<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 Enamel hypoplasia and can you explain it in depth? [/INST] Enamel hypoplasia is a defect of the teeth in which the enamel is deficient in quantity, caused by defective enamel matrix formation during enamel development, as a result of inherited and acquired systemic condition(s). It can be identified as missing tooth structure and may manifest as pits or grooves in the crown of the affected teeth, and in extreme cases, some portions of the crown of the tooth may have no enamel, exposing the dentin. It may be generalized across the dentition or localized to a few teeth. Defects are categorized by shape or location. Common categories are pit-form, plane-form, linear-form, and localised enamel hypoplasia. Hypoplastic lesions are found in areas of the teeth where the enamel was being actively formed during a systemic or local disturbance. Since the formation of enamel extends over a long period of time, defects may be confined to one well-defined area of the affected teeth. Knowledge of chronological development of deciduous and permanent teeth makes it possible to determine the approximate time at which the developmental disturbance occurred. Enamel hypoplasia varies substantially among populations and can be used to infer health and behavioural impacts from the past. Defects have also been found in a variety of non-human animals.

Causes
Enamel hypoplasia is believed to result from the dysfunction of ameloblasts—enamel-producing cells—either for a short period of time or throughout their lifespan. Enamel hypoplasia has a wide variety of known causes. Some causes are hereditary and others are from environmental exposure. The severity and localization of disease presentation is dependent on the timing and stage of tooth development in which the defective enamel formation occurred.
Hereditary causes of enamel hypoplasia include:

Primary abnormalities in enamel development, such as amelogenesis imperfecta
Certain dermatological conditions, such as Ehlers-Danlos syndrome
Other complex hereditary conditions such as Usher syndrome, Seckel syndrome, Treacher-Collins syndrome, Heimler syndrome & Ellis-Van Creveld syndromeEnvironmental causes of enamel hypoplasia include:

Nutritional deficits, such as Vitamin D, iron or calcium deficiency
Birth injury or preterm birth
Smoking during pregnancy
Trauma
Radiation
Certain infections (e.g. congenital syphilis, cytomegalovirus, congenital rubella)
Certain diseases (such as undiagnosed and untreated celiac disease, chicken pox, congenital syphilis)
High fever
Hypoxia (i.e. from severe cardiac defect)
Excessive fluoride exposure (dental fluorosis)
Tetracycline
Vitamin A, C, or D deficiency

Clinical relevance
Enamel hypoplasia is a risk factor for dental caries in children including early childhood caries (ECC), which continues to be a burden for many children. This association has been identified as significant and independent, and is believed that the formation of pits and missing enamel provides a suitable local environment for adhesion and colonization of cariogenic bacteria. Historically, enamel hypoplasia has been under-appreciated as a risk factor for ECC.
Developmental defects in enamel that affect tooth appearance in the esthetic zone (i.e. upper front teeth) may cause individuals to experience social embarrassment or anxiety regarding the appearance of their teeth.

Guidelines for Treatment of Enamel Hypoplasia
Dental sealants may be indicated for the prevention of caries in hypoplastic pit & fissure systems.
According to clinical trials, topical fluoride treatment in the form of gel or varnish is effective in preventing tooth decay in children with enamel defects </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 Vocal cord paresis and can you explain it in depth? [/INST] Vocal cord paresis, also known as recurrent laryngeal nerve paralysis or vocal fold paralysis, is an injury to one or both recurrent laryngeal nerves (RLNs), which control all intrinsic muscles of the larynx except for the cricothyroid muscle. The RLN is important for speaking, breathing and swallowing.The primary larynx-related functions of the mainly efferent nerve fiber RLN, include the transmission of nerve signals to the muscles responsible for regulation of the vocal folds position and tension to enable vocalization, as well as the transmission of sensory nerve signals from the mucous membrane of the larynx to the brain.
A unilateral injury of the nerve typically results in hoarseness caused by a reduced mobility of one of the vocal folds. It may also cause minor shortages of breath as well as aspiration problems especially concerning liquids. A bilateral injury causes the vocal folds to impair the air flow resulting in breathing problems, stridor and snoring sounds, and fast physical exhaustion. This strongly depends on the median or paramedian position of the paralyzed vocal folds. Hoarseness rarely occurs in bilaterally paralyzed vocal folds.

Signs and symptoms
Typically, patients with vocal fold paresis or paralysis are able to identify the onset of their symptoms. The most commonly reported symptom patients with either vocal fold paresis or paralysis make is having a rough voice quality. It is important to note that the symptoms of vocal fold paresis are not specific to the condition and tend to be common symptoms of other voice disorders as well. Vocal fold bowing, decreased vocal fold mobility, especially decreased mobility of the arytenoid cartilage, are often observed in vocal fold paresis. Glottal insufficiency is another common symptom observed in vocal fold paresis. In this case, the vocal folds do not come together properly. Glottal insufficiency may be hard to identify, especially when the area above the vocal folds is hyperfunctional. Hyperfunction may also make it difficult to detect the presence of vocal fold paresis. Hyperfunction of the area above the vocal folds may be considered a sign of glottal insufficiency and potentially, vocal fold paresis.In some cases, glottal closure may appear to be normal, however, asymmetries in the vocal folds may still be present. Though voice qualities may appear normal in some cases of vocal fold paresis or paralysis, mild differences in tension between the two vocal folds of the larynx can result in changes of voice pitch, intensity and reduced vocal stamina.Patients with either vocal fold paresis or paralysis may exhibit a breathy voice quality. This voice quality results from the increased activity of the vocal folds to compensate for the immobility of the PCA muscle(s). Patients may need to use more effort than normal when speaking and may find that their voice quiets or grows tired after speaking for a long time. This is known as vocal fatigue. Patients may also complain about having a limited pitch range and trouble varying their pitch at quick rate. It is often difficult for the speaker to project their voice and speak loud enough to be heard in noisy environments, over background noise, or when speaking to someone from a distance. It is possible for symptoms to surface only in situations where the environmental acoustics are poor, such as outdoors. Patients may report feeling pain in the throat or experiencing bouts of choking. A patient presenting with diplophonia is of major concern as this typically means that the mass and tension of their vocal folds are asymmetrical which may also indicate vocal fold paresis.Swallowing difficulties (dysphagia) are not commonly seen in vocal fold paresis that results from RLN damage. Dysphagia may however, suggest SLN damage. Symptoms of sensory nerve damage include: chronic coughing, the feeling of having a lump in the throat (globus sensation), hypersensitivity or abnormal sensation, spasms of the vocal folds (laryngospasms), dysphagia, pain from vocal use, and voice loss in high pitch ranges. It is possible for both the RLN and the SLN to be damaged simultaneously, so the symptoms of RLN and SLN damage may be seen independently or alongside one another.If maladaptive compensatory strategies are used more and more to try to offset the voice difficulties, the vocal mechanisms will fatigue and the above symptoms will worsen.

Causes
There are a wide variety of possible causes of vocal fold (VF) paresis, including congenital (i.e. present at birth) causes, infectious causes, tumors, traumatic causes, endocrinologic diseases (i.e. thyroid disease), and systemic neurologic diseases.

Congenital
Congenital conditions that are implicated in VFP include neurological disorders like hydrocephalus and Arnold-Chiari malformation, dysmorphic neurological disorders such as Moebius syndrome or Goldenhar Syndrome, anatomical abnormalities such as a tracheoesophageal fistula, vascular anomalies (e.g. vascular ring) affecting the vocal mechanism, syndromes affecting brainstem function or atrophic diseases such as Charcot-Marie-Tooth.In the absence of imaging, either invasive (e.g. laryngoscopy) or non-invasive (e.g. computed tomography scan), congenital VFP can be detected in infants through the presence of stridor (i.e. a high-pitched wheezing resulting from a blockage in the larynx or trachea), difficulties feeding, an abnormal sounding cry or excessive hoarseness.Recovery from congenital VFP varies and is reliant on the severity of the condition. Some cases of VFP recover spontaneously, often within the first year. If the paresis is persistent, surgical options such as vocal fold injections or tracheotomy can be taken into consideration.

Infection
Many viral infections have been reported as a cause for VF paresis, including herpes simplex virus, Epstein-Barr virus, Varicella-Zoster, cytomegalovirus, HIV, West Nile virus, and upper respiratory infection. Bacterial infections have also been reported to cause VF paresis, such as syphilis and Lyme disease.

Tumors
When abnormal cells group together in the body, they are said to form a tumor. Tumors can be either malignant (cancerous) or benign (non-cancerous). Tumors may lead to paralysis of the vocal folds when they affect the recurrent laryngeal nerves (RLNs) either directly or indirectly:

RLN paralysis can be caused by tumors of the thyroid, lung, esophagus, and mediastinum.
Radiation as a treatment for malignant head and neck tumors can reduce the number of blood vessels in the treatment area and lead to scarring. In some cases, this can paralyze the vagus nerve, of which the RLNs are branches.
Tumors of the vagus nerve, called vagal neurilemmomas, can also paralyze the vocal folds.

Trauma
VF paresis can result from trauma to one of more laryngeal nerves during intubation, surgery (e.g. thyroidectomy, spine surgery, carotid endartectomy, vagal nerve stimulator implantation), injection of botulinum neurotoxin, or penetrating neck trauma.

Thyroid disease
Causes of VF paresis also include diseases of the thyroid gland, such as hypothyroidism, goiter, and thyroiditis.

Systemic neurologic diseases
Several neurological diseases can cause VF paresis including:

Myasthenia Gravis (MG), a rare neuromuscular autoimmune disease. MGs dominant characteristic is muscles weakness including facial, jaw, pharyngeal and laryngeal muscles.
Charcot-Marie-Tooth (CMT), a neurological heredity disease that affects both motor and sensory functions. CMT affects the nerve cells and interrupts the transmission of nerve impulses as it concerns the axons and the myelination of the nerve cells.
Multiple Sclerosis (MS), which is an autoimmune disease that damages the myelin sheet surrounding the axons of the cranial nerves and the spinal nerves. There are several types of MS depending on the course of the disease.
Spinocerebellar Degeneration, a term that refers to a rare yet diverse chronic disease that affects the brain and the spinal cord. Spinocerebellar Degeneration is usually an inherited progressive disease; however, toxicity and vitamin deficiency can result in the acquired type of cerebellar degeneration disease.Additionally, there are pieces of evidence that some Systemic Rheumatological Diseases such as sarcoidosis, rheumatoid, scleroderma can result in having VF paresis.

Cardiovascular
A rare cause of vocal cord paresis that often presents itself as unexplained hoarseness is cardiovocal syndrome or Ortners syndrome. Although it was originally identified in patients with left atrial enlargement, the definition has expanded to include aneurysms of the aortic arch, pulmonary hypertension due to mixed connective tissue disease, or aberrant subclavian artery syndrome among other causes of left recurrent laryngeal nerve palsy with cardiovascular origin.

Diagnosis
There are a variety of ways to diagnose vocal fold paralysis. Important indications of possible causes can be revealed in the patients medical history, which may inform which diagnostic approach is taken. Voice diagnostics are used to assess voice quality and vocal performance. Voice assessment is necessary to plan and estimate the success of a possible speech therapy.[12]An auditory-perceptual evaluation is conducted by a Speech-Language Pathologist (S-LP), and allows changes in voice quality to be monitored over time. There are two scales which can be used to subjectively measure voice quality: the GRBAS (grade, roughness, breathiness, asthenia, strain) and the CAPE-V (Consensus Auditory Perceptual Evaluation of Voice). The GRBAS is used to rate the patients voice quality on 5 dimensions: grade (overall severity), roughness, breathiness, asthenia (weakness) and strain. Each dimension will receive a severity rating from 0 (not present) to 3 (severe). This allows the S-LP to make a judgment about the overall severity of the voice quality. The CAPE-V is used in a similar manner, rating of the dimensions of voice quality on a subjective scale from 0–100, and using this to determine an overall severity score.In the presence of neural lesions with unknown cause, a thorough ENT endoscopy with additional imaging techniques (computed tomography (CT) of the chest, particularly in the case of left-sided paralyses, and magnetic resonance imaging (MRI) of the neck including the base of the skull and the brain, ultrasound examination of the neck) are performed to exclude tumors along the laryngeal nerves. When tumor formation is suspected, parts of the hypopharynx and the upper esophagus and passive mobility of the arytenoid cartilage are endoscopically examined under anesthesia.Voice diagnostics are used to assess voice quality and vocal performance. Voice assessment is necessary to plan and estimate the success of a possible speech therapy. In incompletely or only partially healed paralyses, stroboscopic larynx examinations yield a type of slow motion picture to assess tension and fine mobility of the vocal folds during vocalization. Stroboscopy and voice assessment are important to establish an individual treatment plan to improve the voice.
Breathing tests (spirometry, body plethysmography) are used to measure impairment of respiratory flow through the larynx, particularly in patients with bilateral paralysis.
Electromyography of the larynx muscles (larynx EMG), which measures the electrical activity of the larynx muscles via thin needle electrodes, allows better differentiation between a neural lesion and other causes of impaired mobility of the vocal fold and localization of the lesion along the nerve. The larynx EMG can, within limits, provide a prognosis of the development of a recurrent laryngeal nerve paralysis. Patients with a poor chance of healing can be identified at an early stage. Unfortunately, this advanced examination technique is not available in all treatment centers.
The treating physician must view all examination results combined and establish an individual diagnosis and treatment plan for each patient.

Classification
Vocal fold paresis refers to a partial loss of input to the nerve of the vocal folds.  This loss of neural input leads to reduced vocal fold mobility. It is a condition with a variable profile, as the severity of the paresis can range on a wide continuum from minor to major loss of vocal fold mobility. Vocal fold paralysis, distinguished from vocal paresis, is the total loss of vocal fold mobility due to a lack of neural input to the vocal folds. These conditions result from continuous damage to the laryngeal nerves and often lead to vocal disability. Recurrent laryngeal nerve damage is the most common cause of vocal fold paresis. The RLN is responsible for motor input to the vocal folds. Physicians may also use the term recurrent laryngeal nerve paralysis. Additionally, superior laryngeal nerve damage (SLN) can also lead to vocal fold paresis. The SLN  is responsible for sensory input to the vocal folds. Due to its variable nature, the progression of vocal fold paresis may fluctuate, so it may be characterized differently from one evaluation to the next. Fluctuating vocal fold paresis has been observed in neurodegenerative disorders like Guillain–Barré syndrome or myasthenia gravis.The posterior cricoarytenoid (PCA) is a muscle of the larynx that is responsible for pulling the vocal folds apart from one another. Vocal fold paresis describes the weakness of the PCA and an impairment to its functioning. Unilateral vocal fold paresis is the term used when there is damage to the RLN on one side of the body. In unilateral vocal fold paresis, there is a lack of nerve supply to one side of the vocal folds PCA muscle. This lack of nerve supply renders the arytenoid cartilage immobile. The RLN may be damaged during surgical procedures. The right RLN in particular, has a greater chance of being damaged during surgery due to its position in the neck. When both of the vocal folds PCA muscles lack a nerve supply, the term bilateral vocal fold paresis is used. With bilateral vocal fold paresis, a persons airway may become blocked as the muscles are unable to pull the vocal folds apart fully.

Treatment
The treatment of vocal fold paralysis varies depending on its cause and main symptoms. For example, if laryngeal nerve paralysis is caused by a tumor, suitable therapy should be initiated. In the absence of any additional pathology, the first step of clinical management should be observation to determine whether spontaneous nerve recovery will occur. Voice therapy with a speech-language pathologist is suitable at this time, to help manage compensatory vocal behaviours which may manifest in response to the paralysis.

Voice therapy
The overall goal of voice therapy is to narrow the glottis without causing hyperfunction of the surrounding muscles. In the past, forced adduction exercises were used to push the vocal folds together, but often resulted in additional stress on the vocal folds. Current methods focus more generally on improving abdominal support, muscle strength and agility.

Hard glottal attacks
Hard glottal attacks involve building up subglottal pressure (air pressure below the vocal folds) before letting out a vowel sound. Often, this method is beneficial for clients who compensate by use of a falsetto register.

Half-swallow boom
The half-swallow boom allows for a repositioning of the vocal folds by taking advantage of laryngeal positioning when swallowing. The client is asked to take a breath and then initiate the movement of swallowing, followed by forcefully saying "boom". When performed properly, the "boom" sounds loud and clear. Eventually, this sound can be generalized to other words and phrases.

Abdominal breathing
Training in breath support is essential for those clients who identify as professional voice users. Shifting the awareness of the breath to the belly (diaphragmatic breathing) aids in efficient vocal function, reducing the risk of hyperfunction and muscular tension.

Lip and tongue trills
Lip and tongue trills aid in the balance of resonance, as well as coordinate the muscles of respiration, phonation and articulation. In addition, subglottal pressure may increase during lip trills, and result in the generation greater vocal fold vibration.

Surgery
After 9 months of observation, should the paralysis not resolve and the patient be dissatisfied with the outcomes of voice therapy, the next option is temporary injection medialization.  In this procedure, a variety of materials can be injected into the body of the vocal fold in order to bring it closer to the midline of the glottis. Materials such as Teflon, autologous fat, collagens acellular dermis, fascia, hydroxyapatite and hyaluronates are available to be used in the procedure. The choice of substance is dependent on several factors, taking into consideration the specific condition and preference of the patient as well as the clinical practice of the surgeon. The materials serve the purpose of filling up the vocal folds and increasing their volume. This allows the paralyzed vocal fold to make contact with the alternate fold, in order to more efficiently produce phonation. While injection augmentation has been long considered best practice, neither technique nor materials used have been standardized across clinicians. With this, results prove to be both safe and effective, but variable in their duration, lasting anywhere from 2 to 12 months.For patients with significant paralysis at 12 months post-onset, medialization thyroplasty may be suggested. This surgical procedure introduces a shim between the inner wall of the larynx and the soft tissue supporting the vocal fold. As a result, the paralyzed vocal fold is supported in a position closer to the midline of the glottis, and retains its ability to vibrate and phonate efficiently.In addition to medialization thyroplasty, arytenoid adduction can be performed to improve phonation results. This medical procedure consists of pulling the vocal processes of the arytenoid medially while monitoring the voicing quality being produced by the patient. When the best phonation appears to be achieved, the vocal processes are then maintained in place by a thread.A further surgical intervention used to mitigate vocal fold paresis is laryngeal reinnervation </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 Tracheobronchitis and can you explain it in depth? [/INST] Tracheobronchitis is inflammation of the trachea and bronchi. It is characterised by a cough, fever, and purulent (containing pus) sputum and is therefore suggestive of pneumonia. It is classified as a respiratory tract infection.Tracheobronchitis is often a hospital-acquired infection, particularly in an intensive care setting, associated with the use of mechanical ventilators, and the need for inserting a tracheal tube. In these cases it is known as ventilator-associated tracheobronchitis. The infection begins in the trachea where it colonises and spreads to the bronchi.
The characteristic increased sputum produced can give problems in the removal of the tracheal tube (extubation). Tracheobronchial infections are responsible for up to 80% of exacerbations in chronic obstructive pulmonary disease.

Causes
Ventilator-associated tracheobronchitis is a hospital-acquired infection usually contracted in an intensive care unit when a mechanical ventilator is used. The insertion of a tracheal tube can cause an infection in the trachea which then colonises and spreads to the bronchi. If there is further spread and development into the lungs this will give rise to ventilator-associated pneumonia </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 Repetitive strain injury and can you explain it in depth? [/INST] A repetitive strain injury (RSI) is an injury to part of the musculoskeletal or nervous system caused by repetitive use, vibrations, compression or long periods in a fixed position.  Other common names include repetitive stress disorders, cumulative trauma disorders (CTDs), and overuse syndrome.

Signs and symptoms
Some examples of symptoms experienced by patients with RSI are aching, pulsing pain, tingling and extremity weakness, initially presenting with intermittent discomfort and then with a higher degree of frequency.

Definition
Repetitive strain injury (RSI) and associative trauma orders are umbrella terms used to refer to several discrete conditions that can be associated with repetitive tasks, forceful  exertions, vibrations,  mechanical compression, sustained or awkward positions, or repetitive eccentric contractions. The exact terminology is controversial, but the terms now used by the United States Department of Labor and the National Institute of Occupational Safety and Health (NIOSH) are musculoskeletal disorders (MSDs) and work-related muscular skeletal disorders (WMDs).Examples of conditions that may sometimes be attributed to such causes include tendinosis (or less often tendinitis), carpal tunnel syndrome, cubital tunnel syndrome, De Quervain syndrome, thoracic outlet syndrome, intersection syndrome, golfers elbow (medial epicondylitis), tennis elbow (lateral epicondylitis), trigger finger (so-called stenosing tenosynovitis), radial tunnel syndrome, ulnar tunnel syndrome, and focal dystonia.A general worldwide increase since the 1970s in RSIs of the arms, hands, neck, and shoulder has been attributed to the widespread use in the workplace of keyboard entry devices, such as typewriters and computers, which require long periods of repetitive motions in a fixed posture. Extreme temperatures have also been reported as risk factor for RSI.

Risk factors
Occupational risk factors
Workers in certain fields are at risk of repetitive strains. Most occupational injuries are musculoskeletal disorders, and many of these are caused by cumulative trauma rather than a single event.  Miners and poultry workers, for example, must make repeated motions which can cause tendon, muscular, and skeletal injuries. Jobs that involve repeated motion patterns or prolonged posture within a work cycle, or both, may be repetitive. Young athletes are predisposed to RSIs due to an underdeveloped musculoskeletal system.

Psychosocial factors
Factors such as personality differences to work-place organization problems.  Certain workers may negatively perceive their work organization due to excessive work rate, long work hours, limited job control, and low social support.  Previous studies shown elevated urinary catecholamines (stress-related chemicals) in workers with RSI.  Pain related to RSI may evolve into chronic pain syndrome particularly for workers who do not have supports from co-workers and supervisors.

Non-occupational factors
Age and gender are important risk factors for RSIs. The risk of RSI increases with age.   Women are more likely affected than men because of their smaller frame, lower muscle mass and strength, and due to endocrine influences. In addition, lifestyle choices such as smoking and alcohol consumption are recognizable risk factors for RSI. Recent scientific findings indicate that obesity and diabetes may predispose an individual to RSIs by creating a chronic low grade inflammatory response that prevents the body from effectively healing damaged tissues.

Diagnosis
RSIs are assessed using a number of objective clinical measures. These include effort-based tests such as grip and pinch strength, diagnostic tests such as Finkelsteins test for De Quervains tendinitis, Phalens contortion, Tinels percussion for carpal tunnel syndrome, and nerve conduction velocity tests that show nerve compression in the wrist. Various imaging techniques can also be used to show nerve compression such as x-ray for the wrist, and MRI for the thoracic outlet and cervico-brachial areas. Utilization of routine imaging  is useful in early detection and treatment of overuse injuries in at risk populations, which is important in preventing long term adverse effects.

Treatment
There are no quick fixes for RSI. Early diagnosis is critical to limiting damage. For Upper Limb Repetitive Strain Injury (RSI), Occupational Therapists create interventions that include education to facilitate ergonomics. This will minimize the possibility of an upper limb strain injury by learning the correct approach during facilitating functional task movements. The RICE treatment is used as the first treatment for many muscle strains, ligament sprains, or other bruises and injuries. RICE is used immediately after an injury happens and for the first 24 to 48 hours after the injury. These modalities can help reduce the swelling and pain. Commonly prescribed treatments for early-stage RSIs include analgesics, myofeedback, biofeedback, physical therapy, relaxation, and ultrasound therapy. Low-grade RSIs can sometimes resolve themselves if treatments begin shortly after the onset of symptoms. However, some RSIs may require more aggressive intervention including surgery and can persist for years.Although there are no "quick fixes" for RSI, there are effective approaches to its treatment and prevention. One is that of ergonomics, the changing of ones environment (especially workplace equipment) to minimize repetitive strain.
General exercise has been shown to decrease the risk of developing RSI.  Doctors sometimes recommend that those with RSI engage in specific strengthening exercises, for example to improve sitting posture, reduce excessive kyphosis, and potentially thoracic outlet syndrome. Modifications of posture and arm use are often recommended.

History
Although seemingly a modern phenomenon, RSIs have long been documented in the medical literature </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 Reactive airway disease and can you explain it in depth? [/INST] Reactive airway disease (RAD) is an informal label that physicians apply to patients with symptoms similar to those of asthma. An exact definition of the condition does not exist. Individuals who are typically labeled as having RAD generally have a history of wheezing, coughing, dyspnea, and production of sputum that may or may not be caused by asthma. Symptoms may also include, but are not limited to, coughing, shortness of breath, excess mucus in the bronchial tube, swollen mucous membrane in the bronchial tube, and/or hypersensitive bronchial tubes. Physicians most commonly label patients with RAD when they are hesitant about formally diagnosing a patient with asthma, which is most prevalent in the pediatric setting. While some physicians may use RAD and asthma synonymously, there is controversy over this usage.
More generally, there is controversy over the use of RAD as a label in the healthcare setting, largely due to the ambiguous definition that the term has. Since RAD is not recognized as a real clinical diagnosis, its meaning is highly inconsistent and may cause confusion and misdiagnosis within the medical community. There are also concerns with overtreatment and undertreatment with RAD amongst physicians, since there is little formality with the label. Other problems that healthcare workers have with the use of the RAD label include its exclusion in the International Statistical Classification of Diseases and Related Health Problems, which can lead to billing issues in hospitals and other health care facilities, and the creation of a fabricated sense of security when using it has a diagnosis.RAD can be confused with reactive airways dysfunction syndrome, an asthma-like disorder that results from high exposure to vapors, fumes, and/or smoke. Unlike RAD, reactive airways dysfunction syndrome is recognized by multiple societies as a real clinical syndrome, including the American Thoracic Society and the American College of Chest Physicians.

Terminology
The term reactive airway disease originally began to appear in medical literature in the 1980s in reference to asthmatic patients with hyperactive airways, which is a common feature of asthma. This feature is characterized by increased bronchoconstriction reactions in response to stimuli that should not elicit so strong of response. These stimuli can include methacholine, histamine, and distilled water. However, while this was how the term initially was introduced, RAD soon began to be used interchangeably with the term asthma itself, which has led to the current controversy over its place in medical diagnoses.More commonly, RAD is now mostly used by physicians when they are hesitant to diagnose a patient with asthma. This is most prominent in pediatric settings for a variety of reasons. While infants tend to wheeze more often than adults, only one third of them eventually go on to actually have asthma. Asthma and viral bronchiolitis can also be nearly identical to each other when presented in very young children, since they both consist of wheezing, coughing, and nasal congestion. In addition, typical tests used to accurately diagnose children with asthma, such as the bronchial challenge test, are not considered to be accurate for children under the age of five. This can be due to failure of very young children to cooperate. Diagnosing a child with asthma also carries a certain negative connotation, causing hesitancy from some physicians to do so. All of these factors lead physicians to label young children with RAD instead of asthma, since the disease is often only suspected and unable to be confirmed with pediatric patients.Physicians will generally label an adult with RAD if they have no prior diagnosis or history of asthma while exhibiting symptoms of wheezing, production of sputum, and/or the use of an inhaler. Symptoms may also include, but are not limited to, coughing, shortness of breath, excess mucus in the bronchial tube, swollen mucous membrane in the bronchial tube, and/or hypersensitive bronchial tubes. In order to make a formal asthma diagnosis in adult patients, there is requirement to have documentation of either airway hyperreactivity or some sort of reversible airway obstruction. If none of these symptoms are present in an adult patients medical history or documentation, the physician may label the patient with RAD instead of asthma in order to still indicate there is an airway issue without formal diagnosis.

Reactive airways dysfunction syndrome
While the acronyms are similar, reactive airway disease (RAD) and reactive airways dysfunction syndrome (RADS) are not the same.Reactive airways dysfunction syndrome was first identified by Stuart M. Brooks and colleagues in 1985 as an asthma-like syndrome developing after a single exposure to high levels of an irritating vapor, fume, or smoke. It can manifest in adults with exposure to high levels of chlorine, ammonia, acetic acid, or sulphur dioxide, creating symptoms like asthma. These symptoms can vary from mild to fatal and can even create long-term airway damage, depending on the amount of exposure and the concentration of chlorine. Patients that have been diagnosed with RADS will likely have methacholine airway hyperreactivity, yet other tests that also measure pulmonary functions may appear normal. Some experts classify RADS as occupational asthma. Those with exposure to highly irritating substances should receive treatment to mitigate harmful effects. Treatment for RADS is similar to treatment for other disorders that result from acute inhalation. Preexisting allergies can be a risk factor for developing RADS.The main difference between RAD and RADS is that RADS can occur after just one exposure to the inhalants and without any prior sensitization. In addition, although the symptoms of RADS are very similar to those of asthma, they may be resolved. While some physicians argue that RADS is also not a real clinical syndrome, it is more commonly recognized in legitimate associations than RAD. These associations include the American Thoracic Society and the American College of Chest Physicians.

Controversy over use
There remains controversy over the use of RAD as an unofficial diagnosis. With its use not only being limited to clinical lexicon, but also transitioning to clinical literature now, more physicians are now increasingly disapproving its use in the healthcare setting.One of the largest problems with the using RAD as a diagnostic label lies in the ambiguity of its meaning, as RAD has no true clinical definition </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 Chronic traumatic encephalopathy and can you explain it in depth? [/INST] Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repeated trauma to the head. The encephalopathy symptoms can include behavioral problems, mood problems, and problems with thinking. The disease often gets worse over time and can result in dementia. It is unclear if the risk of suicide is altered.Most documented cases have occurred in athletes involved in striking-based combat sports, such as boxing, kickboxing, mixed martial arts, and Muay Thai—hence its original name dementia pugilistica (Latin for "fistfighters dementia")—and contact sports such as American football, Australian rules football, professional wrestling, ice hockey, rugby, and association football (soccer), in semi-contact sports such as baseball and basketball, and military combat arms occupations. Other risk factors include being in the military, prior domestic violence, and repeated banging of the head. The exact amount of trauma required for the condition to occur is unknown, and as of 2022 definitive diagnosis can only occur at autopsy. The disease is classified as a tauopathy.There is no specific treatment for the disease. Rates of CTE have been found to be about 30% among those with a history of multiple head injuries; however, population rates are unclear. Research in brain damage as a result of repeated head injuries began in the 1920s, at which time the condition was known as dementia pugilistica or "fistfighters dementia", "boxers madness", or "punch drunk syndrome". It has been proposed that the rules of some sports be changed as a means of prevention.

Signs and symptoms
Symptoms of CTE, which occur in four stages, generally appear eight to ten years after an individual experiences repetitive mild traumatic brain injuries.First-stage symptoms are confusion, disorientation, dizziness, and headaches. Second-stage symptoms include memory loss, social instability, impulsive behavior, and poor judgment. Third and fourth stages include progressive dementia, movement disorders, hypomimia, speech impediments, sensory processing disorder, tremors, vertigo, deafness, depression and suicidality.Additional symptoms include dysarthria, dysphagia, cognitive disorders such as amnesia, and ocular abnormalities, such as ptosis. The condition manifests as dementia, or declining mental ability, problems with memory, dizzy spells or lack of balance to the point of not being able to walk under ones own power for a short time and/or Parkinsonism, or tremors and lack of coordination. It can also cause speech problems and an unsteady gait. Patients with CTE may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia.

Cause
Most documented cases have occurred in athletes with mild repetitive head impacts (RHI) over an extended period of time. Evidence indicates that repetitive concussive and subconcussive blows to the head cause CTE. Specifically contact sports such as boxing, American football, Australian rules football, wrestling, mixed martial arts, ice hockey, rugby, and association football. In association football (soccer), whether this is just associated with prolific headers or other injuries is unclear as of 2017. Other potential risk factors include military personnel (repeated exposure to explosive charges or large caliber ordnance), domestic violence, and repeated banging of the head. The exact amount of trauma required for the condition to occur is unknown although it is believed that it may take years to develop.

Pathology
The neuropathological appearance of CTE is distinguished from other tauopathies, such as Alzheimers disease. The four clinical stages of observable CTE disability have been correlated with tau pathology in brain tissue, ranging in severity from focal perivascular epicenters of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions.The primary physical manifestations of CTE include a reduction in brain weight, associated with atrophy of the frontal and temporal cortices and medial temporal lobe. The lateral ventricles and the third ventricle are often enlarged, with rare instances of dilation of the fourth ventricle. Other physical manifestations of CTE include anterior cavum septi pellucidi and posterior fenestrations, pallor of the substantia nigra and locus ceruleus, and atrophy of the olfactory bulbs, thalamus, mammillary bodies, brainstem and cerebellum. As CTE progresses, there may be marked atrophy of the hippocampus, entorhinal cortex, and amygdala.On a microscopic scale, a pathognomonic CTE lesion involves p-tau aggregates in neurons, with or without thorn-shaped astrocytes, at the depths of the cortical sulcus around a small blood vessel, deep in the parenchyma, and not restricted to the subpial and superficial region of the sulcus; the pathognomonic lesion must include p-tau in neurons to distinguish CTE from ARTAG. Supporting features of CTE are: superficial neurofibrillary tangles (NFTs); p–tau in CA2 and CA4 hippocampus; p-tau in: mammillary bodies, hypothalamic nuclei, amygdala, nucleus accumbens, thalamus, midbrain tegmentum, nucleus basalis of Meynert, raphe nuclei, substantia nigra and locus coeruleus; p-tau thorn-shaped astrocytes (TSA) in the subpial region; p-tau dot-like neurites. Purely astrocytic perivascular p-tau pathology represents ARTAG and does not meet the criteria for CTE. Beta-amyloid is not a feature of CTE, however a person with CTE may have comorbid pathologies such as Alzheimers disease.A small group of individuals with CTE have chronic traumatic encephalomyopathy (CTEM), which is characterized by symptoms of motor-neuron disease and which mimics amyotrophic lateral sclerosis (ALS). Progressive muscle weakness and balance and gait problems (problems with walking) seem to be early signs of CTEM.Exosome vesicles created by the brain are potential biomarkers of TBI, including CTE.Loss of neurons, scarring of brain tissue, collection of proteinaceous senile plaques, hydrocephalus, attenuation of the corpus callosum, diffuse axonal injury, neurofibrillary tangles, and damage to the cerebellum are implicated in the syndrome. Neurofibrillary tangles have been found in the brains of dementia pugilistica patients, but not in the same distribution as is usually found in people with Alzheimers. One group examined slices of brain from patients having had multiple mild traumatic brain injuries and found changes in the cells cytoskeletons, which they suggested might be due to damage to cerebral blood vessels.Increased exposure to concussions and subconcussive blows is regarded as the most important risk factor. This exposure can depend on the total number of fights, number of knockout losses, the duration of career, fight frequency, age of retirement, and boxing style.

Diagnosis
Diagnosis of CTE cannot be made in living individuals; a clear diagnosis is only possible during an autopsy. Though there are signs and symptoms some researchers associate with CTE, there is no definitive test to prove the existence in a living person. Signs are also very similar to that of other neurological conditions such as Alzheimers.The lack of distinct biomarkers is the reason CTE cannot typically be diagnosed while a person is alive. Concussions are non-structural injuries and do not result in brain bleeding, which is why most concussions cannot be seen on routine neuroimaging tests such as CT or MRI. Acute concussion symptoms (those that occur shortly after an injury) should not be confused with CTE. Differentiating between prolonged post-concussion syndrome (PCS, where symptoms begin shortly after a concussion and last for weeks, months, and sometimes even years) and CTE symptoms can be difficult. Research studies are examining whether neuroimaging can detect subtle changes in axonal integrity and structural lesions that can occur in CTE. Recently, more progress in in-vivo diagnostic techniques for CTE has been made, using DTI, fMRI, MRI, and MRS imaging; however, more research needs to be done before any such techniques can be validated.PET tracers that bind specifically to tau protein are desired to aid diagnosis of CTE in living individuals. One candidate is the tracer [18F]FDDNP, which is retained in the brain in individuals with a number of dementing disorders such as Alzheimers disease, Down syndrome, progressive supranuclear palsy, corticobasal degeneration, familial frontotemporal dementia, and Creutzfeldt–Jakob disease. In a small study of 5 retired NFL players with cognitive and mood symptoms, the PET scans revealed accumulation of the tracer in their brains. However, [18F]FDDNP binds to beta-amyloid and other proteins as well. Moreover, the sites in the brain where the tracer was retained were not consistent with the known neuropathology of CTE. A more promising candidate is the tracer [18F]-T807, which binds only to tau. It is being tested in several clinical trials.A putative biomarker for CTE is the presence in serum of autoantibodies against the brain. The autoantibodies were detected in football players who experienced a large number of head hits but no concussions, suggesting that even sub-concussive episodes may be damaging to the brain. The autoantibodies may enter the brain by means of a disrupted blood-brain barrier, and attack neuronal cells which are normally protected from an immune onslaught. Given the large numbers of neurons present in the brain (86 billion), and considering the poor penetration of antibodies across a normal blood-brain barrier, there is an extended period of time between the initial events (head hits) and the development of any signs or symptoms. Nevertheless, autoimmune changes in blood of players may constitute the earliest measurable event predicting CTE.According to 2017 study on brains of deceased gridiron football players, 99% of tested brains of NFL players, 88% of CFL players, 64% of semi-professional players, 91% of college football players, and 21% of high school football players had various stages of CTE. Players still alive are not able to be tested.

Imaging
Although the diagnosis of CTE cannot be determined by imaging, the effects of head trauma may be seen with the use of structural imaging. Imaging techniques include the use of magnetic resonance imaging, nuclear magnetic resonance spectroscopy, CT scan, single-photon emission computed tomography, Diffusion MRI, and Positron emission tomography (PET). One specific use of imaging is the use of a PET scan is to evaluate for tau deposition, which has been conducted on retired NFL players.

Prevention
The use of helmets and mouth-guards has been put forward as a possible preventative measure; though neither has significant research to support its use, both have been shown to reduce direct head trauma. Although there is no significant research to support the use of helmets to reduce the risk of concussions, there is evidence to support that helmet use reduces impact forces. Mouth guards have been shown to decrease dental injuries, but again have not shown significant evidence to reduce concussions. Because repeated impacts are thought to increase the likelihood of CTE development, a growing area of practice is improved recognition and treatment for concussions and other head trauma; removal from sport participation during recovery from these traumatic injuries is essential. Proper return-to-play protocol after possible brain injuries is also important in decreasing the significance of future impacts.Efforts are being made to change the rules of contact sports to reduce the frequency and severity of blows to the head. Examples of these rule changes are the evolution of tackling technique rules in American football, such as the banning of helmet-first tackles, and the addition of rules to protect defenseless players. Likewise, another growing area of debate is better implementation of rules already in place to protect athletes.Because of the concern that boxing may cause CTE, there is a movement among medical professionals to ban the sport. Medical professionals have called for such a ban as early as the 1950s.

Management
No cure exists for CTE, and because it cannot be tested for until an autopsy is performed, people cannot know if they have it. Treatment is supportive as with other forms of dementia. Those with CTE-related symptoms may receive medication and non-medication related treatments.

Epidemiology
Rates of disease have been found to be about 30% among those with a history of multiple head injuries. Population rates, however, are unclear.Professional level athletes are the largest group with CTE, due to frequent concussions and sub-concussive impacts from play in contact sport. These contact-sports include American football, Australian rules football, ice hockey, Rugby football (Rugby union and Rugby league), boxing, kickboxing, mixed martial arts, association football, and wrestling. In association football, only prolific headers are known to have developed CTE.Cases of CTE were also recorded in baseball.According to a 2017 study on brains of deceased gridiron football players, 99% of tested brains of NFL players, 88% of CFL players, 64% of semi-professional players, 91% of college football players, and 21% of high school football players had various stages of CTE.Other individuals diagnosed with CTE were those involved in military service, had a previous history of chronic seizures, were domestically abused, or were involved in activities resulting in repetitive head collisions.

History
CTE was originally studied in boxers in the 1920s as "punch-drunk syndrome." Punch-drunk syndrome was first described in 1928 by a forensic pathologist, Dr. Harrison Stanford Martland, who was the chief medical examiner of Essex County in Newark, New Jersey, in a Journal of the American Medical Association article, in which he noted the tremors, slowed movement, confusion and speech problems typical of the condition. The term "punch-drunk" was replaced with "dementia pugilistica" in 1937 by J.A. Millsbaugh, as he felt the term was condescending to former boxers. The initial diagnosis of dementia pugilistica was derived from the Latin word for boxer pugil (akin to pugnus  fist, pugnāre  to fight).Other terms for the condition have included chronic boxers encephalopathy, traumatic boxers encephalopathy, boxers dementia, pugilistic dementia, chronic traumatic brain injury associated with boxing (CTBI-B), and punch-drunk syndrome.The seminal work on the disease came from British neurologist Macdonald Critchley, who in 1949 wrote a paper titled "Punch-drunk syndromes: the chronic traumatic encephalopathy of boxers". CTE was first recognized as affecting individuals who took considerable blows to the head, but was believed to be confined to boxers and not other athletes. As evidence pertaining to the clinical and neuropathological consequences of repeated mild head trauma grew, it became clear that this pattern of neurodegeneration was not restricted to boxers, and the term chronic traumatic encephalopathy became most widely used.In 1990, a patient nicknamed Wilma was diagnosed postmortem with dementia pugilistica; she was the first woman diagnosed with dementia pugilistica from domestic violence.In 2002, American football player Mike Webster died following unusual and unexplained behavior. In 2005 Nigerian-American neuropathologist Bennet Omalu, along with colleagues in the Department of Pathology at the University of Pittsburgh, published their findings in a paper titled "Chronic Traumatic Encephalopathy in a National Football League Player", followed by a paper on a second case in 2006 describing similar pathology.In June 2007 professional wrestler Chris Benoit murdered his wife and son before committing suicide days after appearing on television. His autopsy revealed he was in very advanced stages of CTE with his brain being said to resemble that of an 87-year-old with advanced Alzheimers.
In 2008, the Sports Legacy Institute joined with the Boston University School of Medicine (BUSM) to form the Center for the Study of Traumatic Encephalopathy (now the BU CTE Center). Brain Injury Research Institute (BIRI) also studies the impact of concussions.In 2014, Patrick Grange of Albuquerque was the first US soccer player with CTE at autopsy. He was well known for his heading and had died in 2012.On April 7, 2021, former National Football League player Phillip Adams was found to have shot and killed six people, before killing himself a day later. A subsequent autopsy revealed at that the time of the shooting, Adams had an "unusually severe" case of chronic traumatic encephalopathy.

Research
In 2005, forensic pathologist Bennet Omalu, along with colleagues in the Department of Pathology at the University of Pittsburgh, published a paper, "Chronic Traumatic Encephalopathy in a National Football League Player", in the journal Neurosurgery, based on analysis of the brain of deceased former NFL center Mike Webster. This was then followed by a paper on a second case in 2006 describing similar pathology, based on findings in the brain of former NFL player Terry Long.In 2008, the Center for the Study of Traumatic Encephalopathy at the BU School of Medicine (now the BU CTE Center) started the VA-BU-CLF Brain Bank at the Bedford Veterans Administration Hospital to analyze the effects of CTE and other neurodegenerative diseases on the brain and spinal cord of athletes, military veterans, and civilians. To date, the VA-BU-CLF Brain Bank is the largest CTE tissue repository in the world, with over 1000 brain donors.On 21 December 2009, the National Football League Players Association announced that it would collaborate with the BU CTE Center to support the centers study of repetitive brain trauma in athletes. Additionally, in 2010 the National Football League gave the BU CTE Center a $1 million gift with no strings attached. In 2008, twelve living athletes (active and retired), including hockey players Pat LaFontaine and Noah Welch as well as former NFL star Ted Johnson, committed to donate their brains to VA-BU-CLF Brain Bank after their deaths. In 2009, NFL Pro Bowlers Matt Birk, Lofa Tatupu, and Sean Morey pledged to donate their brains to the VA-BU-CLF Brain Bank.In 2010, 20 more NFL players and former players pledged to join the VA-BU-CLF Brain Donation Registry, including Chicago Bears linebacker Hunter Hillenmeyer, Hall of Famer Mike Haynes, Pro Bowlers Zach Thomas, Kyle Turley, and Conrad Dobler, Super Bowl Champion Don Hasselbeck and former pro players Lew Carpenter, and Todd Hendricks. In 2010, professional wrestlers Mick Foley, Booker T and Matt Morgan also agreed to donate their brains upon their deaths. Also in 2010, MLS player Taylor Twellman, who had to retire from the New England Revolution because of post-concussion symptoms, agreed to donate his brain upon his death. As of 2010, the VA-BU-CLF Brain Donation Registry consists of over 250 current and former athletes.In 2011, former North Queensland Cowboys player Shaun Valentine became the first Australian National Rugby League player to agree to donate his brain upon his death, in response to recent concerns about the effects of concussions on Rugby League players, who do not use helmets. Also in 2011, boxer Micky Ward, whose career inspired the film The Fighter, agreed to donate his brain upon his death. In 2018, NASCAR driver Dale Earnhardt Jr., who retired in 2017 citing multiple concussions, became the first auto racing competitor agreeing to donate his brain upon his death.In related research, the Center for the Study of Retired Athletes, which is part of the Department of Exercise and Sport Science at the University of North Carolina at Chapel Hill, is conducting research funded by National Football League Charities to "study former football players, a population with a high prevalence of exposure to prior Mild Traumatic Brain Injury (MTBI) and sub-concussive impacts, in order to investigate the association between increased football exposure and recurrent MTBI and neurodegenerative disorders such as cognitive impairment and Alzheimers disease (AD)".In February 2011, former NFL player Dave Duerson committed suicide via a gunshot to his chest, thus leaving his brain intact. Duerson left text messages to loved ones asking that his brain be donated to research for CTE. The family got in touch with representatives of the Boston University center studying the condition, said Robert Stern, the co-director of the research group. Stern said Duersons gift was the first time of which he was aware that such a request had been made by someone who had committed suicide that was potentially linked to CTE. Stern and his colleagues found high levels of the protein tau in Duersons brain. These elevated levels, which were abnormally clumped and pooled along the brain sulci, are indicative of CTE.In July 2010, NHL enforcer Bob Probert died of heart failure. Before his death, he asked his wife to donate his brain to CTE research because it was noticed that Probert experienced a mental decline in his 40s. In March 2011, researchers at Boston University concluded that Probert had CTE upon analysis of the brain tissue he donated </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 Post-schizophrenic depression and can you explain it in depth? [/INST] Post-schizophrenic depression is a "depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present." Someone that has post-schizophrenic depression experiences both symptoms of depression and can also continue showing mild symptoms of schizophrenia. Unfortunately, depression is a common symptom found in patients with schizophrenia and can fly under the radar for years before others become aware of its presence in a patient. However, very little research has been done on the subject, meaning there are few answers to how it should be systematically diagnosed, treated, or what course the illness will take. Some scientists would entirely deny the existence of post-schizophrenic depression, insisting it is a phase in schizophrenia as a whole. As of late, post-schizophrenic depression has become officially recognized as a syndrome and is considered a sub-type of schizophrenia.

Symptoms
Because the nature of acute schizophrenia is similar to depression, it is difficult to differentiate normal levels of depression in patients with schizophrenia from depressive levels in post-schizophrenic depression. "Prominent subjectively low mood, suggesting depression, and prominent blunting of affect, suggesting negative symptoms, are the two features which are most helpful in differentiating [schizophrenia and depression]." A number of researchers believe that depression is actually a symptom of schizophrenia that has been hidden by the psychosis. However, symptoms usually arise after the first psychotic episodes if they will arise at all. Officially, diagnosing post-schizophrenia depression in a patient requires for the patient to be experiencing a depressive episode of either short or long term following the overcoming of schizophrenia. The patient must still demonstrate some schizophrenic symptoms but those symptoms must no longer be the focus of the illness. Typically, the depressive symptoms are not severe enough to be classified as a severe depressive episode. Formally, diagnosis entails the patient having had schizophrenia within the past year, a number of schizophrenic symptoms, and depression being present for two weeks or more. Mild schizophrenic signs may be withdrawing socially, agitation or hostility, and irregular sleep such as in the case of insomnia and hypersomnia.

Causes
There is no clear cause to how certain patients with schizophrenia develop post-schizophrenic depression while others may surpass this stage. However, there are a few theories as to possible causes. Those with post-schizophrenic depression often experience social isolation due to their illness, which may increase depression levels. There is strong evidence of stigma-related isolation against those with mental illnesses in a variety of societies, especially those with schizophrenia as they are often viewed as dangerous and unpredictable. Because of this isolation and studies linking social isolation and depression, it is possible that patients under these stigmas eventually develop post-schizophrenic depression. Depression in patients with schizophrenia may also be caused by substance abuse, which is fairly common among those with schizophrenia, as depressants such as alcohol and cannabis can be relaxing. Furthermore, with what little information is currently known about post-schizophrenic depression, the onset may be caused by not giving patients with schizophrenia antipsychotic medications. After being taken off of antipsychotic medication, schizophrenic patients antidepressant medication had to be increased, while those under antipsychotic medication reported having fewer depressive symptoms, further giving reason to believe that a lack of antipsychotic medication in earlier stages of schizophrenia may lead to post-schizophrenic depression. However, some psychology professionals still push for the reduction of neuroleptic drugs, as there is a popular belief that post-schizophrenic depression is caused by neuroleptic treatment. Therapists are also believed to engage the depression in people with schizophrenia, having given too much psychotherapy after the patient had overcome their schizophrenic symptoms. Schizophrenia itself should not be overlooked as a key player in causing post-schizophrenic depression, though. A study done over a two-year time period shadowing patients with schizophrenia and monitoring their depression was unable to locate possible triggers such as the ones previously listed, so it is possible the nature of schizophrenia itself is the primary cause of post-schizophrenic depression.

Suicide
Those with post-schizophrenic depression are also commonly at risk for suicidal tendencies. There is a trend correlated between suicide and post-schizophrenic depression according to Mulholland and Coopers research in "The Symptoms of Depression in Schizophrenia and its Management." Furthermore, depression and schizophrenia have both been studied individually to try to determine if there is a correlation, and research has indicated that there is a very strong tendency for people with depression or schizophrenia to attempt suicide. Statistically, out of all patients with schizophrenia, "10%...commit suicide.  Depressed patients with schizophrenia are at a particularly high risk for suicide the first few months after diagnosis and after hospital discharge." Risk factors increasing the chance of suicide are, from highest to lowest, previous depressive orders, previous suicide attempts, drug abuse, and several other factors </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 Cryptorchidism and can you explain it in depth? [/INST] Cryptorchidism is the absence of one or both testes from the scrotum. The word is from Greek κρυπτός (kryptos) hidden and ὄρχις (orchis) testicle. It is the most common birth defect of the male genital tract. About 3% of full-term and 30% of premature infant boys are born with at least one undescended testis.
However, about 80% of cryptorchid testes descend by the first year of life (the majority within three months), making the true incidence of cryptorchidism around 1% overall. Cryptorchidism may develop after infancy, sometimes as late as young adulthood, but that is exceptional.

Cryptorchidism is distinct from monorchism, the condition of having only one testicle. Though the condition may occur on one or both sides, it more commonly affects the right testis.A testis absent from the normal scrotal position may be:

Anywhere along the "path of descent" from high in the posterior (retroperitoneal) abdomen, just below the kidney, to the inguinal ring
In the inguinal canal
Ectopic, having "wandered" from the path of descent, usually outside the inguinal canal and sometimes even under the skin of the thigh, the perineum, the opposite scrotum, or the femoral canal
Undeveloped (hypoplastic) or severely abnormal (dysgenetic)
Missing (also see anorchia).About two-thirds of cases without other abnormalities are unilateral; most of the other third involve both testes. In 90% of cases, an undescended testis can be felt in the inguinal canal. In a small minority of cases, missing testes may be found in the abdomen or appear to be nonexistent (truly "hidden").
Undescended testes are associated with reduced fertility, increased risk of testicular germ-cell tumors, and psychological problems when fully-grown. Undescended testes are also more susceptible to testicular torsion (and subsequent infarction) and inguinal hernias. Without intervention, an undescended testicle will usually descend during the first year of life, but to reduce these risks, undescended testes can be brought into the scrotum in infancy by a surgical procedure called an orchiopexy.Although cryptorchidism nearly always refers to congenital absence or maldescent, a testis observed in the scrotum in early infancy can occasionally "reascend" (move back up) into the inguinal canal. A testis that can readily move or be moved between the scrotum and canal is referred to as retractile.
Cryptorchidism, hypospadias, testicular cancer, and poor semen quality make up the syndrome known as testicular dysgenesis syndrome.

Signs and symptoms
Infertility
Many men who were born with undescended testes have reduced fertility, even after orchiopexy in infancy. The reduction with unilateral cryptorchidism is subtle, with a reported infertility rate of about 10%, compared with about 6% reported by the same study for the general population of adult men.
The fertility reduction after orchiopexy for bilateral cryptorchidism is more marked, about 38%, or six times that of the general population. The basis for the universal recommendation for early surgery is research showing degeneration of spermatogenic tissue and reduced spermatogonia counts after the second year of life in undescended testes. The degree to which this is prevented or improved by early orchiopexy is still uncertain.

Cancer risk
One of the strongest arguments for early orchiopexy is reducing the risk of testicular cancer. About one in 500 men born with one or both testes undescended develops testicular cancer, roughly a four- to 40-fold increased risk. The peak incidence occurs in the third and fourth decades of life. The risk is higher for intra-abdominal testes and somewhat lower for inguinal testes, but even the normally descended testis of a man whose other testis was undescended has about a 20% higher cancer risk than those of other men.The most common type of testicular cancer occurring in undescended testes is seminoma. It is usually treatable if caught early, so urologists often recommend that boys who had orchiopexy as infants be taught testicular self-examination, to recognize testicular masses and seek early medical care for them. Cancer developing in an intra-abdominal testis would be unlikely to be recognized before considerable growth and spread, and one of the advantages of orchiopexy is that a mass developing in a scrotal testis is far easier to recognize than an intra-abdominal mass.
Orchidopexy was originally thought to result in easier detection of testicular cancer, but did not lower the risk of actually developing cancer.  However, recent data have shown a paradigm shift.  The New England Journal of Medicine published in 2007 that orchidopexy performed before puberty resulted in a significantly reduced risk of testicular cancer than if done after puberty.The risk of malignancy in the undescended testis is four to 10 times higher than that in the general population and is about one in 80 with a unilateral undescended testis and one in 40 to one in 50 for bilateral undescended testes. The peak age for this tumor is 15–45 years old. The most common tumor developing in an undescended testis is a seminoma (65%); in contrast, after orchiopexy, seminomas represent only 30% of testicular tumors.

Causes
In most full-term infant boys with cryptorchidism but no other genital abnormalities, a cause cannot be found, making this a common, sporadic, unexplained (idiopathic) birth defect. A combination of genetics, maternal health, and other environmental factors may disrupt the hormones and physical changes that influence the development of the testicles.

Severely premature infants can be born before descent of testes.  Low birth weight is also a known factor.
A contributing role of environmental chemicals called endocrine disruptors that interfere with normal fetal hormone balance has been proposed.  The Mayo Clinic lists "parents exposure to some pesticides" as a known risk factor.
Risk factors may include exposure to regular alcohol consumption during pregnancy (five or more drinks per week, associated with a three-fold increase in cryptorchidism when compared to nondrinking mothers.  Cigarette smoking is also a known risk factor.
Family history of undescended testicles or other problems of genital development
Cryptorchidism occurs at a much higher rate in a large number of congenital malformation syndromes. Among the more common are Down syndrome, Prader–Willi syndrome, and Noonan syndrome.
In vitro fertilization, use of cosmetics by the mother, and pre-eclampsia have also been recognized as risk factors for development of cryptorchidism.In 2008, a study was published that investigated the possible relationship between cryptorchidism and prenatal exposure to a chemical called phthalate (DEHP), which is used in the manufacture of plastics. The researchers found a significant association between higher levels of DEHP metabolites in pregnant mothers and several sex-related changes, including incomplete descent of the testes in their sons.  According to the lead author of the study, a national survey found that 25% of U.S. women had phthalate levels similar to the levels that were found to be associated with sexual abnormalities.A 2010 study  examined the prevalence of congenital cryptorchidism among offspring whose mothers had taken mild analgesics, primarily over-the-counter pain medications including ibuprofen (e.g. Advil) and paracetamol (acetaminophen). Combining the results from a survey of pregnant women prior to their due date in correlation with the health of their children and an ex vivo rat model, the study found  that pregnant women who had been exposed to mild analgesics had a higher prevalence of baby boys born with congenital cryptorchidism.New insight into the testicular descent mechanism has been hypothesized by the concept of a male programming window derived from animal studies. According to this concept, testicular descent status is "set" during the period from eight to 14 weeks of gestation in humans. Undescended testis is a result of disruption in androgen levels only during this programming window.

Mechanism
Normal development
The testes begin as an immigration of primordial germ cells into testicular cords along the gonadal ridge in the abdomen of the early embryo. The interaction of several male genes organizes this developing gonad into a testis rather than an ovary by the second month of gestation. During the third to fifth months, the cells in the testes differentiate into testosterone-producing Leydig cells, and anti-Müllerian hormone-producing Sertoli cells. The germ cells in this environment become fetal spermatogonia. Male external genitalia develops during the third and fourth months of gestation and the fetus continues to grow, develop, and differentiate.
The testes remain high in the abdomen until the seventh month of gestation when they move from the abdomen through the inguinal canals into the two sides of the scrotum. Movement has been proposed to occur in two phases, under the control of somewhat different factors. The first phase, movement across the abdomen to the entrance of the inguinal canal, appears controlled (or at least greatly influenced) by anti-Müllerian hormone (AMH). The second phase, in which the testes move through the inguinal canal into the scrotum, is dependent on androgens (most importantly testosterone). In rodents, androgens induce the genitofemoral nerve to release calcitonin gene-related peptide, which produces rhythmic contractions of the gubernaculum, a ligament which connects the testis to the scrotum, but a similar mechanism has not been demonstrated in humans. Maldevelopment of the gubernaculum or deficiency or insensitivity to either AMH or androgen can, therefore, prevent the testes from descending into the scrotum. Some evidence suggests an additional paracrine hormone, referred to as descendin, may be secreted by the testes.
In many infants with inguinal testes, further descent of the testes into the scrotum occurs in the first six months of life. This is attributed to the postnatal surge of gonadotropins and testosterone that normally occurs between the first and fourth months of life.
Spermatogenesis continues after birth. In the third to fifth months of life, some of the fetal spermatogonia residing along the basement membrane become type A spermatogonia. More gradually, other fetal spermatogonia become type B spermatogonia and primary spermatocytes by the fifth year after birth. Spermatogenesis arrests at this stage until puberty.
Most normal-appearing undescended testes are also normal by microscopic examination, but reduced spermatogonia can be found. The tissue in undescended testes becomes more markedly abnormal ("degenerates") in microscopic appearance between two and four years after birth. Some evidence indicates early orchiopexy reduces this degeneration.

Pathophysiology
At least one contributing mechanism for reduced spermatogenesis in cryptorchid testes is temperature. The temperature of testes in the scrotum is at least a few degrees cooler than in the abdomen. Animal experiments in the middle of the 20th century suggested that raising the temperature could damage fertility. Some circumstantial evidence suggests tight underwear and other practices that raise the testicular temperature for prolonged periods can be associated with lower sperm counts. Nevertheless, research in recent decades suggests that the issue of fertility is more complex than a simple matter of temperature. Subtle or transient hormone deficiencies or other factors that lead to a lack of descent also may impair the development of spermatogenic tissue.
The inhibition of spermatogenesis by ordinary intra-abdominal temperature is so potent that continual suspension of normal testes tightly against the inguinal ring at the top of the scrotum by means of special "suspensory briefs" has been researched as a method of male contraception, and was referred to as "artificial cryptorchidism" by one report.
An additional factor contributing to infertility is the high rate of anomalies of the epididymis in boys with cryptorchidism (over 90% in some studies). Even after orchiopexy, these may also affect sperm maturation and motility at an older age.

Diagnosis
The most common diagnostic dilemma in otherwise normal boys is distinguishing a retractile testis from a testis that will not descend spontaneously into the scrotum. Retractile testes are more common than truly undescended testes and do not need to be operated on. In normal males, as the cremaster muscle relaxes or contracts, the testis moves lower or higher ("retracts") in the scrotum. This cremasteric reflex is much more active in infant boys than older men. A retractile testis high in the scrotum can be difficult to distinguish from a position in the lower inguinal canal. Though various maneuvers are used to do so, such as using a cross-legged position, soaping the examiners fingers, or examining in a warm bath, the benefit of surgery in these cases can be a matter of clinical judgment.
In the minority of cases with bilaterally nonpalpable testes, further testing to locate the testes, assess their function, and exclude additional problems is often useful. Scrotal ultrasound or magnetic resonance imaging performed and interpreted by a radiologist can often locate the testes while confirming absence of a uterus. At ultrasound, the undescended testis usually appears small, less echogenic than the contralateral normal testis and usually located in the inguinal region.  With color Doppler ultrasonography, the vascularity of the undescended testis is poor.A karyotype can confirm or exclude forms of dysgenetic primary hypogonadism, such as Klinefelter syndrome or mixed gonadal dysgenesis. Hormone levels (especially gonadotropins and AMH) can help confirm that hormonally functional testes are worth attempting to rescue, as can stimulation with a few injections of human chorionic gonadotropin to elicit a rise of the testosterone level. Occasionally, these tests reveal an unsuspected and more complicated intersex condition.
In the even smaller minority of cryptorchid infants who have other obvious birth defects of the genitalia, further testing is crucial and has a high likelihood of detecting an intersex condition or other anatomic anomalies. Ambiguity can indicate either impaired androgen synthesis or reduced sensitivity. The presence of a uterus by pelvic ultrasound suggests either persistent Müllerian duct syndrome (AMH deficiency or insensitivity) or a severely virilized genetic female with congenital adrenal hyperplasia. An unambiguous micropenis, especially accompanied by hypoglycemia or jaundice, suggests congenital hypopituitarism.

Treatment
The primary management of cryptorchidism is watchful waiting, due to the high likelihood of self-resolution. Where this fails, orchiopexy is effective if inguinal testes have not descended after 4–6 months.  Surgery is often performed by a pediatric urologist or pediatric surgeon, but in many communities still by a general urologist or surgeon.
When the undescended testis is in the inguinal canal, hormonal therapy is sometimes attempted and very occasionally successful. The most commonly used hormone therapy is human chorionic gonadotropin (hCG). A series of hCG injections (10 injections over five weeks is common) is given and the status of the testis/testes is reassessed at the end. Although many trials have been published, the reported success rates range widely, from roughly 5% to 50%, probably reflecting the varying criteria for distinguishing retractile testes from low inguinal testes. Hormone treatment does have the occasional incidental benefits of allowing confirmation of Leydig cell responsiveness (proven by a rise of the testosterone by the end of the injections) or inducing additional growth of a small penis (via the testosterone rise). Some surgeons have reported facilitation of surgery, perhaps by enhancing the size, vascularity, or healing of the tissue. A newer hormonal intervention used in Europe is the use of GnRH analogs such as nafarelin or buserelin; the success rates and putative mechanism of action are similar to hCG, but some surgeons have combined the two treatments and reported higher descent rates. Limited evidence suggests that germ cell count is slightly better after hormone treatment; whether this translates into better sperm counts and fertility rates at maturity has not been established. The cost of either type of hormone treatment is less than that of surgery and the chance of complications at appropriate doses is minimal. Nevertheless, despite the potential advantages of a trial of hormonal therapy, many surgeons do not consider the success rates high enough to be worth the trouble, since the surgery itself is usually simple and uncomplicated.
In cases where the testes are identified preoperatively in the inguinal canal, orchiopexy is often performed as an outpatient and has a very low complication rate. An incision is made over the inguinal canal. The testis with accompanying cord structure and blood supply is exposed, partially separated from the surrounding tissues ("mobilized"), and brought into the scrotum. It is sutured to the scrotal tissue or enclosed in a "subdartos pouch". The associated passage back into the inguinal canal, an inguinal hernia, is closed to prevent reascent.
In patients with intra-abdominal maldescended testis, laparoscopy is useful to see for oneself the pelvic structures, position of the testis and decide upon surgery (single or staged procedure ).
Surgery becomes more complicated if the blood supply is not ample and elastic enough to be stretched into the scrotum. In these cases, the supply may be divided, some vessels sacrificed with expectation of adequate collateral circulation. In the worst case, the testis must be "autotransplanted" into the scrotum, with all connecting blood vessels cut and reconnected (anastomosed).
When the testis is in the abdomen, the first stage of surgery is exploration to locate it, assess its viability, and determine the safest way to maintain or establish the blood supply. Multistage surgeries, or autotransplantation and anastomosis, are more often necessary in these situations. Just as often, intra-abdominal exploration discovers that the testis is nonexistent ("vanished"), or dysplastic and not salvageable.
The principal major complication of all types of orchiopexy is a loss of the blood supply to the testis, resulting in loss of the testis due to ischemic atrophy or fibrosis.

Other animals
Cryptorchidism is seen in all domestic animals, most commonly in stallions, boars, and canines. The prevalence of this condition can vary depending on species and breed. Evidence of this condition is more likely in companion animals and swine than ruminants. The cause of this condition can vary from a combination of genetics, environment, and epigenetics.

Dogs
Cryptorchidism is common in male dogs, occurring at a rate  up to 10%.  This condition is one of the most common congenital defects in purebred dogs (11%), with 14% reported in Siberian Huskies. Although the genetics are not fully understood, it is thought to be a recessive, and probably polygenetic, trait.  Some have speculated that it is a sex-limited autosomal recessive trait; however, it is unlikely to be simple recessive. Dog testes usually descend by 10 days of age and it is considered to be cryptorchidism if they do not descend by the age of eight weeks.  Cryptorchidism can be either bilateral (causing sterility) or unilateral, and inguinal or abdominal (or both).  Because it is an inherited trait, affected dogs should not be bred and should be castrated.  The parents should be considered carriers of the defect and a breeder should thoughtfully consider whether to breed the carrier parent or not.  Littermates may be normal, carriers, or cryptorchid.  Castration of the undescended teste(s) should be considered for cryptorchid dogs due to the high rate of testicular cancer, especially Sertoli cell tumors </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 Cytomegalovirus and can you explain it in depth? [/INST] Cytomegalovirus (CMV) (from cyto- cell via Greek κύτος kútos- container + μέγας mégas big, megalo- + -virus via Latin vīrus poison) is a genus of viruses in the order Herpesvirales, in the family Herpesviridae, in the subfamily Betaherpesvirinae. Humans and other primates serve as natural hosts. The 11 species in this genus include human betaherpesvirus 5 (HCMV, human cytomegalovirus, HHV-5), which is the species that infects humans. Diseases associated with HHV-5 include mononucleosis and pneumonia. In the medical literature, most mentions of CMV without further specification refer implicitly to human CMV. Human CMV is the most studied of all cytomegaloviruses.MX2/MXB was identified as a restriction factor for herpesviruses, which acts at a very early stage of the replication cycle and MX2/MXB restriction of herpesvirus requires GTPase activity.

Taxonomy
Within the Herpesviridae, CMV belongs to the Betaherpesvirinae subfamily, which also includes the genera Muromegalovirus and Roseolovirus (human herpesvirus 6 and human betaherpesvirus 7). It is also related to other herpesviruses within the Alphaherpesvirinae subfamily, which includes herpes simplex viruses 1 and 2 and varicella-zoster virus, and the Gammaherpesvirinae subfamily, which includes Epstein–Barr virus and Kaposis sarcoma-associated herpesvirus.Several species of Cytomegalovirus have been identified and classified for different mammals. The most studied is Human cytomegalovirus (HCMV), which is also known as Human betaherpesvirus 5 (HHV-5). Other primate CMV species include Chimpanzee cytomegalovirus (CCMV) that infects chimpanzees and orangutans, and Simian cytomegalovirus (SCCMV) and Rhesus cytomegalovirus (RhCMV) that infect macaques; CCMV is known as both Panine beta herpesvirus 2 (PaHV-2) and Pongine betaherpesvirus 4 (PoHV-4). SCCMV is called cercopithecine betaherpesvirus 5 (CeHV-5) and RhCMV, Cercopithecine betaherpesvirus 8 (CeHV-8). A further two viruses found in the night monkey are tentatively placed in the genus Cytomegalovirus, and are called Herpesvirus aotus 1 and Herpesvirus aotus 3. Rodents also have viruses previously called cytomegaloviruses that are now reclassified under the genus Muromegalovirus; this genus contains Mouse cytomegalovirus (MCMV) is also known as Murid betaherpesvirus 1 (MuHV-1) and the closely related Murid betaherpesvirus 2 (MuHV-2) that is found in rats.

Species
The genus consists of these 11 species:
Aotine betaherpesvirus 1
Cebine betaherpesvirus 1
Cercopithecine betaherpesvirus 5
Human betaherpesvirus 5
Macacine betaherpesvirus 3
Macacine betaherpesvirus 8
Mandrilline betaherpesvirus 1
Panine betaherpesvirus 2
Papiine betaherpesvirus 3
Papiine betaherpesvirus 4
Saimiriine betaherpesvirus 4

Structure
Viruses in Cytomegalovirus are enveloped, with icosahedral, spherical to pleomorphic, and round geometries, and T=16 symmetry. The diameter is around 150–200 nm. Genomes are linear and nonsegmented, around 200 kb in length.

Genome
Herpesviruses have some of the largest genomes among human viruses, often encoding hundreds of proteins. For instance, the double‑stranded DNA (dsDNA) genome of wild-type HCMV strains has a size of around 235 kb and encodes at least 208 proteins. It is thus longer than all other human herpesviruses and one of the longest genomes of all human viruses in general. It has the characteristic herpesvirus class E genome architecture, consisting of two unique regions (unique long UL and unique short US), both flanked by a pair of inverted repeats (terminal/internal repeat long TRL/IRL and internal/terminal repeat short IRS/TRS). Both sets of repeats share a region of a few hundred bps, the so-called "a sequence"; the other regions of the repeats are sometimes referred to as "b sequence" and "c sequence".

Life cycle
Viral replication is nuclear and lysogenic </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 Steatocystoma simplex 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 Generalized eruptive histiocytoma 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 Proximal femoral focal deficiency and can you explain it in depth? [/INST] Proximal femoral focal deficiency (PFFD), also known as Congenital Femoral Deficiency (CFD),   is a rare, non-hereditary birth defect that affects the pelvis, particularly the hip bone, and the proximal femur.  The disorder may affect one side or both, with the hip being deformed and the leg shortened.
It is commonly linked with the absence or shortening of a leg bone (fibular hemimelia) and the absence of a kneecap.  Other linked birth defects include the dislocation or instability of the joint between the femur and the kneecap, a shortened tibia or fibula, and foot deformities.

Causes
The cause of PFFD is uncertain.  Two hypotheses have been advanced.  The theory of sclerotome subtraction posits injury to neural crest cells that are the precursors to sensory nerves at the level of L4 and L5. Histologic studies of a fetus with unilateral PFFD have prompted an alternative hypothesis that PFFD is caused by a defect in maturation of chondrocytes (cartilage cells) at the growth plate.  In either hypothesis, the agent causing the injury is usually not known. Thalidomide is known to cause PFFD when the mother is exposed to it in the fifth or sixth week of pregnancy, and it is speculated that exposure to other toxins during pregnancy may also be a cause.  Other etiologies that have been suggested, but not proven, include anoxia, ischemia, radiation, infection, hormones, and mechanical force. PFFD occurs sporadically, and does not appear to be hereditary.

Diagnosis
Classifications
There are typically four classes (or types) of PFFD, ranging from class A to class D, as detailed by Aitken.Types of PFFD
Type A — The femur bone is slightly shorter on the proximal end (near the hip), and the femoral head (the ball of the thigh bone that goes into the hip socket) may not be solid enough to be seen on X-rays at birth, but later hardens (ossifies). This deformity is sometimes called congenital short femur, because the child’s anatomy from hip to knee is contiguous and similar to their peers except for the one shortened bone. In some cases, children with type A deformities will also have an externally rotated femur, which could lead to bowing of the legs (genu varum).
Type B — The femur bone is shorter on the proximal end (near the hip) and the defect affects both the femoral head (the ball) and the femoral shaft (the long part of the bone). This defect is more severe than type A deformities because it will not heal spontaneously and, at skeletal maturity, the proximal femur (lower part near the knee) will not connect with the femoral head.
Type C — The entire top half of the femur bone is absent, including the trochanters (the part of the bone in which muscles are attached to the upper thigh), and the femoral head </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 Cystic eyeball 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 Lupoid sycosis 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 Aneurysm of sinus of Valsalva and can you explain it in depth? [/INST] Aneurysm of the aortic sinus, also known as the sinus of Valsalva, is a rare abnormality of the aorta, the largest artery in the body.  The aorta normally has three small pouches that sit directly above the aortic valve (the sinuses of Valsalva), and an aneurysm of one of these sinuses is a thin-walled swelling.  Aneurysms may affect the right (65–85%), non-coronary (10–30%), or rarely the left (< 5%) coronary sinus. These aneurysms may not cause any symptoms but if large can cause shortness of breath, palpitations or blackouts. Aortic sinus aneurysms can burst or rupture into adjacent cardiac chambers, which can lead to heart failure if untreated.
Aortic sinus aneurysms may occur in isolation, or may been seen in association with other diseases of the aorta including Marfan syndrome, Loeys-Dietz syndrome, and bicuspid aortic valve.  They can be diagnosed using an echocardiogram or cardiac magnetic resonance imaging (MRI) scan.  Treatment includes blood pressure control but surgical repair may be needed, especially if the aneurysm ruptures.

Symptoms and signs
If unruptured, sinus of Valsalva aneurysm (commonly abbreviated SVA or SOVA) is usually asymptomatic and typically goes undetected until symptoms appear or medical imaging is performed for other reasons. If symptoms do occur, the most common are shortness of breath, palpitations, myocardial ischemia, and syncope. Even less common, but more serious, presentations are embolic stroke and myocardial infarction due to blockage of a coronary artery by the aneurysm.A ruptured aneurysm typically leads to an aortocardiac shunt and progressively worsening heart failure.An aneurysm of the aortic sinus may rupture due to infective endocarditis involving the aortic wall and tertiary-stage syphilis.The manifestations appear depending on the site where the sinus has ruptured. For example, if the sinus ruptures in a low pressure area like the right atrium or right ventricle then a continuous type of murmur is heard. The murmur is located in the left parasternal region mainly confined to the lower sternum. It is also accompanied by a superficial thrill. A ruptured Sinus of Valsalva abscess represents a surgical emergency.

Causes
This type of aneurysm is typically congenital and may be associated with heart defects </s>