<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Polydactyly and can you explain it in depth? [/INST] Polydactyly or polydactylism (from Greek  πολύς (polys) many, and  δάκτυλος (daktylos) finger), also known as hyperdactyly, is an anomaly in humans and animals resulting in supernumerary fingers and/or toes. Polydactyly is the opposite of oligodactyly (fewer fingers or toes).

Signs and symptoms
In humans/animals this condition can present itself on one or both hands. The extra digit is usually a small piece of soft tissue that can be removed. Occasionally it contains bone without joints; rarely it may be a complete functioning digit. The extra digit is most common on the ulnar (little finger) side of the hand, less common on the radial (thumb) side, and very rarely within the middle three digits. These are respectively known as postaxial (little finger), preaxial (thumb), and central (ring, middle, index fingers) polydactyly. The extra digit is most commonly an abnormal fork in an existing digit, or it may rarely originate at the wrist as a normal digit does.The incidence of congenital deformities in newborns is approximately 2%, and 10% of these deformities involve the upper extremity. Congenital anomalies of the limb can be classified in seven categories, proposed by Frantz and O’Rahilly and modified by Swanson, based on the embryonic failure causing the clinical presentation. These categories are failure of formation of parts, failure of differentiation, duplication, overgrowth, undergrowth, congenital constriction band syndrome, and generalized skeletal abnormalities. Polydactyly belongs to the category of duplication.
Because there is an association between polydactyly and several syndromes, children with a congenital upper extremity deformity should be examined by a geneticist for other congenital anomalies. This should also be done if a syndrome is suspected, or if more than two or three generations of the family are affected.
Research has shown that the majority of congenital anomalies occur during the 4-week embryologic period of rapid limb development. Polydactyly has been associated with 39 genetic mutations. More specific loci and genetic mechanisms responsible for disorders of duplications will be defined with time, as molecular research continues.
Polydactyly can be divided into three major types, which are discussed below.

Ulnar or postaxial polydactyly
This is the most common situation, in which the extra digit is on the ulnar side of the hand, thus the side of the little finger. This can also be called postaxial polydactyly. It can manifest itself very subtly, for instance only as a nubbin on the ulnar side of the little finger, or very distinctly, as a fully developed finger. Most commonly, the extra finger is rudimentary, consisting of an end phalanx with a nail, and connected to the hand with a small skin pedicle. Mostly one neurovascular bundle can be identified, with no tendons present in the extra digit. In case of a fully developed extra finger, the duplication usually presents itself at the level of the metacarpophalangeal joint. A triplication of the little finger is very rare. Ulnar polydactyly occurs ten times more often in African populations. The incidence in Caucasians is reported as 1 in 1,339 live births, compared with 1 in 143 live births in Africans and African Americans. Ulnar polydactyly is also often part of a syndrome. In patients with African ancestry ulnar polydactyly mostly occurs isolated, whereas the presentation in Caucasians is often associated with a syndrome, though in a retrospective review, only 4 of 37 cases of ulnar polydactyly in Caucasians were syndromic.

Radial or preaxial polydactyly
This is a less common situation, in which the affectation is on the side of the hand towards the thumb. Radial polydactyly refers to the presence of an extra digit (or extra digits) on the radial side of the hand. It is most frequent in Indian populations and it is the second most common congenital hand disorder. The incidence of radial polydactyly is reported as 1 in every 3,000 live births. The clinical features of radial polydactyly will depend upon the extent of duplication.
Radial polydactyly varies from a barely visible radial skin tag to complete duplication. Thumb polydactyly varies from barely visible broadening of the distal phalanx to full duplication of the thumb including the first metacarpal.
Radial polydactyly is frequently associated with several syndromes.

Central polydactyly
This is a very rare situation, in which the extra digit is on the ring, middle or index finger. Of these fingers, the index finger is most often affected, whereas the ring finger is rarely affected.
This type of polydactyly can be associated with syndactyly, cleft hand and several syndromes.
Polysyndactyly presents various degrees of syndactyly affecting fingers three and four.

Causes
Polydactyly is associated with different mutations, either mutations in a gene itself or in a cis-regulatory element responsible for the expression of a specific gene. Mutations in Hoxa- or Hoxd clusters are reported leading to polydactyly. Interactions of Hoxd13 and GLI3 induce synpolydactyly, a combination of extra and consolidated digits. Other signal transduction pathways in this context are the Wnt signaling pathway or Notch.In the specific case of preaxial polydactyly (Hemingway mutant), a cis-acting mutation approximately 1Mb upstream of SHH gene has been implicated. Normally SHH is expressed in an organiser region, called the zone of polarizing activity (ZPA) on the posterior limb side. From there it diffuses anteriorly, laterally to the growth direction of the limb. In the mutant, smaller ectopic expression in a new organiser region is seen on the anterior side of the limb. This ectopic expression causes cell proliferation delivering the raw material for one or more new digits.In addition to the study of genetic causes of polydactyly, limb patterning models are used to simulate the congenital disorder at the limb, being able to explain the development paths of polydactyly.Polydactyly can occur by itself, or more commonly, as one feature of a syndrome of congenital anomalies. When it occurs by itself, it is associated with autosomal dominant mutations in single genes, i.e. it is not a multifactorial trait. But mutation in a variety of genes can give rise to polydactyly. Typically the mutated gene is involved in developmental patterning, and a syndrome of congenital anomalies results, of which polydactyly is one feature or two.Polydactyly has been linked to the prenatal environment, however, with a recent study showing a relationship to maternal pollution exposure in China.Types include:

97 genetic syndromes have been associated with different kinds of polydactyly.

Ulnar polydactyly
Ulnar polydactyly is often bilateral and associated with syndactyly and polydactyly of the feet. This can be a simple or complex polydactyly. Ulnar polydactyly occurs as an isolated congenital condition, but can also be part of a syndrome. The syndromes which occur with ulnar polydactyly are: Trisomy 13, Greig cephalopolysyndactyly syndrome, Meckel syndrome, Ellis–van Creveld syndrome, McKusick–Kaufman syndrome, Down syndrome, Bardet–Biedl syndrome, Smith–Lemli–Opitz syndrome

Radial polydactyly
Type VII of radial polydactyly is associated with several syndromes:
Holt–Oram syndrome, Fanconi anemia (aplastic anemia by the age of 6), Townes–Brocks syndrome, and Greig cephalopolysyndactyly (also known to occur with ulnar polydactyly).

Central polydactyly
The syndromes associated with central polydactyly are:
Bardet–Biedl syndrome, Meckel syndrome, Pallister–Hall syndrome, Legius syndrome, Holt–Oram syndrome. Also, central polydactyly can be associated with syndactyly and cleft hand. Other syndromes including polydactyly include acrocallosal syndrome, basal cell nevus syndrome, Biemond syndrome, ectrodactyly-ectodermal dysplasias-cleft lip/palate syndrome, mirror hand deformity, Mohr syndrome, oral-facial-digital syndrome, Rubinstein-Taybi syndrome, short rib polydactyly, and VATER association.
It can also occur with a triphalangeal thumb.

Diagnosis
Classification is performed by using x-ray imaging to see the bone structures.

Ulnar polydactyly
The classification of ulnar polydactyly exists of either two or three types. The two-stage classification, according to Temtamy and McKusick, involves type A and B. In type A there is an extra little finger at the metacarpophalangeal joint, or more proximal including the carpometacarpal joint. The little finger can be hypoplastic or fully developed. Type B varies from a nubbin to an extra, non-functional little finger part on a pedicle. According to the three-type classification, type I includes nubbins or floating little fingers, type II includes duplications at the MCPJ, and type III includes duplications of the entire ray.

Radial polydactyly
The Wassel classification is the most widely used classification of radial polydactyly, based upon the most proximal level of skeletal duplication. The most common type is Wassel 4 (about 50% of such duplications) followed by Wassel 2 (20%) and Wassel 6 (12%).

Central polydactyly
The classification of central polydactyly is based on the extent of duplication and involves the following three types:
Type I is a central duplication, not attached to the adjacent finger by osseous or ligamentous attachments; it frequently does not include bones, joints, cartilage, or tendons.
Type IIA is a nonsyndactylous duplication of a digit or part of a digit with normal components, and articulates with a broad or bifid metacarpal or phalanx.
Type IIB is a syndactylous duplication of a digit or part of a digit with normal components, and articulates with a broad or bifid metacarpal or phalanx.
Type III is a complete digital duplication, which has a well-formed duplicated metacarpal.

Treatment
Ulnar polydactyly
Ulnar polydactyly usually does not interfere with hand function, but for social reasons it can be treated operatively.

Type A ulnar polydactyly
The treatment of Type A ulnar polydactyly is complex as its goal is to remove the accessory digit while maintaining a stable, functional small finger. When the duplicated proximal phalanx articulates with a common, broad metacarpal head, the ulnar collateral ligament must be considered. In those cases with a common articulation or with a sixth metacarpal the muscle executing the abduction of the little finger (abductor digiti minimi) must be preserved.
In patients with a common metacarpal articulation an elliptical incision at the base of the post-axial digit is made. This incision may be extended proximally in order to adequately expose the abductor digiti minimi. The ulnar collateral ligament and the insertions of the abductor digiti minimi are then elevated with a periosteal sleeve. The duplicated extensor and flexor tendons to the ulnar digit are transected and after that the digit is amputated at its articulation with the metacarpal. If the articular surface is wide the metacarpal may be shaved. At last the collateral ligament and abductor digiti minimi are reinserted at the base of the preserved proximal phalanx and a wire is then placed across the reconstructed joint.
In patients with a duplicated metacarpal, the accessory digit is amputated in a standard ray fashion with transfer of the abductor digiti minimi to the retained small finger.

Type B ulnar polydactyly
In this situation there is an absence of osseous and ligamentous structures. The surgical technique is analogous to radial polydactyly, in which the level of duplication and anatomical components should guide operative treatment.
The pedicled ulnar extra digit can be removed by  suture ligation to devise the skin bridge of the newborn child. This might be easier than an excision of the extra digit when the child is 6 to 12 months old. Ligation occludes the vascular supply to the duplicated digit, resulting in dry gangrene and subsequent autoamputation. This must be done with consideration of the presence of a neurovascular bundle, even in very small skin bridges. When the ligation is done inappropriately it can give a residual nubbin. Also, a neuroma can develop in the area of the scar. An excision can prevent the development of a residual nubbin and the sensitivity due to a neuroma.
For infants with ulnar type B polydactyly the recommended treatment is ligation in the neonatal nursery. Studies have shown that excision of the extra digit in the neonatal nursery is a safe and simple procedure with a good clinical and cosmetic outcome.

Radial polydactyly
Because neither of the two thumb components is normal, a decision should be taken on combining which elements to create the best possible composite digit. Instead of amputating the most hypoplastic thumb, preservation of skin, nail, collateral ligaments and tendons is needed to augment the residual thumb. Surgery is recommended in the first year of life, generally between 9 and 15 months of age.
Surgical options depend on type of polydactyly.

Bilhaut-Cloquet procedure
This type of procedure is recommended for Wassel types 1 and 2 (in which both thumbs are severely hypoplastic) by some congenital hand surgeons. The technique contains a composite wedge resection of the central bone and soft-tissue. This will be achieved with approach of the lateral tissue of each thumb. The goal is to achieve a normal thumb, what concerns the size, which is possible. If the width of the nail bed is greater than 70% of the contralateral thumb, it may be split.

Ablation with collateral ligament reconstruction
This type of procedure is used for all Wassel types of polydactyly and is the most commonly used technique. It is recommended in all cases of thumb duplication with a hypoplastic, less-functional thumb. Otherwise, one could consider the Bilhaut-Cloquet. The ulnar thumb is preferably preserved as it is the more developed one in most cases.By detaching the radial collateral ligament from distal to proximal, a periosteal sleeve can be preserved.
In this way, the radial collateral band of the radial digit, will function as the absent radial collateral ligament of the preserved ulnar thumb.
Elevation of the APB and FPB is performed in Wassel type 4 duplication; this can be accomplished via the periosteum or separately. As the tendons insert proximally, the elevation is performed proximally too to potentially rebalance the ulnar thumb. After the radial thumb is amputated, the ulnar elements are centralized and fixed with a Kirschner wire. In most cases, a longitudinal and sagittal osteotomy is needed to centralize the bony parts of the ulnar thumb. While the soft-tissue of the radial thumb was preserved, it is now attached to the radial side of the ulnar thumb together with the periosteal sleeve. The APB and FPB of the ablated radial thumb are attached to the distal phalanx for more stability. If necessary, the extensor pollicis longus and the flexor pollicis longus are reattached to centralize their course.In Wassel type 5 and 6 the opponens pollicis muscle must be transferred to the ulnar metacarpal. Soft tissue with collateral ligament reconstruction is used to avoid any angular deformity in the preserved thumb. Tendon centralization is also often used for correction. Still, cases with osseous deformities may happen. To provide alignment, osteotomies are necessary to be done. This operation may need bone grafting, which is obtained from the amputated thumb.

On top plasty procedure
This type is indicated when one thumb is larger proximally and the other thumb has a larger distal component. (The procedure is initially described as a way to lengthen amputated digits.) The goal is to create a functional thumb by combining less-hypoplastic components. On top plasty procedure is rarely employed in the treatment of congenital thumb duplication. It might be necessary for Wassel types 4, 5, 6.At the level of the mid-proximal phalanx or mid-metacarpal, the distal component is transferred to the proximal component. The tendons of the distal component are preserved as the rest of the distal component is amputated. The neurovascular bundle which supplies the distal component is reserved and transferred proximally.

Central polydactyly
Early osteotomy and ligament reconstructions should be done to prevent deformities, such as angular growth deformities.The surgical treatment of central polydactyly is highly variable. After the surgery the hand must be functional and stable, but also aesthetically pleasing. This requires intraoperative creativity and flexibility. The surgeon must also consider whether retention of a fully functional supranumerary digit is preferable to surgical intervention. In contrast, a functional, four-fingered hand achieved via ray amputation may be preferable to a five-fingered hand with a deformed or stiff reconstructed finger.Cases of polysyndactyly are approached through a standard opposing zig-zag incision. The incision is favored toward the accessory digit, preserving extra skin for subsequent closure. Depending on the level and extent of duplication, the flexor and extensor tendons may require centralization or rebalancing. Also, the collateral ligaments must be preserved or reconstructed. Wide articular surfaces should be narrowed and phalangeal wedge osteotomies may be required to provide an axial alignment. Attention must also be given to reconstruct the intermetacarpal ligament. Furthermore, one should take in mind the provision for adequate web-space soft tissue.

Prognosis
Ulnar polydactyly
Type A ulnar polydactyly
There are no substantive outcome studies regarding the function of these hands following surgical intervention. This is mainly caused by the fact that there is a generally normal function of these patients’ hands following ablation with collateral ligament reconstruction. In a study on 27 patients undergoing surgical excision for Type A ulnar polydactyly, only one complication was noted in the form of an infection
However, no investigators have objectively reviewed functional range of motion or articular stability.

Type B ulnar polydactyly
In a study on 21 patients with Type B ulnar polydactyly treated with suture ligation it was found that the duplicated digit was typically amputated at an average of 10 days and no complications of infection or bleeding were reported.
In a large study on 105 patients treated with suture ligation an overall complication rate of 23.5% was reported, citing a residual tender or unacceptable bump in 16%, infection in 6%, and bleeding in 1% of patients.
In general, suture ligation is safe and effective when applied to appropriate cases of Type B polydactyly in which no substantial ligamentous or osseous structures are present within the pedicle. Parents should be educated as to the progression of necrosis, and that revision of residual tissue or scar may be necessary when the child is six months of age or older.

Radial polydactyly
Bilhaut procedure
Advantages:
By combining two hypoplastic thumbs a sufficient thumb size is acquired. Furthermore, the IP and MCP joints are very stable as the collateral ligaments are not violated during reconstruction.
Disadvantages:
Violation during reconstruction can lead to growth arrest or asymmetric growth. Nail deformity could also occur after reconstruction. Although the joints are stable, restriction of flexion may be possible.
The average IP flexion in a reconstructed thumb is 55 degrees less than the contralateral thumb. MCP flexion averaged 55 degrees in reconstructed thumbs, compared to 75 degrees in the contralateral thumb.

Ablation with collateral ligament reconstruction
Advantages:
The reconstructed joints tend to remain flexible. Also, it preserves the nail bed and physis, this increases the prevention of nail deformities over time.
Disadvantages:
Although surgeons try to obtain a stable thumb of appropriate size, instability of the IP and MCP joint may occur, as well as a size mismatch. Thumbs are defined as unacceptable if IP joint deviation exceeds 15 degrees, MCP joint deviation exceeds 30 degrees, and thumb size is inappropriate based on the examiners assessment. Also, thumb size one-third greater or less than the contralateral thumb is defined as unacceptable.

On-top plasty procedure
No surgical outcomes studies exist for evaluating the function of the thumbs after an on-top plasty reconstruction.

Central polydactyly
Few clinical outcome studies exist regarding the treatment of central polydactyly. Tada and colleagues note that satisfactory surgical correction of central polydactyly is difficult to achieve and that outcomes are generally poor. In Tadas study, 12 patients were reviewed. All patients required secondary surgical procedures to address flexion contractures and angular deviation at the IP joint level.
However, several primary factors contribute to the complexity of central polydactyly reconstruction. Hypoplastic joints and soft tissues that predispose the reconstructed finger to joint contracture, and angular deformities as well as complex tendon anomalies, are often difficult to address. Therefore, treatment is wholly dependent on the anatomic components present, the degree of syndactyly, and the function of the duplicated finger.

Epidemiology
The condition has an estimated occurrence of 0.3–3.6 per 1000 live births. Postaxial hand polydactyly is most frequent in the United States in Black males. Preaxial polydactyly occurs in 0.08 to 1.4 in 1,000 live births. In the United States, it is more common in White people and also relatively frequent in Native American and Asian people. A 1994 study by Finley et al. combined data from Jefferson County, Alabama, United States, and Uppsala County, Sweden. This study found incidence of all types of polydactyly at rates of 2.3 per 1000 live births of White males, 0.6 per 1000 live births of White females, 13.5 per 1000 live births of Black males, and 11.1 per 1000 live births of Black females.

Society and culture
People with polydactyly
Antonio Alfonseca, retired MLB professional baseball pitcher known as "El Pulpo" – Spanish for "the Octopus" with regard to his extra digit on each extremity.
Endre Ady, Hungarian poet born with six fingers, but one was removed as a child. The poet later interpreted it as a sign of his selection (according to the ancient Hungarian belief, the táltos are born with more bones, such as six fingers).
Brites de Almeida, a legendary Portuguese woman who killed seven hiding Castilian soldiers in her oven after the Battle of Aljubarrota, had six fingers on each hand.
The actress Gemma Arterton was born with six fingers on each hand, the additional fingers being removed after birth.
Anne Boleyn, former Queen of England, was rumoured to have six fingers on one hand. However, considering that this rumour first emerged in the 1580s from a Catholic dissenter, it is generally deemed false.
Robert Chambers, purported author of Vestiges of the Natural History of Creation, and his brother William had six digits on each limb.
Lucille Clifton, an African-American poet and civil rights advocate.
Zerah Colburn, American prodigious math calculating savant.
Calvin Choy, a Hong Konger singer and actor nicknamed "Sir One One" (Sir11) as he has six digits on his right hand.
Several members of a Da Silva family in São Paulo, Brazil, have two thumbs on each hand.
Vicente Fox, former President of Mexico, has six toes on each foot.
Danny Garcia, boxing champion, has six toes on his right foot.
Yoandri Hernández Garrido, nicknamed "Veinticuatro" ("twenty four" in Spanish), has six fully formed fingers on both hands and six perfect toes on each foot.
Hampton Hawes, jazz pianist, was born with six fingers on each hand (the extra fingers were surgically removed shortly after birth).
Henry II the Pious, High Duke of Poland 1238–1241, had six toes on his left foot.
A boy named Hong Hong born in Pingjiang County, Hunan province, China, has 31 fingers and toes.
Kamani Hubbard, a boy in California was born in 2009 with a rare case of polydactyly, with 12 fingers and 12 toes, all fully functional.
Johann Jacob Freiherr von Moscon (1621–1661), Lower Styrian baron, is depicted with six fingers at his left hand on a portrait from Brežice, Slovenia.
Jiang Qing, Mao Zedongs fourth wife, reportedly had six toes on her right foot.
Hrithik Roshan, a Bollywood actor born with a supernumerary thumb on his right hand.
Nayanthara, an Indian actress who is a polydactyl, with a rudimentary finger on her left hand.
Akshat Saxena from Uttar Pradesh, India is the world record holder for highest number of digits. He was born in 2010 with seven digits on each hand and 10 digits on each foot, for a total of 34 digits.
Garfield Sobers, West Indian cricketer, had an extra finger on each hand which he removed himself during childhood "with the aid of catgut and a sharp knife".
Theodore Roosevelt "Hound Dog" Taylor, American Chicago-based blues guitarist, was born with polydactyly on both hands, although around age 41, he removed the extra finger on his right hand.
Varalakshmi V, a girl from Bangalore with eight fingers on each hand and about four to five extra toes on each foot.
Volcacius Sedigitus, a Roman poet of the 1st century, probably received his epithet, signifying "Sixfinger", because he was born with six fingers on each hand, according to Pliny,
Zhu Yunming, a Chinese calligrapher, had six fingers on his right hand.
Reggy B, a drag queen and contestant on the second season of Drag Race Holland, revealed on the show that she was born with an extra thumb on her left hand, three extra toes on one foot, and two extra toes on her other foot. Her extra fingers and toes were surgically removed at a young age.
Ish Madon (איש מדון), a biblical Philistean figure who fought against King Davids army. The Bible mentions he was a relative to Goliath.

Fictional people
In The Silence of the Lambs, Hannibal Lecter is described as having mid-ray duplication polydactyly (a duplicated middle finger) on his left hand, which he later removes in Hannibal as part of his cosmetic surgery to disguise himself.
In the cartoon series Gravity Falls, Stanford Pines ("Grunkle Ford") has six fingers on both of his hands, a trait which also identifies him in the shows mythology.
Tyrone Rugen, a Count in The Princess Bride, is described many times as the "six-fingered man."
Void, an antagonist of the manga series Berserk, has six fingers on each hand.
Billy, a character from Adventure Time had six fingers on each hand.

Other animals
Polydactyly occurs in numerous types of animals. The condition is sporadically seen in livestock, where it affects cattle, sheep, pigs, and occasionally horses. Conversely, it is a common trait in several heritage chicken breeds. Chickens normally have 4 toes on each foot. The chicken breeds known for being polydactyl are the Dorking, Faverolle, Houdan, Lincolnshire Buff, Meusienne, Sultan, and non-bearded Silkie Bantams. The breed standard of these varieties of chickens calls for five toes on each foot, although sometimes more than five toes will occur. The extra digit in these breeds presents as an extra "thumb" that does not touch the ground. Mixed-breed chickens may also have extra digits if the aforementioned breeds are part of their genetic makeup.Polydactyly also occurs in dogs, cats, and small mammals such as guinea pigs and mice </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Right ventricular hypertrophy and can you explain it in depth? [/INST] Right ventricular  (RVH) is a condition defined by an abnormal enlargement of the cardiac muscle surrounding the right ventricle. The right ventricle is one of the four chambers of the heart. It is located towards the lower-end of the heart and it receives blood from the right atrium and pumps blood into the lungs.
Since RVH is an enlargement of muscle it arises when the muscle is required to work harder. Therefore, the main causes of RVH are pathologies of systems related to the right ventricle such as the pulmonary artery, the tricuspid valve or the airways.
RVH can be benign and have little impact on day-to-day life or it can lead to conditions such as heart failure, which has a poor prognosis.

Signs and symptoms
Symptoms
Although presentations vary, individuals with right ventricular hypertrophy can experience symptoms that are associated with pulmonary hypertension, heart failure and/or a reduced cardiac output. These include:
Difficulty breathing on exertion
Chest pain (angina) on exertion
Fainting (syncope) on exertion
General fatigue/lethargy
Dizziness
Feeling of fullness in the upper abdominal area
Discomfort or pain in the right upper abdomen
Reduced appetite
Swelling (oedema) of the legs, ankles or feet
Racing heart beat (palpitations)People may rarely present with the symptoms of Ortners syndrome, which include cough, haemoptysis and hoarseness.

Signs
On physical examination, the most prominent features are due to the development of right-sided heart failure. These can include a raised jugular venous pressure, ascites, left parasternal heave and a tender, enlarged liver on palpation.
On inspection, patients may be chronically ill, cyanotic, cachectic and occasionally jaundiced.On auscultation, an accentuated second pulmonary sound (S2), a third heart sound termed a ‘right ventricular gallop’, as well as a systolic murmur over the tricuspid area accentuated by inspiration may be present. On occasion, the systolic murmur can be transmitted and auscultated over the liver. Less typically, diastolic murmur may also be heard as a result of pulmonary insufficiency.

Causes
RVH usually occurs due to chronic lung disease or structural defects in the heart. One of the most common causes of RVH is pulmonary hypertension (PH), defined as increased blood pressure in the vessels supplying blood to the lungs. PH leads to increased pulmonary artery pressure. The right ventricle tries to compensate for this increased pressure by changing its shape and size. Hypertrophy of individual myocytes results in an increase in right ventricular wall thickness. The worldwide incidence of PH is 4 per million people. RVH occurs in approximately 30% of these cases.PH is broadly split into five categories by the World Health Organization, based on the underlying cause. The incidence of RVH varies between the groups. Common causes of PH include chronic obstructive pulmonary disease (COPD), pulmonary embolism, and other restrictive lung diseases. RVH often occurs as a result of these disorders. RVH is seen in 76% of patients with advanced COPD and 50% of patients with restrictive lung disease.RVH also occurs in response to structural defects in the heart. One common cause is tricuspid insufficiency. This is a disorder where the tricuspid valve fails to close properly, allowing backward flow of blood. Other structural defects which lead to RVH include tetralogy of Fallot, ventricular septal defects, pulmonary valve stenosis, and atrial septal defects. RVH is also associated with abdominal obesity, elevated fasting blood glucose, high systolic blood pressure, and fractional shortening of the left ventricular mid-wall.Other risk factors for RVH include smoking, sleep apnea, and strenuous activity. These increase the risk of heart and lung disease and hence RVH.

Pathophysiology
Right ventricular hypertrophy can be both a physiological and pathophysiological process. It becomes pathophysiological (damaging) when there is excessive hypertrophy. The pathophysiological process mainly occurs through aberrant signalling of the neuroendocrine hormones; angiotensin II, endothelin-1 and the catecholamines (e.g. noradrenaline).

Angiotensin-II and endothelin-1
Angiotensin-II and endothelin-1 are hormones that bind to the angiotensin (AT) and endothelin (ET) receptors. These are G-protein coupled receptors that act via internal signalling pathways. Through several intermediates, these pathways directly or indirectly increase reactive oxygen species (ROS) production causing accumulation in myocardial cells. This can subsequently induce necrotic cell death, fibrosis, and mitochondrial dysfunction.This has been demonstrated in animal studies. Protein Kinase C (PKC) is an intermediate molecule in the signalling pathway and mice lacking PKC shown resistance to heart failure compared to mice overexpressing PKC which shown heart dysfunction.Targeting the renin–angiotensin (RAAS) system (using angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers) are a well-recognized clinical approach for reversing maladaptive cardiac hypertrophy independently of blood pressure.

Catecholamines
Catecholamines levels increase due to increased sympathetic nervous system activity. Catecholamines can act on the alpha-adrenergic receptors and beta-adrenergic receptors which are G-protein coupled receptors. This binding initiates the same intracellular signalling pathways as angiotensin and endothelin. There is also activation of cAMP and an increase in intracellular Ca2+ which leads to contractile dysfunction and fibrosis.

Others
Hormones are not the only cause of RVH. Hypertrophy can also be caused by mechanical forces, mTOR pathways, nitric oxide and immune cells. Immune cells can cause hypertrophy by inducing inflammation.

Diagnosis
The two main diagnostic tests used to confirm right ventricular hypertrophy are electrocardiography and echocardiography.

Electrocardiography
The use of electrocardiogram (ECG) to measure cardiac chamber hypertrophy is well established but since the left ventricular activity is dominant on the ECG a large degree of RVH is often required for any detectable changes. Nonetheless, the ECG is used to assist with the diagnosis of RVH. A post mortem study on 51 adult male patients concluded that anatomical RVH may be diagnosed using one or more of the following ECG criteria:
Right axis deviation of more than (or equal to) 110° (see hexaxial reference figure)
R-wave dominant over S-wave in V1 or V2
S-wave dominant over R-wave in V6However, the American Heart Association recommended the use of additional diagnostic tests to diagnose RVH because no single criteria or set of criteria were considered sufficiently reliable.

Echocardiography
Echocardiography can be used to directly visualise right ventricular wall thickness. The preferred technique is the trans-oesophageal approach giving a view of 4 chambers. The normal thickness of a right ventricular free wall ranges from 2-5 millimetres, with a value above 5 mm considered to be hypertrophic.

Treatment
It is important to understand that right ventricular hypertrophy in itself is not the main issue, but what right ventricular hypertrophy represents is. Right ventricular hypertrophy is the intermediate stage between increased right ventricular pressure (in the early stages) and right ventricle failure (in the later stages). As such, management of right ventricular hypertrophy is about either preventing the development of right ventricular hypertrophy in the first place, or preventing the progression towards right ventricle failure. Right ventricular hypertrophy in itself has no (pharmacological) treatment.

Treating the cause
Since the main causes of right ventricular hypertrophy is tricuspid regurgitation or pulmonary hypertension (discussed above), management involves treatment of these conditions.
Tricuspid regurgitation is typically treated conservatively by aiming to treat the underlying cause and following up the patient regularly </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Galactosemia and can you explain it in depth? [/INST] Galactosemia (British galactosaemia, from Greek γαλακτόζη + αίμα, meaning galactose + blood, accumulation of galactose in blood) is a rare genetic metabolic disorder that affects an individuals ability to metabolize the sugar galactose properly. Galactosemia follows an autosomal recessive mode of inheritance that confers a deficiency in an enzyme responsible for adequate galactose degradation.
Friedrich Goppert (1870–1927), a German physician,  first described the disease in 1917, with its cause as a defect in galactose metabolism being identified by a group led by Herman Kalckar in 1956. Galactosemia was the second disorder found to be detectable through newborn screening methods by Robert Guthrie.Its incidence is about 1 per 60,000 births for people of European ancestry.  In other populations the incidence rate differs. Galactosaemia is about one hundred times more common (1:480 births) in the Irish Traveller population.

Symptoms
Adults
Infants
Infants may appear asymptomatic at birth, however, upon ingestion of galactose a few days later (via breast and/or formula feeding), children start to experience life-threatening symptoms, which include:
poor feeding, and weight gain
vomiting and diarrhea
hepatocellular damage
lethargy, and hypotoniaProgression of this acute neonatal toxicity syndrome may include the development of sepsis, cataracts, and even pseudotumor cerebri (which may cause a bulging of fontanelle).

Cause
Lactose in food (such as dairy products) is broken down by the enzyme lactase into glucose and galactose. In individuals with galactosemia, the enzymes needed for further metabolism of galactose (Galactokinase and galactose-1-phosphate uridyltransferase) are severely diminished or missing entirely, leading to toxic levels of galactose or galactose 1-phosphate (depending on which enzyme is missing) in various tissues as in the case of classic galactosemia, resulting in hepatomegaly (an enlarged liver), cirrhosis, kidney failure, cataracts, vomiting, seizure, low blood sugar (hypoglycemia), lethargy, brain damage, and ovarian failure. Without treatment, mortality in infants with galactosemia is about 75%.Galactosemia is inherited in an autosomal recessive manner, meaning a child must inherit one defective gene from each parent to show the disease. Heterozygotes are carriers, because they inherit one normal gene and one defective gene. Carriers show no symptoms of galactosemia.

Accumulation of galactose
Reduction to galactitol
In galactosemic patients, the accumulation of galactose becomes the substrate for enzymes that catalyze the polyol pathway of carbohydrate metabolism. The first reaction of this pathway is the reduction of aldoses, types of sugars including galactose, to sugar alcohols. Recent data suggests that aldose reductase is the enzyme responsible for the primary stage of this pathway. Therefore, aldose reductase reduces galactose to its sugar alcohol form, galactitol. Galactitol, however, is not a suitable substrate for the next enzyme in the polyol pathway, polyol dehydrogenase. Thus, galactitol accumulates in body tissues and is excreted in the urine of galactosemic patients. Accumulation of galactitol has been attributed to many of the negative effects of galactosemia, and high concentrations of galactitol have been found in people with classic galactosemia (GALT deficiency or Galactose-1-phosphate uridylyltransferase deficiency), galactokinase deficiency, and epimerase deficiency with glucose.

Oxidation to galactonate
Accumulated galactose can also undergo an alternative reaction: Oxidation to galactonate. The mechanism of galactonate formation is still unclear. However, recent studies suggest that galactose dehydrogenase is responsible for converting galactose to galactonolactone, which then spontaneously or enzymatically converts to galactonate. Once formed, galactonate may enter the pentose phosphate pathway. Thus, Oxidation to galactonate serves as an alternate pathway for metabolizing galactose. This oxidative pathway renders accumulated galactonate less harmful than accumulated galactitol.

Diagnosis
In many states throughout the world, infants routinely undergo newborn screening (NBS) for galactosemia. This allows a diagnosis to be made while the person is still an infant. Infants affected by galactosemia typically present with symptoms of lethargy, vomiting, diarrhea, failure to thrive, and jaundice. None of these symptoms are specific to galactosemia, often leading to diagnostic delays. If the family of the baby has a history of galactosemia, doctors can test prior to birth by taking a sample of fluid from around the fetus (amniocentesis) or from the placenta (chorionic villus sampling or CVS). Galactosemia is normally first detected through newborn screening which if available, is able to diagnose the majority of affected infants.
A galactosemia test is a blood test (from the heel of the infant) or urine test that checks for three enzymes that are needed to change galactose sugar that is found in milk and milk products into glucose, a sugar that the human body uses for energy. A person with galactosemia doesnt have one of these enzymes. This causes high levels of galactose in the blood or urine.Affected children can have serious, irreversible effects or even die within days from birth.  It is important that newborns be screened for metabolic disorders without delay.  Galactosemia can even be detected through NBS before any ingestion of galactose-containing formula or breast milk.
Detection of the disorder through NBS does not depend on protein or lactose ingestion, and, therefore, it should be identified on the first specimen unless the infant has been transfused. A specimen should be taken prior to transfusion.  The enzyme is prone to damage if analysis of the sample is delayed or exposed to high temperatures.  The routine NBS is accurate for detection of galactosemia.  Two screening tests are used to screen infants affected with galactosemia—the Beutlers test and the Hill test </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Receptive aphasia and can you explain it in depth? [/INST] Wernickes aphasia, also known as receptive aphasia, sensory aphasia or posterior aphasia, is a type of aphasia in which individuals have difficulty understanding written and spoken language. Patients with Wernickes aphasia demonstrate fluent speech, which is characterized by typical speech rate, intact syntactic abilities and effortless speech output. Writing often reflects speech in that it tends to lack content or meaning. In most cases, motor deficits (i.e. hemiparesis) do not occur in individuals with Wernickes aphasia. Therefore, they may produce a large amount of speech without much meaning. Individuals with Wernickes aphasia are typically unaware of their errors in speech and do not realize their speech may lack meaning. They typically remain unaware of even their most profound language deficits.
Like many acquired language disorders, Wernickes aphasia can be experienced in many different ways and to many different degrees. Patients diagnosed with Wernickes aphasia can show severe language comprehension deficits; however, this is dependent on the severity and extent of the lesion. Severity levels may range from being unable to understand even the simplest spoken and/or written information to missing minor details of a conversation. Many diagnosed with Wernickes aphasia have difficulty with repetition in words and sentences and/or working memory.Wernickes aphasia was named after German physician Carl Wernicke, who is credited with discovering the area of the brain responsible for language comprehension (Wernickes area).

Signs and symptoms
The following are common symptoms seen in patients with Wernickes aphasia:

Impaired comprehension: deficits in understanding (receptive) written and spoken language. This is because Wernickes area is responsible for assigning meaning to the language that is heard, so if it is damaged, the brain cannot comprehend the information that is being received.
Poor word retrieval: ability to retrieve target words is impaired. This is also referred to as anomia.
Fluent speech: individuals with Wernickes aphasia do not have difficulty with producing connected speech that flows. Although the connection of the words may be appropriate, the words they are using may not belong together or make sense (see Production of jargon below).
Production of jargon: speech that lacks content, consists of typical intonation, and is structurally intact. Jargon can consist of a string of neologisms, as well as a combination of real words that do not make sense together in context. The jargon may include word salads.
Awareness: Individuals with Wernickes aphasia are often not aware of their incorrect productions, which would further explain why they do not correct themselves when they produce jargon, paraphasias, or neologisms.
Paraphasias:Phonemic (literal) paraphasias: involves the substitution, addition, or rearrangement of sounds so that an error can be defined as sounding like the target word. Often, half of the word is still intact which allows for easy comparison to the appropriate, original word.
E.g. "bap" for "map"
Semantic (verbal) paraphasias: saying a word that is related to the target word in meaning or category; frequently observed in Wernickes aphasia.
E.g. "jet" for "airplane" or "knife" for "fork"
Neologisms: nonwords that have no relation to the target word.E.g. "dorflur" for "shoe"
Circumlocution: talking around the target word.E.g. "uhhh its white... its flat... you write on it..." (when referencing paper)
Press of speech: run-on speech.If a clinician asks, "what do you do at a supermarket?" And the individual responds with "Well, the supermarket is a place. It is a place with a lot of food. My favorite food is Italian food. At a supermarket, I buy different kinds of food. There are carts and baskets. Supermarkets have lots of customers, and workers..."
Lack of hemiparesis: typically, no motor deficits are seen with a localized lesion in Wernickes area.
Reduced retention span: reduced ability to retain information for extended periods of time.
Impairments in reading and writing: impairments can be seen in both reading and writing with differing severity levels.How to differentiate from other types of aphasia
Expressive aphasia (non-fluent Brocas aphasia): individuals have great difficulty forming complete sentences with generally only basic content words (leaving out words like "is" and "the").
Global aphasia: individuals have extreme difficulties with both expressive (producing language) and receptive (understanding language).
Anomic aphasia: the biggest hallmark is ones poor word-finding abilities; ones speech is fluent and appropriate, but full of circumlocutions (evident in both writing and speech).
Conduction aphasia: individuals can comprehend what is being said and are fluent in spontaneous speech, but they cannot repeat what is being said to them.

Causes
The most common cause of Wernickes aphasia is stroke. Strokes may occur when blood flow to the brain is completely interrupted or severely reduced. This has a direct effect on the amount of oxygen and nutrients being able to supply the brain, which causes brain cells to die within minutes."The middle cerebral arteries supply blood to the cortical areas involved in speech, language and swallowing. The left middle cerebral artery provides Brocas area, Wernickes area, Heschls gyrus, and the angular gyrus with blood". Therefore, in patients with Wernickes aphasia, there is typically an occlusion to the left middle cerebral artery.As a result of the occlusion in the left middle cerebral artery, Wernickes aphasia is most commonly caused by a lesion in the posterior superior temporal gyrus (Wernickes area). This area is posterior to the primary auditory cortex (PAC) which is responsible for decoding individual speech sounds. Wernickes primary responsibility is to assign meaning to these speech sounds. The extent of the lesion will determine the severity of the patients deficits related to language. Damage to the surrounding areas (perisylvian region) may also result in Wernickes aphasia symptoms due to variation in individual neuroanatomical structure and any co-occurring damage in adjacent areas of the brain.

Diagnosis
Aphasia is usually first recognized by the physician who treats the person for his or her brain injury. Most individuals will undergo a magnetic resonance imaging (MRI) or computed tomography (CT) scan to confirm the presence of a brain injury and to identify its precise location. In circumstances where a person is showing possible signs of aphasia, the physician will refer him or her to a speech-language pathologist (SLP) for a comprehensive speech and language evaluation. SLPs will examine the individuals ability to express him or herself through speech, understand language in written and spoken forms, write independently, and perform socially.The American Speech, Language, Hearing Association (ASHA) states a comprehensive assessment should be conducted in order to analyze the patients communication functioning on multiple levels; as well as the effect of possible communication deficits on activities of daily living. Typical components of an aphasia assessment include: case history, self report, oral-motor examination, language skills, identification of environmental and personal factors, and the assessment results. A comprehensive aphasia assessment includes both formal and informal measures.Formal assessments include:

Boston Diagnostic Aphasia Examination (BDAE): diagnoses the presence and type of aphasia, focusing on location of lesion and the underlying linguistic processes.
Western Aphasia Battery – Revised (WAB): determines the presence, severity, and type of aphasia; and can also determine baseline abilities of patient.
Communication Activities of Daily Living - Second Edition (CADL-2): measures functional communication abilities; focuses on reading, writing, social interactions, and varying levels of communication.
Revised Token Test (RTT): assess receptive language and auditory comprehension; focuses on patients ability to follow directions.Informal assessments, which aid in the diagnosis of patients with suspected aphasia, include:
Conversational speech and language sample
Family interview
Case history or medical chart review
Behavioral observationsDiagnostic information should be scored and analyzed appropriately. Treatment plans and individual goals should be developed based on diagnostic information, as well as patient and caregiver needs, desires, and priorities.

Treatment
According to Bates et al. (2005), "the primary goal of rehabilitation is to prevent complications, minimize impairments, and maximize function". The topics of intensity and timing of intervention are widely debated across various fields. Results are contradictory: some studies indicate better outcomes with early intervention, while other studies indicate starting therapy too early may be detrimental to the patients recovery. Recent research suggests, that therapy be functional and focus on communication goals that are appropriate for the patients individual lifestyle.Specific treatment considerations for working with individuals with Wernickes aphasia (or those who exhibit deficits in auditory comprehension) include using familiar materials, using shorter and slower utterances when speaking, giving direct instructions, and using repetition as needed.

Role of neuroplasticity in recovery
Neuroplasticity is defined as the brains ability to reorganize itself, lay new pathways, and rearrange existing ones, as a result of experience. Neuronal changes after damage to the brain such as collateral sprouting, increased activation of the homologous areas, and map extension demonstrate the brains neuroplastic abilities. According to Thomson, "Portions of the right hemisphere, extended left brain sites, or both have been shown to be recruited to perform language functions after brain damage. All of the neuronal changes recruit areas not originally or directly responsible for large portions of linguistic processing. Principles of neuroplasticity have been proven effective in neurorehabilitation after damage to the brain. These principles include: incorporating multiple modalities into treatment to create stronger neural connections, using stimuli that evoke positive emotion, linking concepts with simultaneous and related presentations, and finding the appropriate intensity and duration of treatment for each individual patient.

Auditory comprehension treatment
Auditory comprehension is a primary focus in treatment for Wernickes aphasia, as it is the main deficit related to this diagnosis. Therapy activities may include:

Single-word comprehension: A common treatment method used to support single-word comprehension skills is known as a pointing drill. Through this method, clinicians lay out a variety of images in front of a patient. The patient is asked to point to the image that corresponds to the word provided by the clinician.
Understanding spoken sentences: "Treatment to improve comprehension of spoken sentences typically consists of drills in which patients answer questions, follow directions or verify the meaning of sentences".
Understanding conversation: An effective treatment method to support comprehension of discourse includes providing a patient with a conversational sample and asking him or her questions about that sample. Individuals with less severe deficits in auditory comprehension may also be able to retell aspects of the conversation.

Word retrieval
Anomia is consistently seen in aphasia, so many treatment techniques aim to help patients with word finding problems. One example of a semantic approach is referred to as semantic feature analyses. The process includes naming the target object shown in the picture and producing words that are semantically related to the target. Through production of semantically similar features, participants develop more skilled in naming stimuli due to the increase in lexical activation.

Restorative therapy approach
Neuroplasticity is a central component to restorative therapy to compensate for brain damage. This approach is especially useful in Wernickes aphasia patients that have had a stroke to the left brain hemisphere.Schuells stimulation approach is a main method in traditional aphasia therapy that follows principles to retrieve function in the auditory modality of language and influence surrounding regions through stimulation. The guidelines to have the most effective stimulation are as follows:
Auditory stimulation of language should be intensive and always present when other language modalities are stimulated.
The stimulus should be presented at a difficulty level equal to or just below the patients ability.
Sensory stimulation must be present and repeated throughout the treatment.
Each stimulus applied should produce a response; if there is no response more stimulation cues should be provided.
Response to stimuli should be maximized to create more opportunities for success and feedback for the speech-language pathologist.
The feedback of the speech-language pathologist should promote further success and patient and encouragement.
Therapy should follow an intensive and systemic method to create success by progressing in difficulty.
Therapies should be varied and build off of mastered therapy tasks.Schuells stimulation utilizes stimulation through therapy tasks beginning at a simplified task and progressing to become more difficult including:

Point to tasks. During these tasks the patient is directed to point to an object or multiple objects. As the skill is learned the level of complexity increases by increasing the number of objects the patient must point to.Simple: "Point to the book."
Complex: "Point to the book and then to the ceiling after touching your ear."
Following directions with objects. During these tasks the patient is instructed to follow the instruction of manually following directions that increase in complexity as the skill is learned.Simple: "Pick up the book."
Complex: "Pick up the book and put it down on the bench after I move the cup."
Yes or no questions – This task requires the patient to respond to various yes or no questions that can range from simple to complex.Paraphrasing and retelling – This task requires the patient to read a paragraph and, afterwards, paraphrase it aloud. This is the most complex of Schuells stimulation tasks because it requires comprehension, recall, and communication.

Social approach to treatment
The social approach involves a collaborative effort on behalf of patients and clinicians to determine goals and outcomes for therapy that could improve the patients quality of life. A conversational approach is thought to provide opportunities for development and the use of strategies to overcome barriers to communication. The main goals of this treatment method are to improve the patients conversational confidence and skills in natural contexts using conversational coaching, supported conversations, and partner training.
Conversational coaching involves patients with aphasia and their speech language pathologists, who serve as a "coach" discussing strategies to approach various communicative scenarios. The "coach" will help the patient develop a script for a scenario (such as ordering food at a restaurant), and help the patient practice and perform the scenario in and out of the clinic while evaluating the outcome.
Supported conversation also involves using a communicative partner who supports the patients learning by providing contextual cues, slowing their own rate of speech, and increasing their messages redundancy to promote the patients comprehension.Additionally, it is important to include the families of patients with aphasia in treatment programs. Clinicians can teach family members how to support one another, and how to adjust their speaking patterns to facilitate their loved ones treatment and rehabilitation.

Prognosis
Prognosis is strongly dependent on the location and extent of the lesion (damage) to the brain. Many personal factors also influence how a person will recover, which include age, previous medical history, level of education, gender, and motivation. All of these factors influence the brains ability to adapt to change, restore previous skills, and learn new skills. It is important to remember that all the presentations of Receptive Aphasia may vary. The presentation of symptoms and prognosis are both dependent on personal components related to the individuals neural organization before the stroke, the extent of the damage, and the influence of environmental and behavioral factors after the damage occurs. The quicker a diagnosis of a stroke is made by a medical team, the more positive the patients recovery may be </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ocular dysmetria and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Femoroacetabular impingement and can you explain it in depth? [/INST] Femoroacetabular impingement (FAI) is a condition involving one or more anatomical abnormalities of the hip joint, which is a ball and socket joint. It is a common cause of hip pain and discomfort in young and middle-aged adults. It occurs when the ball shaped femoral head contacts the acetabulum abnormally or does not permit a normal range of motion in the acetabular socket. Damage can occur to the articular cartilage, or labral cartilage (soft tissue, ring-shaped bumper of the socket), or both. The condition may be symptomatic or asymptomatic. It may cause osteoarthritis of the hip. Treatment options range from conservative management to surgery.

Signs and symptoms
Pain is the most common complaint in those with FAI. It is experienced in a number of areas, making the diagnosis challenging, but commonly occurs in the groin, upper buttock/lower back, the buttock or beneath the buttock, side of the affected hip and posterior upper leg. Onset of symptoms has been reported to present in both an acute and more gradual manner.  The pain is often significant enough to cause a decrease in activity level and movement. Some will also describe decreased range of motion of the affected hip. Another symptom is groin pain associated with activity and no prior history of trauma. Inability to perform activities such as high hip flexion or prolong sitting can also be seen in individuals with FAI.

Cause
FAI is characterized by abnormal contact between the proximal femur and rim of the acetabulum (hip socket). In most cases, patients present with a deformity in the femoral head, or acetabulum, a poorly positioned femoral-acetabular junction, or any or all of the foregoing. The cause of FAI is currently unknown, but both congenital and acquired etiologies have been put forth. Studies have shown an increased incidence in siblings, suggesting a genetic component. At least one study has also shown a predilection in the white population. It has also been reported to be more common in males. However, there is no concrete evidence to suggest a genetic trait and instead, the most favored theory currently supports that FAI (the cam type in particular) is due to repetitive movements involving the hip (e.g. squatting) in young athletes. Aggravating activities that are commonly reported include repetitive or prolonged squatting, twisting movements of the hip, like pivoting during athletics, getting in and out of cars, and even sitting for prolonged periods. A combination of these factors may also predispose to a form of FAI; predominantly, a marginal developmental hip abnormality together with environmental factors such as recurrent motion of the legs within a supraphysiologic range.Three types of FAI are recognized (see title image). The first involves an excess of bone along the upper surface of the femoral head, known as a cam deformity (abbreviation for camshaft, which the shape of the femoral head and neck resembles). The second is due to an excess of growth of the upper lip of the acetabular cup and is known as a pincer deformity.  The third is a combination of the two, generally referred to as mixed. The most common type seen, approximately 70% of the time, is the mixed type. A complicating issue is that some of the radiographic findings of FAI have also been described in asymptomatic subjects.Current literature suggests that the cam type of impingement is associated with the development of hip osteoarthritis. Thus far, no correlation has been seen between the pincer type and development of hip osteoarthritis.

Anatomy
The hip joint is classified as a ball and socket joint. This type of synovial joint allows for multidirectional movement and rotation. There are two bones that make up the hip joint and create an articulation between the femur and pelvis. This articulation connects the axial skeleton with the lower extremity. The pelvic bone, also known as the innominate bone, is formed by three bones fused together: the ilium, ischium, and pubis. The musculature of the hip is divided into anterior hip muscles and posterior hip muscles. The major nerve supply that runs through the hip joint is the femoral nerve and the sciatic nerve.

Diagnosis
Clinical evaluation is the first step in diagnosis, but will rarely lead to the diagnosis on its own, due to inconsistent and vague nature of the pain. Childhood and current activity should be inquired about. Physical exam should also involve assessing passive internal rotation of the hip during flexion, as range of motion is reduced in proportion to the size of a cam lesion. Flexing the hip to 90 degrees, adducting, and internally rotating the hip, known as the FADDIR test, should also be performed. It is positive when it causes pain. The FABER test should also be performed, this test involves flexing, abducting, and externally rotating the hip. The FABER test is useful when diagnosing concurrently with a labral pathology and is considered positive if the position elicits pain. Additional non-invasive ways to observe possible FAI is changes in gait that include a lower peak hip extension and internal rotation to compensate for bony growth.

X-ray
Projectional radiography ("X-ray")is often considered first line for FAI. Anterior-posterior pelvis and a lateral image of the hip in question should be attained. A 45-degree Dunn view is also recommended.

Other modalities
MRI imaging may follow, particularly if there is no specific evidence on radiographs, producing a three-dimensional reconstruction of the joint for better definition, to evaluate the hip cartilage, or measure hip socket angles (e.g. the alpha-angle as described by Nötzli in 2-D and by Siebenrock in 3-D). MR arthrogram had been used in the past, as it was more sensitive for picking up soft tissue lesions; however, due to improvement in technology, MRI is now considered comparable for picking up such lesions. CT is not usually used due to radiation exposure and no benefit above MRI. It is possible to perform dynamic simulation of hip motion with CT or MRI assisting to establish whether, where, and to what extent, impingement is occurring.
The diagnosis is often made in conjunction with a labral tear.

Differential Diagnosis
Piriformis syndrome or strain
Labral tear without FAI
Adductor muscle strain
Sciatica
Athletic pubalgia
Gluteus medius/minimus or illiopsoas tendinopathy
Stress fracture
Femoral head osteonecrosis
Other impingements, including anterior inferior iliac spine, ischiofemoral and iliopsoas
Loose body in the joint (intra-articular body)

Prevention
Prevention is currently being investigated. The goal of prevention would be to avoid joint damage and premature hip osteoarthritis. Studies are examining the effectiveness of screening adolescents in school and targeting at-risk individuals for education, physical therapy and decreasing participation in possibly harmful activities/sports as referenced in the epidemiology section.

Treatment
Treatment of FAI can be divided into those that are non-operative (conservative) and operative. Conservative treatment is often prescribed for those who have not yet received any therapy. Conservative treatment includes physical therapy, avoidance of those activities that produce pain, and  nonsteroidal anti-inflammatory drugs. It may also include joint injections with cortisone or hyaluronic acid, particularly for those who wish to avoid surgery.Physical therapy is implemented for the purpose of improving joint mobility, strengthening muscles surrounding the joint, correcting posture, and treating any other muscle or joint deficits that may be exacerbating the condition. A movement analysis may also be performed to identify specific movement patterns that may be causing injury. Studies to demonstrate the effectiveness of physical therapy are currently underway, with no conclusive results to date.Operative treatment is generally recommended to those who continue to have symptoms. It involves the surgical correction of any bony abnormalities causing the impingement and correction of any soft tissue lesions, such as labral tears. The primary aim of surgery is to correct the fit of the femoral head and acetabulum to create a hip socket that reduces contact between the two, allowing a greater range of movement. This includes femoral head sculpting and/or trimming of the acetabular rim.Surgery may be arthroscopic or open. A 2011 study analyzing current surgical methods for management of symptomatic femoral acetabular impingement, suggested that the arthroscopic method had surgical outcomes equal to or better than other methods with a lower rate of major complications when performed by experienced surgeons; consequently, the surgery is now rarely done open.Outcomes of arthroscopic surgery are currently being studied, but have generally been positive. According to a 2019 meta-analysis, the risk of having surgery fail or need to be re-operated on is about 5.5% whereas the complication rate is 1.7%. Additionally, patient reported outcomes show that approximately three to six months post-operative hip arthroscopy is when pain reduction and activities of daily life are improved. For sport function this timeline is about six months to a year. Failure of hip arthroscopy is more likely to fail in older patients, females, or those who have experienced the symptoms of FAI for a long period of time.When performed on elite athletes, most are able to return their previous level of competition. These athletes also have a higher rate of return to sport than recreational and collegiate athletes.Long term, randomized controlled trials evaluating the efficacy of conservative and operative treatments are underway.

Epidemiology
There has been limited research on the prevalence of FAI among a general population according to a literature review by Algarni. On the other hand, there are many sources that discuss the prevalence of athletes with the condition especially those that are younger and white. Hockey, tennis, soccer, and equestrian are all sports where the prevalence of a femoral neck abnormalities are higher due to the nature of the sport to force athletes into forced, loaded flexion and internal rotation.Cam lesions are more common in males, where pincer lesions are more common in females due to differences in anatomical development of the pelvis.

History
FAI is a relatively recent discovery </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Angioma serpiginosum and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tuberculoid leprosy and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Caffeine dependence and can you explain it in depth? [/INST] Caffeine dependence is the condition of having a substance dependence on caffeine, a commonplace central nervous system stimulant drug which occurs in nature in coffee, tea, yerba mate, cocoa, and other plants. Caffeine is also an additive in many consumer products, including beverages such as caffeinated alcoholic beverages, energy drinks, and colas.
Caffeines mechanism of action is somewhat different from that of cocaine and the substituted amphetamines; caffeine blocks adenosine receptors A1 and A2A. Adenosine is a by-product of cellular activity, and stimulation of adenosine receptors produces feelings of tiredness and the need to sleep. Caffeines ability to block these receptors means the levels of the bodys natural stimulants, dopamine and norepinephrine, continue at higher levels.
The Diagnostic and Statistical Manual of Mental Disorders describes four caffeine-related disorders including intoxication, withdrawal, anxiety, and sleep.

Dependence
Mild physical dependence can result from long-term caffeine use.  Caffeine addiction, or a pathological and compulsive form of use, has been documented in humans.

Addiction vs. Dependence
Caffeine use is classified as a dependence, not an addiction. For a drug to be considered addictive, it must activate the brains reward circuit. Caffeine, like addictive drugs, enhances dopamine signaling in the brain (is eugeroic), but not enough to activate the brains reward circuit like addictive substances such as cocaine, morphine, and nicotine. Caffeine dependence forms due to caffeine antagonizing the adenosine A2A receptor, effectively blocking adenosine from the adenosine receptor site. This delays the onset of drowsiness and releases dopamine.Studies have demonstrated that people who take in a minimum of 100 mg of caffeine per day (about the amount in one cup of coffee) can acquire a physical dependence that would trigger withdrawal symptoms that include headaches, muscle pain and stiffness, lethargy, nausea, vomiting, depressed mood, and marked irritability.  Professor Roland R. Griffiths, a professor of neurology at Johns Hopkins in Baltimore strongly believes that caffeine withdrawal should be classified as a psychological disorder. His research suggested that withdrawal affects 50% of habitual coffee drinkers,  beginning within  12–24 hours after cessation of caffeine intake, and peaking in 20–48 hours, lasting as long as 9 days.Continued exposure to caffeine leads the body to create more adenosine-receptors in the central nervous system, which makes it more sensitive to the effects of adenosine. It reduces the stimulatory effects of caffeine by increasing tolerance, and it increases the withdrawal symptoms of caffeine as the body becomes more sensitive to the effects of adenosine once caffeine intake decreases. Caffeine tolerance develops very quickly. Tolerance to the sleep disruption effects of caffeine were seen after consumption of 400 mg of caffeine 3 times a day for 7 days, whereas complete tolerance was observed after consumption of 300 mg taken 3 times a day for 18 days.

Physiological effects
When a person becomes caffeine dependent, it can cause a person to suffer different physiological effects which could lead to withdrawal. Symptoms can range from mild to severe that are dependent on the amount of caffeine consumed daily. Tests are still being done to get a better understanding of the effects that occur to someone when they become dependent on different forms of caffeine to make it through the day.

Adults
Caffeine is consumed by many each day and from this a dependence is formed. For the most part caffeine consumption is safe, but consuming over 400 mg of caffeine has shown adverse physiological and psychological effects; especially in people that have pre-existing conditions. When adults form a dependence on caffeine, it can cause a range of health problems such as headaches, insomnia, dizziness, cardiac issues, hypertension and others. When an adult is dependent on this substance, they must consume a certain amount of caffeine every day to avoid these effects.

Pregnancy
If pregnant, it is recommended not to consume over 200 mg of caffeine a day (depending on size of person) </s>


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<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Occupational injury and can you explain it in depth? [/INST] An occupational injury is bodily damage resulting from working. The most common organs involved are the spine, hands, the head, lungs, eyes, skeleton, and skin. Occupational injuries can result from exposure to occupational hazards (physical, chemical, biological, or psychosocial), such as temperature, noise, insect or animal bites, blood-borne pathogens, aerosols, hazardous chemicals, radiation, and occupational burnout.While many prevention methods are set in place, injuries may still occur due to poor ergonomics, manual handling of heavy loads, misuse or failure of equipment, exposure to general hazards, and inadequate safety training.

Worldwide
It has been estimated that worldwide there are more than 350,000 workplace fatalities and more than 270 million workplace injuries annually. In 2000 there were approximately 2.9 billion workers worldwide. Occupational injuries resulted in the loss of 3.5 years of healthy life for every 1,000 workers. 300,000 of the occupational injuries resulted in a fatality.The most common occupations associated with these hazards vary throughout the world depending on the major industries in a particular country. Overall, the most hazardous occupations are in farming, fishing, and forestry. In more developed countries, construction  and manufacturing  occupations are associated with high rates of spine, hand, and wrist injuries.

By country
United States
In the United States in 2012, 4,383 workers died from job injuries, 92% of which were men, and nearly 3 million nonfatal workplace injuries & illness were reported which cost businesses a collective loss of $198.2 billion and 60 million workdays. In 2007, 5,488 workers died from job injuries, 92% of which were men, and 49,000 died from work-related injuries. NIOSH estimates that 4 million workers in the U.S. in 2007 sustained non-fatal work related injuries or illnesses.According to data from the National Institute for Occupational Safety and Health (NIOSH) and the Bureau of Labor Statistics, an average of 15 workers die from traumatic injuries each day in the United States, and an additional 200 workers are hospitalized.In a study in the state of Washington, injured workers were followed for 14 years to determine the long term effects of work injury on employment. The work injuries resulted in an average of 1.06 years of lost productivity for each of the 31,588 allowed claims.In 2010, 25% of occupational injuries and illnesses that were not fatal but caused work absences were related to injuries to the upper limb.

Dangerous sectors
In the U.S. the Bureau of Labor Statistics makes available extensive statistics on workplace accidents and injuries. For example:

Common injuries
As in the United Kingdom, slips, trips and falls (STF) are common and account for 20-40% of disabling occupational injuries. Often these accidents result in a back injury that can persist to a permanent disability. In the United States, a high risk of back injuries occurs in the health care industry. 25% of reported injuries in health care workers in the state of Pennsylvania are for back pain. Among nurses, the prevalence of lower back pain may be as high as 72% mostly as a result of transferring patients. Some of these injuries can be prevented with the availability of patient lifts, improved worker training, and allocation of more time to perform work procedures. Another common type of injury is carpal tunnel syndrome associated with overuse of the hands and wrists. Studies on a cohort of newly hired workers have thus far identified forceful gripping, repetitive lifting of > 1 kg, and using vibrating power tools as high risk work activities.Additionally, noise exposure in the workplace can cause hearing loss, which accounted for 14% of reported occupational illnesses in 2007. Many initiatives have been created to prevent this common workplace injury. For example, the Buy Quiet program encourages employers to purchase tools and machines that produce less noise and the Safe-In-Sound Award was created to recognize companies and program that excel in the area of hearing loss prevention.Accidental injection or needlestick injuries are a common injury that plague agriculture workers and veterinarians. The majority of these injuries are located to the hands or legs, and can result in mild to severe reactions, including possible hospitalization. Due to the wide variety of biologics used in animal agriculture, needlestick injuries can result in bacterial or fungal infections, lacerations, local inflammation, vaccine/antibiotic reactions, amputations, miscarriage, and death. Due to daily human-animal interactions, livestock related injuries are also a prevalent injury of agriculture workers, and are responsible for the majority of nonfatal worker injuries on dairy farms. Additionally, approximately 30 people die of cattle and horse-related deaths in the United States annually.

Employees at risk
Perhaps the most important personal factor that predisposes to an increased risk is age. In the United States in 1998 17 million workers were over age 55 and by 2018 this population is expected to more than double. Workers in this age group are more likely to develop lower back pain that may be worsened by work conditions that normally do not affect a younger worker. Older workers are also more likely by be killed in a construction related fall. They are also at higher risk for injury due to age-related hearing loss, visual impairment, and use of multiple prescription medications that has been linked to higher rates of work injuries.  In addition to age, other personal risk factors for injury include obesity  particularly its associated risk with back injury, and depression.Lack of proper education or training can also predispose an individual to an occupational injury. For example, there is limited needlestick injury awareness among agriculture workers, and there is a need for comprehensive programs to prevent needlestick injuries on livestock operations. Proper animal handling techniques and training, or stockmanship, can also decrease the risk of livestock injury. A handlers timing, positioning, speed, direction of movement, and sounds made will affect the behavior of an animal and consequently the safety of the handler. The agriculture industry has begun to focus more on proper education and training, and has made a variety of resources available to producers. For example, organizations like the Upper Midwest Agriculture Safety and Health Center (UMASH) have a variety of informational fact sheets and training videos easily accessible online. Additionally, organizations like Beef Quality Assurance offers stockmanship training seminars and demonstrations.

Regulation
In the United States, the Occupational Safety and Health Administration (OSHA) sets and enforces national standards for occupational safety across all sectors.

United Kingdom
In the UK, a total of 111 fatal injuries happened in a single year. According to the HSE, a total of 111 workers died in work related injuries in the UK during 2019–20. The biggest cause for these fatal injuries was falling from heights that alone was responsible for 29 deaths during the same year. Other causes include injuries from moving vehicles and other objects, and contact with the moving machinery.In the United Kingdom in 2013–2014, 133 people were killed at work. Of those 133 people, 89 were employed, while 44 were self-employed. In 2013–2014, an estimated 629,000 injuries occurred at work </s>