion of the head and neck
retrocollis: hyperextension of head and neck backwardA combination of these movements may often be observed. Torticollis can be a disorder in itself as well as a symptom in other conditions.
Other symptoms include:
Neck pain
Occasional formation of a mass
Thickened or tight sternocleidomastoid muscle
Tenderness on the cervical spine
Tremor in head
Unequal shoulder heights
Decreased neck movement

Causes
A multitude of conditions may lead to the development of torticollis including: muscular fibrosis, congenital spine abnormalities, or toxic or traumatic brain injury.
A rough categorization discerns between congenital torticollis and acquired torticollis.Other categories include:
Osseous
Traumatic
CNS/PNS
Ocular
Non-muscular soft tissue
Spasmodic
Drug induced
Oral ties (lip and tongue ties)

Congenital muscular torticollis
The congenital muscular torticollis is the most common torticollis which is present at birth. The cause of congenital muscular torticollis is unclear. Birth trauma or intrauterine malposition is considered to be the cause of damage to the sternocleidomastoid muscle in the neck. Other alterations to the muscle tissue arise from repetitive microtrauma within the womb or a sudden change in the calcium concentration in the body which causes a prolonged period of muscle contraction.Any of these mechanisms can result in a shortening or excessive contraction of the sternocleidomastoid muscle, which curtails its range of motion in both rotation and lateral bending. The head typically is tilted in lateral bending toward the affected muscle and rotated toward the opposite side. In other words,  the head itself is tilted in the direction towards the shortened muscle with the chin tilted in the opposite direction.Congenital Torticollis is presented at 1–4 weeks of age, and a hard mass usually develops. It is normally diagnosed using ultrasonography and a colour histogram or clinically through evaluating the infants passive cervical range of motion.Congenital torticollis constitutes the majority of cases seen in clinical practice. The reported incidence of congenital torticollis is 0.3-2.0%. Sometimes a mass, such as a sternocleidomastoid tumor, is noted in the affected muscle.  Torticollis does not resolve on its own and may result in plagiocephaly.

Acquired torticollis
Noncongenital muscular torticollis may result from scarring or disease of cervical vertebrae, adenitis, tonsillitis, rheumatism, enlarged cervical glands, retropharyngeal abscess, or cerebellar tumors. It may be spasmodic (clonic) or permanent (tonic). The latter type may be due to Potts Disease (tuberculosis of the spine).
A self-limiting spontaneously occurring form of torticollis with one or more painful neck muscles is by far the most common (stiff neck) and will pass spontaneously in 1–4 weeks. Usually the sternocleidomastoid muscle or the trapezius muscle is involved. Sometimes draughts, colds, or unusual postures are implicated; however, in many cases, no clear cause is found. These episodes are commonly seen by physicians.Most commonly this self-limiting form relates to an untreated dental occlusal dysfunction, which is brought on by clenching and grinding the teeth during sleep. Once the occlusion is treated it will completely resolve. Treatment is accomplished with an occlusal appliance, and equilibration of the dentition.

Tumors of the skull base (posterior fossa tumors) can compress the nerve supply to the neck and cause torticollis, and these problems must be treated surgically.
Infections in the posterior pharynx can irritate the nerves supplying the neck muscles and cause torticollis, and these infections may be treated with antibiotics if they are not too severe, but could require surgical debridement in intractable cases.
Ear infections and surgical removal of the adenoids can cause an entity known as Grisels syndrome, a subluxation of the upper cervical joints, mostly the atlantoaxial joint, due to inflammatory laxity of the ligaments caused by an infection.
The use of certain drugs, such as antipsychotics, can cause torticollis.
Antiemetics - Neuroleptic Class - Phenothiazines
There are many other rare causes of torticollis.  A very rare cause of acquired torticollis is fibrodysplasia ossificans progressiva (FOP), the hallmark of which is malformed great toes.

Spasmodic torticollis
Torticollis with recurrent, but transient contraction of the muscles of the neck and especially of the sternocleidomastoid, is called spasmodic torticollis. Synonyms are "intermittent torticollis", "cervical dystonia" or "idiopathic cervical dystonia", depending on cause.

Trochlear torticollis
Torticollis may be unrelated to the sternocleidomastoid muscle, instead caused by damage to the trochlear nerve (fourth cranial nerve), which supplies the superior oblique muscle of the eye. The superior oblique muscle is involved in depression, abduction, and intorsion of the eye. When the trochlear nerve is damaged, the eye is extorted because the superior oblique is not functioning. The affected person will have vision problems unless they turn their head away from the side that is affected, causing intorsion of the eye and balancing out the extorsion of the eye. This can be diagnosed by the Bielschowsky test, also called the head-tilt test, where the head is turned to the affected side. A positive test occurs when the affected eye elevates, seeming to float up.

Anatomy
The underlying anatomical distortion causing torticollis is a shortened sternocleidomastoid muscle. This is the muscle of the neck that originates at the sternum and clavicle and inserts on the mastoid process of the temporal bone on the same side. There are two sternocleidomastoid muscles in the human body and when they both contract, the neck is flexed. The main blood supply for these muscles come from the occipital artery, superior thyroid artery, transverse scapular artery and transverse cervical artery. The main innervation to these muscles is from cranial nerve XI (the accessory nerve) but the second, third and fourth cervical nerves are also involved. Pathologies in these blood and nerve supplies can lead to torticollis.

Diagnosis
Evaluation of a child with torticollis begins with history taking to determine circumstances surrounding birth and any possibility of trauma or associated symptoms. Physical examination reveals decreased rotation and bending to the side opposite from the affected muscle. Some say that congenital cases more often involve the right side, but there is not complete agreement about this in published studies. Evaluation should include a thorough neurologic examination, and the possibility of associated conditions such as developmental dysplasia of the hip and clubfoot should be examined.  Radiographs of the cervical spine should be obtained to rule out obvious bony abnormality, and MRI should be considered if there is concern about structural problems or other conditions.
Ultrasonography can be used to visualize muscle tissue, with a colour histogram generated to determine cross-sectional area and thickness of the muscle.Evaluation by an optometrist or an ophthalmologist should be considered in children to ensure that the torticollis is not caused by vision problems (IV cranial nerve palsy, nystagmus-associated "null position," etc.).
Differential diagnosis for torticollis includes
Cranial nerve IV palsy
Spasmus nutans
Sandifer syndrome
Myasthenia gravis
Cerebrospinal fluid leakCervical dystonia appearing in adulthood has been believed to be idiopathic in nature, as specific imaging techniques most often find no specific cause.

Treatment
Initially, the condition is treated with physical therapies, such as stretching to release tightness, strengthening exercises to improve muscular balance, and handling to stimulate symmetry. A TOT collar is sometimes applied. Early initiation of treatment is very important for full recovery and to decrease chance of relapse.

Physical therapy
Physical therapy is an option for treating torticollis in a non-invasive and cost-effective manner. In the children above 1 year of age, surgical release of the tight sternocleidomastoid muscle is indicated along with aggressive therapy and appropriate splinting. Occupational therapy rehabilitation in Congenital muscular torticollis concentrates on observation, orthosis, gentle stretching, myofascial release techniques, parents’ counseling-training, and home exercise program. While outpatient infant physiotherapy is effective, home therapy performed by a parent or guardian is just as effective in reversing the effects of congenital torticollis. It is important for physical therapists to educate parents on the importance of their role in the treatment and to create a home treatment plan together with them for the best results for their child. Five components have been recognized as the "first choice intervention" in PT for treatment of torticollis and include neck passive range of motion, neck and trunk active range of motion, development of symmetrical movement, environmental adaptations, and caregiver education. In therapy, parents or guardians should expect their child to be provided with these important components, explained in detail below. Lateral neck flexion and overall range of motion can be regained quicker in newborns when parents conduct physical therapy exercises several times a day.Physical therapists should teach parents and guardians to perform the following exercises:
Stretching the neck and trunk muscles actively. Parents can help promote this stretching at home with infant positioning. For example, prone positioning will encourage the child to lift their chin off the ground, thereby strengthening their bilateral neck and spine extensor muscles, and stretching their neck flexor muscles. Active rotation exercises in supine, sitting or prone position by using toys, lights and sounds to attract infants attention to turn neck and look toward the non-affected side.
Stretching the muscle in a prone position passively. Passive stretching is manual, and does not include infant involvement. Two people can be involved in these stretches, one person stabilizing the infant while the other holds the head and slowly brings it through the available range of motion. Passive stretching should not be painful to the child, and should be stopped if the child resists. Also, discontinue the stretch if changes in breathing or circulation are seen or felt.
Stretching the muscle in a lateral position supported by a pillow (have infant lie on the side with the neck supported by pillow). Affected side should be against the pillow to deviate the neck towards the non-affected side.
Environmental adaptations can control posture in strollers, car seats  and swings (using U-shaped neck pillow or blankets to hold neck in neutral position)
Passive cervical rotation (much like stretching when being supported by a pillow, have affected side down)
Position infant in the crib with affected side by the wall so they must turn to the non-affected side to face outPhysical therapists often encourage parents and caregivers of children with torticollis to modify the environment to improve neck movements and position. Modifications may include:

Adding neck supports to the car seat to attain optimal neck alignment
Reducing time spent in a single position
Using toys to encourage the child to look in the direction of limited neck movement
Alternating sides when bottle or breastfeeding
Encouraging prone playtime (tummy time). Although the Back to Sleep campaign promotes infants sleeping on their backs to avoid sudden infant death syndrome during sleep, parents should still ensure that their infants spend some waking hours on their stomachs.

Microcurrent therapy
A Korean study has recently introduced an additional treatment called microcurrent therapy that may be effective in treating congenital torticollis. For this therapy to be effective the children should be under three months of age and have torticollis involving the entire sternocleidomastoid muscle with a palpable mass and a muscle thickness over 10 mm. Microcurrent therapy sends minute electrical signals into tissue to restore the normal frequencies in cells. Microcurrent therapy is completely painless and children can only feel the probe from the machine on their skin.Microcurrent therapy is thought to increase ATP and protein synthesis as well as enhance blood flow, reduce muscle spasms and decrease pain along with inflammation. It should be used in addition to regular stretching exercises and ultrasound diathermy. Ultrasound diathermy generates heat deep within body tissues to help with contractures, pain and muscle spasms as well as decrease inflammation. This combination of treatments shows remarkable outcomes in the duration of time children are kept in rehabilitation programs: Micocurrent therapy can cut the length of a rehabilitation program almost in half with a full recovery seen after 2.6 months.About 5–10% of cases fail to respond to stretching and require surgical release of the muscle.

Surgery
Surgical release involves the two heads of the sternocleidomastoid muscle being dissected free. This surgery can be minimally invasive and done laparoscopically. Usually surgery is performed on those who are over 12 months old. The surgery is for those who do not respond to physical therapy or botulinum toxin injection or have a very fibrotic sternocleidomastoid muscle. After surgery the child will be required to wear a soft neck collar (also called a Callots cast). There will be an intense physiotherapy program for 3–4 months as well as strengthening exercises for the neck muscles.Other treatments include:
Rest and analgesics for acute cases
Diazepam or other muscle relaxants
Botulinum toxin
Encouraging active movements for children 6–8 months of age
Ultrasound diathermy

Prognosis
Studies and evidence from clinical practice show that 85–90% of cases of congenital torticollis are resolved with conservative treatment such as physical therapy </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Aquarium granuloma and explain in detail? [/INST] Aquarium granuloma (also known as fish tank granuloma and swimming pool granuloma) is a rare skin condition caused by a non-tubercular mycobacterium known as Mycobacterium marinum. Skin infections with M. marinum in humans are relatively uncommon, and are usually acquired from contact with contaminated swimming pools, aquariums or infected fish.

Signs and symptoms
Aquarium granuloma presents as a slow-growing, inflamed red bump (nodule or plaque) at the site of infection. It is characterized by a painful, itchy skin lesion,  and may become ulcerated or crusted. Skin changes usually appear roughly three weeks after the aquatic exposure.If this condition is acquired from an aquarium, then often the dominant hand is affected. If this condition is acquired from a swimming pool, then symptoms can also develop on trauma-prone body zones, such as the elbows, knees, feet and tip of the nose.

Cause
For the infection to develop in humans, the two main factors required are exposure to contaminated water, and abrasion or injury to the skin. Hence, this infection is commonly seen in individuals who clean fish tanks, handle ornamental fish and work in wet fields.Aquatic systems with a high density of fish and warm waters appear to be conditions particularly favorable to this infectious agent, and increase the changes to contract fish tank granuloma. Poor water quality and various nutritional deficiencies are also possible contributing factors.Swimming pool granuloma can occur when there is inadequate chlorination of swimming pools.

Diagnosis
Aquarium granuloma is relatively nonspecific in clinical presentation. Therefore, more common skin conditions, like cellulitis, foreign body reaction, skin cancer, and fungal or parasitic infections, are often explored first. Overall, diagnosis and treatment of this rare skin infection is often delayed because of a lack of suspicion.Lab tests for finding M. marinum include cultures where a swab or sample is taken and grown in the laboratory. Cultures of M. marinum are fairly difficult to grow, and results may take several weeks. The culture may be negative, even if there is an active infection. Treatment may still be considered even if the test results are negative, especially if the patients history supports past fish or fish-tank exposure.
In the absence of positive culture results, a skin or tissue biopsy may be a helpful test to render a microscopic diagnosis. Another technique that can be used to detect the bacteria is Polymerase Chain Reaction (PCR) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hypocapnia and explain in detail? [/INST] Hypocapnia (from the Greek words υπό meaning below normal and καπνός kapnós meaning smoke), also known as hypocarbia, sometimes incorrectly called acapnia, is a state of reduced carbon dioxide in the blood. Hypocapnia usually results from deep or rapid breathing, known as hyperventilation.
Hypocapnia is the opposite of hypercapnia.

Effects
Even when marked, hypocapnia is normally well tolerated. Symptoms include tingling sensation (usually in the limbs), abnormal heartbeat, painful muscle cramps, and seizures. Acute hypocapnia causes hypocapnic alkalosis, which causes cerebral vasoconstriction leading to cerebral hypoxia, and this can cause transient dizziness, fainting, and anxiety. A low partial pressure of carbon dioxide in the blood also causes alkalosis (because CO2 is acidic in solution), leading to lowered plasma calcium ions (Hypocalcaemia), causing increased nerve and muscle excitability. This explains the other common symptoms of hyperventilation—pins and needles, muscle cramps and tetany in the extremities, especially hands and feet.Because the brain stem regulates breathing by monitoring the level of blood CO2 instead of O2, hypocapnia can suppress breathing to the point of blackout from cerebral hypoxia, as exhibited in shallow water blackout.
Hypocapnia also results in bronchoconstriction in order to decrease ventilation. This mechanism is meant to counteract hyperventilation, and decrease the amount of oxygen coming into the lungs </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Calcium pyrophosphate dihydrate crystal deposition disease and explain in detail? [/INST] Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease, also known as pseudogout and pyrophosphate arthropathy, is a rheumatologic disease which is thought to be secondary to abnormal accumulation of calcium pyrophosphate dihydrate crystals within joint soft tissues. The knee joint is most commonly affected.

Signs and symptoms
When symptomatic, the disease classically begins with symptoms that are similar to a gout attack (thus the moniker "pseudogout"). These include:
severe pain
warmth
swelling of one or more jointsThe symptoms can be monoarticular (involving a single joint) or polyarticular (involving several joints). Symptoms usually last for days to weeks, and often recur. Although any joint may be affected, the knees, wrists, and hips are most common.X-ray, CT, or other imaging usually shows accumulation of calcium within the joint cartilage, known as chondrocalcinosis. There can also be findings of osteoarthritis.  The white blood cell count is often raised.

Cause
The cause of CPPD disease is unknown. Increased breakdown of adenosine triphosphate (ATP; the molecule used as energy currency in all living things), which results in increased pyrophosphate levels in joints, is thought to be one reason why crystals may develop.Familial forms are rare. One genetic study found an association between CPPD and a region of chromosome 8q.The gene ANKH is involved in crystal-related inflammatory reactions and inorganic phosphate transport.

Diagnosis
The disease is defined by presence of joint inflammation and the presence of CPPD crystals within the joint. The crystals are usually detected by imaging and/or joint fluid analysis.

Medical imaging, consisting of x-ray, CT, MRI, or ultrasound may detect chondrocalcinosis within the affected joint, indicating a substantial amount of calcium crystal deposition within the cartilage or ligaments. Ultrasound is a reliable method to diagnose CPPD. Using ultrasound, chondrocalcinosis may be depicted as echogenic foci with no acoustic shadow within the hyaline cartilage or fibrocartilage.  By x-ray, CPPD can appear similar to other diseases such as ankylosing spondylitis and gout.

Arthrocentesis, or removing synovial fluid from the affected joint, is performed to test the synovial fluid for the calcium pyrophosphate crystals that are present in CPPD. When stained with H&E stain, calcium pyrophosphate crystals appears deeply blue ("basophilic"). However, CPP crystals are much better known for their rhomboid shape and weak positive birefringence on polarized light microscopy, and this method remains the most reliable method of identifying the crystals under the microscope. However, even this method has poor sensitivity, specificity, and inter-operator agreement.These two modalities currently define CPPD disease, but lack diagnostic accuracy. Thus, the diagnosis of CPPD disease is potentially epiphenomenological.

Treatment
Because any medication that could reduce the inflammation of CPPD bears a risk of causing organ damage, treatment is not advised if the condition is not causing pain.
For acute pseudogout, treatments include intra-articular corticosteroid injection, systemic corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), or, on occasion, high-dose colchicine. In general, NSAIDs are administered in low doses to help prevent CPPD </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Splenogonadal fusion and explain in detail? [/INST] Splenogonadal fusion is a rare congenital malformation that results from an abnormal connection between the primitive spleen and gonad during gestation. A portion of the splenic tissue then descends with the gonad.  Splenogonadal fusion has been classified into two types: continuous, where there remains a connection between the main spleen and gonad; and discontinuous, where ectopic splenic tissue is attached to the gonad, but there is no connection to the orthotopic spleen. Patients can also be have an accessory spleen. Patients with continuous splenogonadal fusion frequently have additional congenital abnormalities including limb defects, micrognathia, skull anomalies, Spina bifida, cardiac defects, anorectal abnormalities, and most commonly cryptorchidism.  Terminal limb defects have been documented in at least 25 cases which makes up a separate diagnosis of splenogonadal fusion limb defect (SGFLD) syndrome.
The anomaly was first described in 1883 by Bostroem.  Since then more than 150 cases of splenogonadal fusion have been documented, predominantly in males.  The condition is considered benign.  A few cases of testicular neoplasm have been reported in association with splenogonadal fusion.  The reported cases have occurred in patients with a history of cryptorchidism, which is associated with an elevated risk of neoplasm.Splenogonadal fusion occurs with a male-to-female ratio of 16:1, and is seen nearly exclusively on the left side. The condition remains a diagnostic challenge, but preoperative consideration of the diagnosis and use of ultrasound may help avoid unnecessary orchiectomy. The presence of splenic tissue may be confirmed with a technetium-99m sulfur colloid scan.

Classification
Splenogonadal fusion is separated into two types:

Continuous (55%): The native spleen is connected to the gonad. The connection occurs through a cord of splenic tissue or fibrous band.
Discontinuous (45%): Ectopic splenic tissue is present and attached to the gonad. An accessory spleen is present and the native spleen lacks the direct attachment to the gonad.

Pathogenesis
The cause of splenogonadal fusion is still unclear, and there are several proposed mechanisms. A developmental field defect that occurs during blastogenesis is the current explanation of pathogenesis. The spleen derives from mesenchymal tissue and an inappropriate fusion can happen between the gonadal ridge during gut rotation, which occurs between weeks 5 and 8 of fetal life. Splenogonadal fusion may result from an unknown teratogenic insult. The timing of this insult may correlate to the severity of associated defects. There is also postulation that fusion may occur due to adhesion after an inflammatory response or a lack of apoptosis between the structures. Siblings documented to have splenogonadal fusion and an accessory spleen provides additional evidence of a possible genetic component.

Associated Conditions
Additional congenital abnormalities are most often found associated with the continuous type of splenogonadal fusion. These abnormalities include micrognathia, macroglossia, anal atresia, and pulmonary hypoplasia. The most commonly associated malformation is cryptorchidism. When limb abnormalities occur, Splenogonadal Fusion with Limb Defects is made as a separate diagnosis. Splenogonadal Fusion with Limb Defects is also of unknown cause but some literature suggests that the condition may be related to Hanhart syndrome and facial femoral syndrome. Splenogonadal fusion has also been identified in infants with Möbius syndrome and Poland syndrome.

Diagnosis
Diagnosis can be challenging pre-operatively, as patients are commonly asymptomatic. Physical examination can aid in diagnosis if the mass is palpated, but further confirmatory tests are necessary. Females are reportedly less affected by splenogonadal fusion, though it is possible that the condition is underdiagnosed due to the difficulty of internal gonad examination in females. On scrotal ultrasound, ectopic splenic tissue may appear as an encapsulated homogeneous extratesticular mass, isoechoic with the normal testis. Subtle hypoechoic nodules may be present in the mass. Limitations of doppler ultrasonography include visualizing the nonspecific paratesticular masses which can mimic malignancies such as rhabdomyosarcoma or embryonal sarcoma. Technetium-99m sulfur colloid scan is sensitive to target the liver, spleen, and bone marrow, therefore the scans can be used to identify ectopic splenic tissue when clinical suspicion is high. When technetium-99m sulfur colloid scans are not included in a patients diagnostic workup, the diagnosis is often not made until the surgeon performs an abdominal exploration using laparoscopy which can visualize the splenic tissue grossly. Evaluation by biopsy including frozen section procedure is confirmatory for splenogonadal fusion </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Olecranon bursitis and explain in detail? [/INST] Olecranon bursitis is a condition characterized by swelling, redness, and pain at the tip of the elbow. If the underlying cause is due to an infection, fever may be present. The condition is relatively common and is one of the most frequent types of bursitis.It usually occurs as a result of trauma or pressure to the elbow, infection, or certain medical conditions such as rheumatoid arthritis or gout. Olecranon bursitis is associated with certain types of work including plumbing, mining, gardening, and mechanics. The underlying mechanism is inflammation of the fluid filled sac between the olecranon and skin. Diagnosis is usually based on symptoms.Treatment involves avoiding further trauma, a compression bandage, and NSAIDs. If there is concern of infection the fluid should be drained and tested and antibiotics are typically recommended. The use of steroid injections is controversial. Surgery may be done if other measures are not effective.

Signs and symptoms
Symptoms include swelling in the elbow, which can sometimes be large enough to restrict motion. There is pain originating in the elbow joint from mild to severe which can spread to the rest of the arm.
If the bursa is infected, there also will be prominent redness and the skin will feel very warm. Another symptom would include the infected bursa possibly opening spontaneously and draining pus.

Causes
Bursitis normally develops as a result either of a single injury to the elbow (for example, a hard blow to the tip of the elbow), or perhaps more commonly due to repeated minor injuries, such as repeated leaning on the point of the elbow on a hard surface. The chance of developing bursitis is higher if ones job or hobby involves a repetitive movement (for example, tennis, golf, or even repetitive computer work involving leaning on ones elbow). The likelihood of developing the condition is increased as one gets older.As a reaction to injury, the lining of the bursa becomes inflamed. It then secretes a much greater than normal amount of fluid into the closed cavity of the bursa, from where it has nowhere to go. The bursa therefore inflates, producing a swelling over the proximal end of the ulna which is usually inflamed and tender.Another possible cause of inflammation of the bursa is infection, which can usually (but not always) be traced to a crack or other lesion in the skin which allowed for bacteria of the normal skin flora to invade deeper layers of tissue.This bursa is located just over the extensor aspect of the extreme proximal end of the ulna </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Lymphangitis and explain in detail? [/INST] Lymphangitis is an inflammation or an infection of the lymphatic channels that occurs as a result of infection at a site distal to the channel. The most common cause of lymphangitis in humans is Streptococcus pyogenes (Group A strep), hemolytic streptococci, and in some cases, mononucleosis, cytomegalovirus, tuberculosis, syphilis, and the fungus Sporothrix schenckii.  Lymphangitis is sometimes mistakenly called "blood poisoning". In reality, "blood poisoning" is synonymous with sepsis.
Lymphatic vessels are smaller than capillaries and tiny venules and are ubiquitous in the body. These vessels are fitted with valves to direct flow in only one direction. Fluid diffusing through the thin-walled small capillaries should be collected and the lymphatic system does just that: a fluid rich in protein, minerals, nutrients, and other substances useful for tissue growth. As well as essential nutrients, the lymphatic system can also transport or carry cancer cells, defective or damaged cells, and pathogens such as bacteria and viruses, as well as foreign bodies and organisms. The lymph nodes are found in close proximity to unique white blood cells that engulf or metabolize pathogens (bacteria and viruses) and defective or cancerous cells, preventing infections and malignant cancer cells from spreading.
 Infection spreads out of the wound site to enter the lymphatic system. The wound may be small or it may be an abscess constantly feeding bacteria into the lymphatic system. After infection, lymph nodes enlarge. Ear, skin, nose, and eye infections can spread into the lymphatic system. Red streaks in the skin along the direction of regional lymph nodes indicate lymphatic involvement. Infection may spread within hours and can cause sepsis and death.

Symptoms and signs
Warm skin over site of infection. The person may also have chills and a high fever - between 38 and 40 degrees Celsius - along with moderate throbbing pain and swelling. The red streaks can be clearly outlined and demarcated or just barely visible, particularly in dark-skinned patients. Malaise, tenderness at the site of infection, skin ulcers (a rare symptom of lymphangitis), rapid pulse, and enlarged, swollen, and tender lymph nodes are also seen. Appetite loss has been documented with the presence of inflammation (inflammation-associated anorexia), but it is unclear whether appetite loss seen in patients with lymphangitis leads to weight loss; in cases that develop after lymphedema—which can be upwards of 8.14% of the time—weight gain has actually been documented.If these symptoms are absent, it is suggestive of other underlying disorders such as tuberculosis, lymphoma, or Hodgkin’s disease. A person with lymphangitis should be hospitalized and closely monitored by medical professionals </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Cholesterol embolism and explain in detail? [/INST] Cholesterol embolism occurs when cholesterol is released, usually from an atherosclerotic plaque, and travels as an embolus in the bloodstream to lodge (as an embolism) causing an obstruction in blood vessels further away. Most commonly this causes skin symptoms (usually livedo reticularis), gangrene of the extremities and sometimes kidney failure; problems with other organs may arise, depending on the site at which the cholesterol crystals enter the bloodstream. When the kidneys are involved, the disease is referred to as atheroembolic renal disease. The diagnosis usually involves biopsy (removing a tissue sample) from an affected organ. Cholesterol embolism is treated by removing the cause and giving supportive therapy; statin drugs have been found to improve the prognosis.

Signs and symptoms
The symptoms experienced in cholesterol embolism depend largely on the organ involved. Non-specific symptoms often described are fever, muscle ache and weight loss. Embolism to the legs causes a mottled appearance and purple discoloration of the toes, small infarcts and areas of gangrene due to tissue death that usually appear black, and areas of the skin that assume a marbled pattern known as livedo reticularis. The pain is usually severe and requires opiates. If the ulcerated plaque is below the renal arteries the manifestations appear in both lower extremities. Very rarely the ulcerated plaque is below the aortic bifurcation and those cases the changes occur only in one lower extremity.Kidney involvement leads to the symptoms of kidney failure, which are non-specific but usually cause nausea, reduced appetite (anorexia), raised blood pressure (hypertension), and occasionally the various symptoms of electrolyte disturbance such as an irregular heartbeat. Some patients report hematuria (bloody urine) but this may only be detectable on microscopic examination of the urine. Increased amounts of protein in the urine may cause edema (swelling) of the skin (a combination of symptoms known as nephrotic syndrome).If emboli have spread to the digestive tract, reduced appetite, nausea and vomiting may occur, as well as nonspecific abdominal pain, gastrointestinal hemorrhage (vomiting blood, or admixture of blood in the stool), and occasionally acute pancreatitis (inflammation of the pancreas).Both the central nervous system (brain and spinal cord) and the peripheral nervous system may be involved. Emboli to the brain may cause stroke-like episodes, headache and episodes of loss of vision in one eye (known as amaurosis fugax). Emboli to the eye can be seen by ophthalmoscopy and are known as plaques of Hollenhorst. Emboli to the spinal cord may cause paraparesis (decreased power in the legs) or cauda equina syndrome, a group of symptoms due to loss of function of the distal part of the spinal cord – loss of control over the bladder, rectum and skin sensation around the anus. If the blood supply to a single nerve is interrupted by an embolus, the result is loss of function in the muscles supplied by that nerve; this phenomenon is called a mononeuropathy.

Causes
It is relatively unusual (25% of the total number of cases) for cholesterol emboli to occur spontaneously; this usually happens in people with severe atherosclerosis of the large arteries such as the aorta. In the other 75% it is a complication of medical procedures involving the blood vessels, such as vascular surgery or angiography. In coronary catheterization, for instance, the incidence is 1.4%. Furthermore, cholesterol embolism may develop after the commencement of anticoagulants or thrombolytic medication that decrease blood clotting or dissolve blood clots, respectively. They probably lead to cholesterol emboli by removing blood clots that cover up a damaged atherosclerotic plaque; cholesterol-rich debris can then enter the bloodstream.

Diagnosis
Differential diagnosis
Findings on general investigations (such as blood tests) are not specific for cholesterol embolism, which makes diagnosis difficult. The main problem is the distinction between cholesterol embolism and vasculitis (inflammation of the small blood vessels), which may cause very similar symptoms - especially the skin findings and the kidney dysfunction. Worsening kidney function after an angiogram may also be attributed to kidney damage by substances used during the procedure (contrast nephropathy). Other causes that may lead to similar symptoms include ischemic kidney failure (kidney dysfunction due to an interrupted blood supply), a group of diseases known as thrombotic microangiopathies and endocarditis (infection of the heart valves with small clumps of infected tissue embolizing through the body).

Blood and urine
Tests for inflammation (C-reactive protein and the erythrocyte sedimentation rate) are typically elevated, and abnormal liver enzymes may be seen. If the kidneys are involved, tests of kidney function (such as urea and creatinine) are elevated. The complete blood count may show particularly high numbers of a type of white blood cell known as eosinophils (more than 0.5 billion per liter); this occurs in only 60-80% of cases, so normal eosinophil counts do not rule out the diagnosis. Examination of the urine may show red blood cells (occasionally in casts as seen under the microscope) and increased levels of protein; in a third of the cases with kidney involvement, eosinophils can also be detected in the urine. If vasculitis is suspected, complement levels may be determined as reduced levels are often encountered in vasculitis; complement is a group of proteins that forms part of the innate immune system. Complement levels are frequently reduced in cholesterol embolism, limiting the use of this test in the distinction between vasculitis and cholesterol embolism.

Tissue diagnosis
The microscopic examination of tissue (histology) gives the definitive diagnosis.  The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax). The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.The sensitivity of small core biopsies is modest, due to sampling error, as the process is often patchy </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Band keratopathy and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Splenosis and explain in detail? [/INST] Splenosis is the result of spleen tissue breaking off the main organ and implanting at another site inside the body.  This is called heterotopic autotransplantation of the spleen.  It most commonly occurs as a result of traumatic splenic rupture or abdominal surgery. Depending on the location of the spleen, the new piece usually implants in another part of the abdominal cavity (including the pelvic cavity).  Single case reports also describe splenosis in the thoracic cavity, in subcutaneous tissue, in the liver or in the cranial cavity. Splenosis must be distinguished from the presence of additional spleens, which are innate and are the result of differences in embryological development. Additionally, splenosis must be differentiated from malignant tumors which may look similar when imaged.

History
Ectopic splenic tissue was first described in 1896 by Albrecht in Germany, whereas the term “splenosis” was first used by Buchbinder and Lipkoffin to describe their findings in 1939

Cause
A necessary requirement for splenosis is the rupture of the spleen, through a traumatic injury (such as a car wreck) or abdominal surgery, especially splenectomy. Splenosis in the abdominal category may occur in up to 65% of traumatic ruptures of the spleen. Splenosis in the thoracic cavity is rarer, because it requires the simultaneous rupture of the diaphragm. The implantation of spleen tissue under the skin may result from abdominal surgery or gunshot wounds.  Splenosis of the brain or liver is hypothesized to be the result of tiny pieces of spleen tissue traveling through the bloodstream.

Pathology
Macroscopically, splenosis manifests as individual pieces of reddish-blue tissue with variable shape, which can be as few as one and as many as 300, mostly in the abdominal cavity, and varying in size from a few millimeters to as large as 12 cm.  Due to the limited blood supply to these nodules, the typical size of splenic implants is usually less than 3 cm </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Mismatch repair cancer syndrome and explain in detail? [/INST] Mismatch repair cancer syndrome (MMRCS) is a cancer syndrome associated with biallelic DNA mismatch repair mutations. It is also known as Turcot syndrome (after Jacques Turcot, who described the condition in 1959) and by several other names.In MMRCS, neoplasia typically occurs in both the gut and the central nervous system (CNS) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Actinic granuloma and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Human serum albumin and explain in detail? [/INST] Human serum albumin is the serum albumin found in human blood. It is the most abundant protein in human blood plasma; it constitutes about half of serum protein. It is produced in the liver. It is soluble in water, and it is monomeric.Albumin transports hormones, fatty acids, and other compounds, buffers pH, and maintains oncotic pressure, among other functions.
Albumin is synthesized in the liver as preproalbumin, which has an N-terminal peptide that is removed before the nascent protein is released from the rough endoplasmic reticulum. The product, proalbumin, is in turn cleaved in the Golgi apparatus to produce the secreted albumin.
The reference range for albumin concentrations in serum is approximately 35–50 g/L (3.5–5.0 g/dL).  It has a serum half-life of approximately 21 days. It has a molecular mass of 66.5 kDa.
The gene for albumin is located on chromosome 4 in locus 4q13.3 and mutations in this gene can result in anomalous proteins. The human albumin gene is 16,961 nucleotides long from the putative cap site to the first poly(A) addition site. It is split into 15 exons that are symmetrically placed within the 3 domains thought to have arisen by triplication of a single primordial domain.
Human serum albumin (HSA) is a highly water-soluble globular monomeric plasma protein with a relative molecular weight of 67 KDa, consisting of 585 amino acid residues, one sulfhydryl group and 17 disulfide bridges. Among nanoparticulate carriers, HSA nanoparticles have long been the center of attention in the pharmaceutical industry due to their ability to bind to various drug molecules, great stability during storage and in vivo usage, no toxicity and antigenicity, biodegradability, reproducibility, scale up of the production process and a better control over release properties. In addition, significant amounts of drug can be incorporated into the particle matrix because of the large number of drug binding sites on the albumin molecule.

Function
Maintains oncotic pressure
Transports thyroid hormones
Transports other hormones, in particular, ones that are fat-soluble
Transports fatty acids ("free" fatty acids) to the liver and to myocytes for utilization of energy
Transports unconjugated bilirubin
Transports many drugs; serum albumin levels can affect the half-life of drugs.  Competition between drugs for albumin binding sites may cause drug interaction by increasing the free fraction of one of the drugs, thereby affecting potency.
Competitively binds calcium ions (Ca2+)
Serum albumin, as a negative acute-phase protein, is down-regulated in inflammatory states. As such, it is not a valid marker of nutritional status; rather, it is a marker of an inflammatory state
Prevents photodegradation of folic acid
Prevent pathogenic effects of Clostridioides difficile toxins

Measurement
Serum albumin is commonly measured by recording the change in absorbance upon binding to a dye such as bromocresol green or bromocresol purple.

Reference ranges
The normal range of human serum albumin in adults (> 3 y.o.) is 3.5–5.0  g/dL (35–50 g/L). For children less than three years of age, the normal range is broader, 2.9–5.5 g/dL.Low albumin (hypoalbuminemia) may be caused by liver disease, nephrotic syndrome, burns, protein-losing enteropathy, malabsorption, malnutrition, late pregnancy, artefact, genetic variations and malignancy.High albumin (hyperalbuminemia) is almost always caused by dehydration. In some cases of retinol (Vitamin A) deficiency, the albumin level can be elevated to high-normal values (e.g., 4.9 g/dL) because retinol causes cells to swell with water. (This is also the reason too much Vitamin A is toxic.)
This swelling also likely occurs during treatment with 13-cis retinoic acid (isotretnoin), a pharmaceutical for treating severe acne, amongst other conditions. In lab experiments it has been shown that all-trans retinoic acid down regulates human albumin production.

Pathology
Hypoalbuminemia
Hypoalbuminemia means low blood albumin levels. This can be caused by:

Liver disease; cirrhosis of the liver is most common
Excess excretion by the kidneys (as in nephrotic syndrome)
Excess loss in bowel (protein-losing enteropathy, e.g., Ménétriers disease)
Burns (plasma loss in the absence of skin barrier)
Redistribution (hemodilution [as in pregnancy], increased vascular permeability or decreased lymphatic clearance)
Acute disease states (referred to as a negative acute-phase protein)
Malnutrition and wasting
Mutation causing analbuminemia (very rare)
Anorexia nervosa (most common cause in adolescents)In clinical medicine, hypoalbuminemia significantly correlates with a higher mortality rates in several conditions such as heart failure, post-surgery, COVID-19.

Hyperalbuminemia
Hyperalbuminemia is an increased concentration of albumin in the blood. Typically, this condition is due to dehydration.  Hyperalbuminemia has also been associated with high protein diets.

Medical use
Human albumin solution (HSA) is available for medical use, usually at concentrations of 5–25%.
Human albumin is often used to replace lost fluid and help restore blood volume in trauma, burns and surgery patients. There is no strong medical evidence that albumin administration (compared to saline) saves lives for people who have hypovolaemia or for those who are critically ill due to burns or hypoalbuminaemia. It is also not known if there are people who are critically ill that may benefit from albumin. Therefore, the Cochrane Collaboration recommends that it should not be used, except in clinical trials.In acoustic droplet vaporization (ADV), albumin is sometimes used as a surfactant.  ADV has been proposed as a cancer treatment by means of occlusion therapy.Human serum albumin may be used to potentially reverse drug/chemical toxicity by binding to free drug/agent.Human albumin may also be used in treatment of decompensated cirrhosis.Human serum albumin has been used as a component of a frailty index.

Glycation
It has been known for a long time that human blood proteins like hemoglobin  and serum albumin may undergo a slow non-enzymatic glycation, mainly by formation of a Schiff base between ε-amino groups of lysine (and sometimes arginine) residues and glucose molecules in blood (Maillard reaction). This reaction can be inhibited in the presence of antioxidant agents. Although this reaction may happen normally, elevated glycoalbumin is observed in diabetes mellitus.Glycation has the potential to alter the biological structure and function of the serum albumin protein.Moreover, the glycation can result in the formation of Advanced Glycation End-Products (AGE), which result in abnormal biological effects. Accumulation of AGEs leads to tissue damage via alteration of the structures and functions of tissue proteins, stimulation of cellular responses, through receptors specific for AGE-proteins, and generation of reactive oxygen intermediates. AGEs also react with DNA, thus causing mutations and DNA transposition. Thermal processing of proteins and carbohydrates brings major changes in allergenicity </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Gastrointestinal perforation and explain in detail? [/INST] Gastrointestinal perforation, also known as ruptured bowel, is a hole in the wall of part of the gastrointestinal tract. The gastrointestinal tract includes the esophagus, stomach, small intestine, and large intestine. Symptoms include severe abdominal pain and tenderness. When the hole is in the stomach or early part of the small intestine, the onset of pain is typically sudden while with a hole in the large intestine onset may be more gradual. The pain is usually constant in nature. Sepsis, with an increased heart rate, increased breathing rate, fever, and confusion may occur.The cause can include trauma such as from a knife wound, eating a sharp object, or a medical procedure such as colonoscopy, bowel obstruction such as from a volvulus, colon cancer, or diverticulitis, stomach ulcers, ischemic bowel, and a number of infections including C. difficile. A hole allows intestinal contents to enter the abdominal cavity. The entry of bacteria results in a condition known as peritonitis or in the formation of an abscess. A hole in the stomach can also lead to a chemical peritonitis due to gastric acid. A CT scan is typically the preferred method of diagnosis; however, free air from a perforation can often be seen on plain X-ray.Perforation anywhere along the gastrointestinal tract typically requires emergency surgery in the form of an exploratory laparotomy. This is usually carried out along with intravenous fluids and antibiotics. A number of different antibiotics may be used such as piperacillin/tazobactam or the combination of ciprofloxacin and metronidazole. Occasionally the hole can be sewn closed while other times a bowel resection is required. Even with maximum treatment the risk of death can be as high as 50%. A hole from a stomach ulcer occurs in about 1 per 10,000 people per year, while one from diverticulitis occurs in about 0.4 per 10,000 people per year.

Signs and symptoms
Signs and symptoms may include a sudden pain in the epigastrium to the right of the midline indicating the perforation of a duodenal ulcer, while a gastric ulcer perforation reveals itself by burning pain in epigastrium, with flatulence and dyspepsia.In intestinal perforation, pain starts from the site of perforation and spreads across the abdomen.Gastrointestinal perforation results in severe abdominal pain intensified by movement, nausea, vomiting and hematemesis </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Ceruminous adenoma and explain in detail? [/INST] A ceruminous adenoma  is a benign glandular neoplasm which arises from the ceruminous glands located within the external auditory canal. These glands are found within the outer one third to one half of the external auditory canal, more common along the posterior surface; therefore, the tumor develops within a very specific location.

Signs and symptoms
Ceruminous adenoma are rare tumors, accounting for less than 1% of all external ear tumors. The patients will present with a mass, perhaps associated pain, and may have changes in hearing (usually a sensorineural or a conductive hearing loss). Some patients have tinnitus. Nerve paralysis is very uncommon.

Pathology findings
The tumors are usually small, with a mean size of about 1.2 cm.
The tumors are separated into three histologic types based on the dominant findings:

Ceruminous adenoma
Ceruminous pleomorphic adenoma
Ceruminous syringocystadenoma papilliferumAll of the tumors are unencapsulated, but are usually well defined or circumscribed. The overlying surface epithelium is not involved. The tumor shows a dual or biphasic appearance, with glandular or cystic spaces showing inner luminal secretory cells with abundant granular, eosinophilic cytoplasm subtended by basal, myoepithelial cells at the periphery, adjacent to the basement membrane. The luminal cells will often have decapitation (apocrine) secretions and will also have yellow-brown, ceroid, lipofuscin-like (cerumen) pigment granules. There is no pleomorphic, limited mitoses, and no necrosis.Immunohistochemistry can be performed to confirm the biphasic nature of the tumor. All cells are positive with pancytokeratin and epithelial membrane antigen; only the luminal cells are positive with CK7; only the basal  cells are positive with CK5/6, p63, S100 protein. CD117 can be positive in either population. The cells are negative with chromogranin, synaptophysin and CK20.

Diagnosis
The major diagnosis from which to separate ceruminous adenoma is ceruminous adenocarcinoma, which shows an infiltrative growth, pleomorphism, mitoses, necrosis, and lacks ceroid pigment granules. Other tumors which need to be excluded include a neuroendocrine adenoma of the middle ear (middle ear adenoma), paraganglioma, and endolymphatic sac tumor.

Management
The tumors are usually removed in small pieces due to the anatomic confines of the area.

Prognosis
Patients treated with complete surgical excision can expect an excellent long term outcome without any problems </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Schizencephaly and explain in detail? [/INST] Schizencephaly (from Greek  skhizein to split, and  enkephalos brain) is a rare birth defect characterized by abnormal clefts lined with grey matter that form the ependyma of the cerebral ventricles to the pia mater. These clefts can occur bilaterally or unilaterally. Common clinical features of this malformation include epilepsy, motor deficits, and psychomotor retardation.

Presentation
Schizencephaly can be distinguished from porencephaly by the fact that in schizencephaly, the fluid-filled component is entirely lined by heterotopic grey matter, while a porencephalic cyst is lined mostly by white matter. Individuals with clefts in both hemispheres, or bilateral clefts, are often developmentally delayed and have delayed speech and language skills and corticospinal dysfunction. Individuals with smaller, unilateral clefts (clefts in one hemisphere) may be weak or paralyzed on one side of the body and may have average or near-average intelligence. Patients with schizencephaly may also have varying degrees of microcephaly, Cognitive impairment, hemiparesis (weakness or paralysis affecting one side of the body), or quadriparesis (weakness or paralysis affecting all four extremities), and may have reduced muscle tone (hypotonia) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Masticatory muscle myositis and explain in detail? [/INST] Masticatory muscle myositis (MMM) is an inflammatory disease in dogs affecting the muscles of mastication (chewing).  It is also known as atrophic myositis or eosinophilic myositis.  MMM is the most common inflammatory myopathy in dogs.  The disease mainly affects large breed dogs.  German Shepherd Dogs  and Cavalier King Charles Spaniels may be predisposed.  There is a similar disease of the eye muscles found in Golden Retrievers.  Symptoms of acute MMM include swelling of the jaw muscles, drooling, and pain on opening the mouth.  Ophthalmic signs may include third eyelid protrusion, red eyes, and exophthalmos (protruding eyeballs).  In chronic MMM there is atrophy of the jaw muscles, and scarring of the masticatory muscles due to fibrosis may result in inability to open the mouth (trismus).  The affected muscles include the temporalis, masseter, and pterygoid muscles </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Progressive muscular atrophy and explain in detail? [/INST] Progressive muscular atrophy (PMA), also called Duchenne–Aran disease and Duchenne–Aran muscular atrophy, is a disorder characterised by the degeneration of lower motor neurons, resulting in generalised, progressive loss of muscle function.
PMA is classified among motor neuron diseases (MND) where it is thought to account for around 4% of all MND cases.PMA affects only the lower motor neurons, in contrast to amyotrophic lateral sclerosis (ALS), the most common MND, which affects both the upper and lower motor neurons, or primary lateral sclerosis, another MND, which affects only the upper motor neurons. The distinction is important because PMA is associated with a better prognosis than ALS.

Signs and symptoms
As a result of lower motor neuron degeneration, the symptoms of PMA include:
muscle weakness
muscle atrophy
fasciculationsSome patients have symptoms restricted only to the arms or legs (or in some cases just one of either). These cases are referred to as flail limb (either flail arm or flail leg) and are associated with a better prognosis.

Diagnosis
PMA is a diagnosis of exclusion, there is no specific test which can conclusively establish whether a patient has the condition. Instead, a number of other possibilities have to be ruled out, such as multifocal motor neuropathy or spinal muscular atrophy. Tests used in the diagnostic process include MRI, clinical examination, and EMG. EMG tests in patients who do have PMA usually show denervation (neuron death) in most affected body parts, and in some unaffected parts too.It typically takes longer to be diagnosed with PMA than ALS, an average of 20 months for PMA vs 15 months in ALS.

Differential diagnosis
In contrast to amyotrophic lateral sclerosis or primary lateral sclerosis, PMA is distinguished by the absence of:
brisk reflexes
spasticity
Babinskis sign
emotional labilityThe importance of correctly recognizing progressive muscular atrophy as opposed to ALS is important for several reasons.

The prognosis is a little better. A recent study found the 5-year survival rate in PMA to be 33% (vs 20% in ALS) and the 10-year survival rate to be 12% (vs 6% in ALS).
Patients with PMA do not have the cognitive change identified in certain groups of patients with MND.
Because PMA patients do not have UMN signs, they usually do not meet the World Federation of Neurology El Escorial Research Criteria for "Definite" or "Probable" ALS and so are ineligible to participate in the majority of clinical trials conducted in ALS.
Because of its rarity (even compared to ALS) and confusion about the condition, some insurance policies or local healthcare policies may not recognize PMA as being the life-changing illness that it is. In cases where being classified as being PMA rather than ALS is likely to restrict access to services, it may be preferable to be diagnosed as "slowly progressive ALS" or "lower motor neuron predominant" ALS.An initial diagnosis of PMA could turn out to be slowly progressive ALS many years later, sometimes even decades after the initial diagnosis </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Lipoatrophia semicircularis and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Curlings ulcer and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Encephalopathy and explain in detail? [/INST] Encephalopathy (; from Ancient Greek: ἐνκέφαλος "brain" + πάθος "suffering") means any disorder or disease of the brain, especially chronic degenerative conditions. In modern usage, encephalopathy does not refer to a single disease, but rather to a syndrome of overall brain dysfunction; this syndrome has many possible organic and inorganic causes.

Signs and symptoms
The hallmark of encephalopathy is an altered mental state or delirium. Characteristic of the altered mental state is impairment of the cognition, attention, orientation, sleep–wake cycle and consciousness. An altered state of consciousness may range from failure of selective attention to drowsiness. Hypervigilance may be present; with or without: cognitive deficits, headache, epileptic seizures, myoclonus (involuntary twitching of a muscle or group of muscles) or asterixis ("flapping tremor" of the hand when wrist is extended).Depending on the type and severity of encephalopathy, common neurological symptoms are loss of cognitive function, subtle personality changes, and an inability to concentrate. Other neurological signs may include dysarthria, hypomimia, problems with movements (they can be clumsy or slow), ataxia, tremor. Other neurological signs may include involuntary grasping and sucking motions, nystagmus (rapid, involuntary eye movement), jactitation (restlessness while in bed), and respiratory abnormalities such as Cheyne-Stokes respiration (cyclic waxing and waning of tidal volume), apneustic respirations and post-hypercapnic apnea. Focal neurological deficits are less common.Wernicke encephalopathy can co-occur with Korsakoff alcoholic syndrome, characterized by amnestic-confabulatory syndrome: retrograde amnesia, anterograde amnesia, confabulations (invented memories), poor recall and disorientation.Anti-NMDA receptor encephalitis is the most common autoimmune encephalitis. It can cause paranoid and grandiose delusions, agitation, hallucinations (visual and auditory), bizarre behavior, fear, short-term memory loss, and confusion.HIV encephalopathy can lead to dementia.

Types
There are many types of encephalopathy. Some examples include:

Mitochondrial encephalopathy: Metabolic disorder caused by dysfunction of mitochondrial DNA. Can affect many body systems, particularly the brain and nervous system.
Glycine encephalopathy: A genetic metabolic disorder involving excess production of glycine.
Hepatic encephalopathy: Arising from advanced cirrhosis of the liver.
Hypoxic ischemic encephalopathy: Permanent or transitory encephalopathy arising from severely reduced oxygen delivery to the brain.
Static encephalopathy: Unchanging, or permanent, brain damage, usually caused by prenatal exposure to ethanol.
Uremic encephalopathy: Arising from high levels of toxins normally cleared by the kidneys—rare where dialysis is readily available.
Wernickes encephalopathy: Arising from thiamine (B1) deficiency, usually in the setting of alcoholism.
Hashimotos encephalopathy: Arising from an auto-immune disorder.
Anti-NMDA receptor encephalitis: An auto-immune encephalitis.
Hyperammonemia: a condition caused by high levels of ammonia, which is due to inborn errors of metabolism (including urea cycle disorder or multiple carboxylase deficiency), a diet with excessive levels of protein, deficiencies of specific nutrients such as  arginine or biotin, or organ failure.
Hypertensive encephalopathy: Arising from acutely increased blood pressure.
Chronic traumatic encephalopathy: a progressive degenerative disease associated with multiple concussions and other forms of brain injury
Lyme encephalopathy: Arising from Lyme disease bacteria, including Borrelia burgdorferi.
Toxic encephalopathy: A form of encephalopathy caused by chemicals and prescription drugs, often resulting in permanent brain damage.
Toxic-metabolic encephalopathy: A catch-all for brain dysfunction caused by infection, organ failure, or intoxication.
Transmissible spongiform encephalopathy: A collection of diseases all caused by prions, and characterized by "spongy" brain tissue (riddled with holes), impaired locomotion or coordination, and a 100% mortality rate. Includes bovine spongiform encephalopathy (mad cow disease), scrapie, and kuru among others.
Neonatal encephalopathy (hypoxic-ischemic encephalopathy): An obstetric form, often occurring due to lack of oxygen in bloodflow to brain-tissue of the fetus during labour or delivery.
Salmonella encephalopathy: A form of encephalopathy caused by food poisoning (especially out of peanuts and rotten meat) often resulting in permanent brain damage and nervous system disorders.
Encephalomyopathy: A combination of encephalopathy and myopathy.  Causes may include mitochondrial disease (particularly MELAS) or chronic hypophosphatemia, as may occur in cystinosis.
Creutzfeldt–Jakob disease (CJD; transmissible spongiform encephalopathy).
HIV encephalopathy (encephalopathy associated with HIV infection and AIDS, characterized by atrophy and ill-defined white matter hyperintensity).
Sepsis-associated encephalopathy (this type can occur in the setting of apparent sepsis, trauma, severe burns, or trauma, even without clear identification of an infection).
Epileptic encephalopathies:
Early infantile epileptic encephalopathy (acquired or congenital abnormal cortical development).
Early myoclonic epileptic encephalopathy (possibly due to metabolic disorders).
Gluten encephalopathy: Focal abnormalities of the white matter (generally area of low perfusion) are appreciated through magnetic resonance. Migraine is the most common symptom reported.

Toxicity from chemotherapy
Chemotherapy medication, for example, fludarabine can cause a
permanent severe global encephalopathy. Ifosfamide can cause
a severe encephalopathy (but it can be reversible with stopping use of the drug and starting the use of methylene blue). Bevacizumab and other anti–vascular endothelial growth factor medication can cause posterior reversible encephalopathy syndrome.

Toxicity from psychotropic medications
All therapeutic interventions are double-edged swords with benefits and adverse effects, and pharmacotherapy is not an exception. Shortly after the introduction of conventional antipsychotic drugs into clinical practice, relatively rare but serious complications with hyperthermia, muscle rigidity, autonomic instability, and disturbed mental status were recognized to develop in some patients treated with antipsychotics. This type of encephalopathy induced by the use of antipsychotics was referred to as neuroleptic malignant syndrome (NMS), and almost all physicians prescribing antipsychotics are nowadays aware of this adverse phenomenon. Another well-known type of encephalopathy associated with psychotropic drug therapy is serotonin toxicity (ST) or serotonin syndrome (SS), which is characterized by autonomic and neuromuscular symptoms and altered mental status. In contrast with the idiosyncratic nature of NMS, ST is a spectrum pathophysiological state assumed to derive from excess serotonergic neural transmission caused by serotonin-related psychotropic agents. In these two decades, pharmacotherapy with psychotropic drugs for mentally ill patients has been dramatically changed, and classical prototypal antipsychotics and antidepressants have been replaced with atypical antipsychotics and selective serotonin reuptake inhibitors (SSRIs), respectively. These newly developed psychotropic drugs are generally safer and more tolerable than older drugs. However, atypical antipsychotics are not free of the risk of development of NMS, and the explosive prevalence of SSRIs prescribed not only for depression but also for a number of psychiatric diagnoses such as anxiety, eating, impulse-control, and personality disorders may increase the incidence of ST. Therefore, these two pathological states still remain as major adverse effects of psychotropic drugs involving altered functioning of the central nervous system (CNS), to which all clinicians prescribing psychoactive drugs should pay attention. The popularity of SSRIs also increased the case reports of patients experiencing discontinuation syndrome, which sometimes includes CNS symptoms like anxiety and irritability. In this chapter, the author provides a comprehensive overview of the above- mentioned adverse effects affecting the CNS function associated with psychotropic pharmacotherapy. In addition, several other pathological conditions potentially causing encephalopathic symptoms in psychiatric patients treated with psychotropic drugs, e.g., hyponatremia, valproate-induced hyperammonemia, transient splenial lesion of the corpus callosum, and so on, are also described.

Diagnosis
Blood tests, cerebrospinal fluid examination by lumbar puncture (also known as spinal tap), brain imaging studies, electroencephalography (EEG), neuropsychological testing and similar diagnostic studies may be used to differentiate the various causes of encephalopathy.
Diagnosis is frequently clinical. That is, no set of tests give the diagnosis, but the entire presentation of the illness with nonspecific test results informs the experienced clinician of the diagnosis.

Treatment
Treatment varies according to the type and severity of the encephalopathy. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some people. In severe cases, dialysis or organ replacement surgery may be needed.
Sympathomimetic drugs can increase motivation, cognition, motor performance and alertness in persons with encephalopathy caused by brain injury, chronic infections, strokes, brain tumors.When the  encephalopathy is caused by untreated celiac disease or non-celiac gluten sensitivity, the gluten-free diet stops the progression of brain damage and improves the headaches.

Prognosis
Treating the underlying cause of the disorder may improve or reverse symptoms. However, in some cases, the encephalopathy may cause permanent structural changes and irreversible damage to the brain </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Tubercle (bone) and explain in detail? [/INST] In the skeleton of humans and other animals, a tubercle, tuberosity or apophysis is a protrusion or eminence that serves as an attachment for skeletal muscles. The muscles attach by tendons, where the enthesis is the connective tissue between the tendon and bone. A tuberosity is generally a larger tubercle.

Main tubercles
Humerus
The humerus has two tubercles, the greater tubercle and the lesser tubercle. These are situated at the proximal end of the bone, that is the end that connects with the scapula.  The greater/lesser tubercule is located from the top of the acromion laterally and inferiorly.  The radius has two, the radial tuberosity and Listers tubercle.

Ribs
On a rib, tubercle is an eminence on the back surface, at the junction between the neck and the body of the rib. It consists of an articular and a non-articular area </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Phoria and explain in detail? [/INST] Phoria are an English art rock band based in Brighton, consisting of Trewin Howard, Ed Sanderson, Jeb Hardwick, James "Cheese" Cheeseman, and Seryn Burden.
Phoria released their debut EP, Yourself Still, in 2010, followed by Bloodworks (2013) and Display (2014). The records earned the band international critical and popular acclaim.
The bands first full-length album, Volition, was released on 3 June 2016.
Their second album, Caught a Black Rabbit, came out on 13 November 2020.

Biography
Phoria members Trewin, Jeb and Ed went to primary as school together in Salisbury, where they learned cello, classical guitar, and violin respectively.
As friends, they spent their youth making music together before leaving for university in 2005.
Jeb and Ed both attended the University of Southampton. Ed continued to study music, specialising in violin and piano. Jeb studied for a sociology degree, though spent much of his time experimenting with music and visual arts.
Trewin attended the Dartington College of Arts in Devon. He  had initially enrolled on as fine arts course but was soon drawn back to music.
Having completed their studies, Trewin, Ed, and Jeb returned to Salisbury and took full time jobs. Jebs included a brief spell as an insurance agent. Ed, with a passion for acting, took large but unfulfilling parts in a series of niche-market films.
It was not long before the three of them realised that their future lay elsewhere, and moved to Brighton to start their musical careers.
While studying at Southampton, Jeb and Ed had met Tim Douglas through a mutual friend. Following successful spells playing guitar in bands across the South West, Tim moved to Brighton to play bass, and complete the Phoria line-up along with then drummer, Ross Crick.
Seryn Burden joined the band in August 2011, twelve months after the release of Yourself Still, following Rosss departure.
In 2016, following the release of Volition, and a string of successful EPs and UK and international tours, Jeb Hardwick left Phoria to pursue a career in filmmaking. He was replaced by James Cheeseman.
Jeb returned for the recording of the second album Caught A Black Rabbit (2020).

Yourself Still EP (2010)
The bands first EP Yourself Still was released in 2010 and earned positive reviews from various music blogs. The blog The Sirens Sound reviewed the EP, stating that [Yourself Still]...carries various musical vibes from cinematic orchestra to post-rock and indie-rock to a stunning pop environment leading the overall outcome of this record to blazed emotion.  Describing Phoria as A band you definitely want to keep an eye on.

Bloodworks EP (2013)
Bloodworks was released through Akira Records in Spring 2013.
Lead single "Red" hit number 2 in The Hype Machine blog aggregator charts within only a few days, cementing the track as one of the standout singles of 2013 from a relatively unknown band. With the single released just days before the EP, ThisIsFakeDIY said of the track [It gives] the impression that this here EPs going to be a game-changer. Glossy production is met midway by a startling, intimate style of songwriting, half Youth Lagoon, half something grander and more orchestral.Several tracks from the EP have been licensed to festival-featured European cinema, and Canadian television series Saving Hope.

Display EP (2014)
Display was released in June 2014. The lead single Emanate received 250,000 plays across YouTube and Soundcloud in the first two weeks.

Volition (2016)
Volition was released in June 2016 following several delays. It received positive reviews across the critical sphere, with The 405 describing the album as gigantic...[yet] effortlessly intimate, praising the cohesion in sound and vision. Ben Yung of therevue.ca gave a glowing review, stating: Volition is stunning, an absolute emotional roller coaster from start to finish. It is easy to understand why it took two years for the Brighton-based five-piece to complete their debut, as every single detail has been given the utmost attention and the production is refined and masterful. Every note, every vocal component, every lyric, every instrumental texture has been attended to and nothing feels out of place. With the precision of a surgeon and the steely aim of an assassin, Phoria hits every mark, including piercing a hole through our hearts with their visceral and emotional electronica.
The album was supported by festival appearances throughout 2016 and a UK and European tour.
In 2018, the song "Evolve" was featured in an episode of the Syfy original show, The Magicians.
Tim Douglas left the band in 2019 citing personal reasons.
Saving Us A Riot was used in Season 3 of Killing Eve. It was announced Jeb Hardwick had rejoined the band in August 2019

Caught A Black Rabbit (2020)
In August 2019, photos were shared of the band recording at Abbey Road Studios. On the 23rd June the band shared the first track from the upcoming album, Intro </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Vestibular papillomatosis and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Chalicosis and explain in detail? [/INST]  </s>