<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 Chickenpox and can you explain it in depth? [/INST] Chickenpox, also known as varicella, is a highly contagious disease caused by the initial infection with varicella zoster virus (VZV). The disease results in a characteristic skin rash that forms small, itchy blisters, which eventually scab over. It usually starts on the chest, back, and face. It then spreads to the rest of the body. The rash and other symptoms, such as fever, tiredness, and headaches, usually last five to seven days. Complications may occasionally include pneumonia, inflammation of the brain, and bacterial skin infections. The disease is usually more severe in adults than in children.Chickenpox is an airborne disease which spreads easily from one person to the next through the coughs and sneezes of an infected person. The incubation period is 10–21 days, after which the characteristic rash appears. It may be spread from one to two days before the rash appears until all lesions have crusted over. It may also spread through contact with the blisters. Those with shingles may spread chickenpox to those who are not immune through contact with the blisters. The disease can usually be diagnosed based on the presenting symptom; however, in unusual cases it may be confirmed by polymerase chain reaction (PCR) testing of the blister fluid or scabs. Testing for antibodies may be done to determine if a person is immune. People usually only get chickenpox once. Although reinfections by the virus occur, these reinfections usually do not cause any symptoms.Since its introduction in 1995, the varicella vaccine has resulted in a decrease in the number of cases and complications from the disease. It protects about 70–90 percent of people from disease with a greater benefit for severe disease. Routine immunization of children is recommended in many countries. Immunization within three days of exposure may improve outcomes in children. Treatment of those infected may include calamine lotion to help with itching, keeping the fingernails short to decrease injury from scratching, and the use of paracetamol (acetaminophen) to help with fevers. For those at increased risk of complications, antiviral medication such as aciclovir are recommended.Chickenpox occurs in all parts of the world. In 2013 there were 140 million cases of chickenpox and shingles worldwide. Before routine immunization the number of cases occurring each year was similar to the number of people born. Since immunization the number of infections in the United States has decreased nearly 90%. In 2015 chickenpox resulted in 6,400 deaths globally – down from 8,900 in 1990. Death occurs in about 1 per 60,000 cases. Chickenpox was not separated from smallpox until the late 19th century. In 1888 its connection to shingles was determined. The first documented use of the term chicken pox was in 1658. Various explanations have been suggested for the use of "chicken" in the name, one being the relative mildness of the disease.

Signs and symptoms
The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity and tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days before recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus ceases. The condition usually resolves by itself within a week or two. The rash may, however, last for up to one month.Chickenpox is rarely fatal, although it is generally more severe in adult men than in women or children. Non-immune pregnant women and those with a suppressed immune system are at highest risk of serious complications. Arterial ischemic stroke (AIS) associated with chickenpox in the previous year accounts for nearly one third of childhood AIS. The most common late complication of chickenpox is shingles (herpes zoster), caused by reactivation of the varicella zoster virus decades after the initial, often childhood, chickenpox infection.

Pregnancy and neonates
During pregnancy the dangers to the fetus associated with a primary VZV infection are greater in the first six months. In the third trimester, the mother is more likely to have severe symptoms.
For pregnant women, antibodies produced as a result of immunization or previous infection are transferred via the placenta to the fetus.
Varicella infection in pregnant women could lead to spread via the placenta and infection of the fetus. If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella syndrome (also known as congenital varicella syndrome). Effects on the fetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation. Possible problems include:

Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
Damage to the eye: optic stalk, optic cup, and lens vesicles, microphthalmia, cataracts, chorioretinitis, optic atrophy
Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horners syndrome
Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction
Skin disorders: (cicatricial) skin lesions, hypopigmentationInfection late in gestation or immediately following birth is referred to as "neonatal varicella". Maternal infection is associated with premature delivery. The risk of the baby developing the disease is greatest following exposure to infection in the period 7 days before delivery and up to 8 days following the birth. The baby may also be exposed to the virus via infectious siblings or other contacts, but this is of less concern if the mother is immune. Newborns who develop symptoms are at a high risk of pneumonia and other serious complications of the disease.

Pathophysiology
Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), postherpetic neuralgia, and sometimes Ramsay Hunt syndrome type II. Varicella zoster can affect the arteries in the neck and head, producing stroke, either during childhood, or after a latency period of many years.

Shingles
After a chickenpox infection, the virus remains dormant in the bodys nerve tissues for about 50 years. This, however, does not mean that VZV cannot be contracted later in life. The immune system usually keeps the virus at bay, however it can still manifest itself at any given age between 1 and 60, causing a different form of the viral infection called shingles (also known as herpes zoster). Since the human immune system efficacy decreases with age, the United States Advisory Committee on Immunization Practices (ACIP) suggests that every adult over the age of 50 years get the herpes zoster vaccine.Shingles affects one in five adults infected with chickenpox as children, especially those who are immune-suppressed, particularly from cancer, HIV, or other conditions. Stress can bring on shingles as well, although scientists are still researching the connection. Adults over the age of 60 who had chickenpox but not shingles are the most prone age demographic.

Diagnosis
The diagnosis of chickenpox is primarily based on the signs and symptoms, with typical early symptoms followed by a characteristic rash. Confirmation of the diagnosis is by examination of the fluid within the vesicles of the rash, or by testing blood for evidence of an acute immunologic response.Vesicular fluid can be examined with a Tzanck smear, or by testing for direct fluorescent antibody. The fluid can also be "cultured", whereby attempts are made to grow the virus from a fluid sample. Blood tests can be used to identify a response to acute infection (IgM) or previous infection and subsequent immunity (IgG).Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (DNA) test of the mothers amniotic fluid can also be performed, though the risk of spontaneous abortion due to the amniocentesis procedure is higher than the risk of the babys developing fetal varicella syndrome.

Prevention
Hygiene measures
The spread of chickenpox can be prevented by isolating affected individuals. Contagion is by exposure to respiratory droplets, or direct contact with lesions, within a period lasting from three days before the onset of the rash, to four days after the onset of the rash. The chickenpox virus is susceptible to disinfectants, notably chlorine bleach (i.e., sodium hypochlorite). Like all enveloped viruses, it is sensitive to drying, heat and detergents.

Vaccine
Chickenpox can be prevented by vaccination. The side effects are usually mild, such as some pain or swelling at the injection site.A live attenuated varicella vaccine, the Oka strain, was developed by Michiaki Takahashi and his colleagues in Japan in the early 1970s. In 1981, Merck & Co. licensed the "Oka" strain of the varicella virus in the United States, and Maurice Hillemans team at Merck invented a varicella vaccine in the same year.The varicella vaccine is recommended in many countries. Some countries require the varicella vaccination or an exemption before entering elementary school. A second dose is recommended five years after the initial immunization. A vaccinated person is likely to have a milder case of chickenpox if they become infected. Immunization within three days following household contact reduces infection rates and severity in children. Being exposed to chickenpox as an adult (for example, through contact with infected children) may boosts immunity to shingles. So it was thought, that when the majority of children are vaccinated against chickenpox, adults might lose this natural boosting, so immunity would drop and more shingles cases would occur. On the other hand, current observations suggest that exposure to children with varicella is not a critical factor in the maintenance of immunity. Multiple subclinical reactivations of varicella zoster virus may occur spontaneously and, despite not causing clinical disease, may still provide an endogenous boost to immunity against zoster.It is part of the routine immunization schedule in the US. Some European countries include it as part of universal vaccinations in children, but not all countries provide the vaccine. In the UK as of 2014, the vaccine is only recommended in people who are particularly vulnerable to chickenpox. This is to keep the virus in circulation thereby exposing the population to the virus at an early age, when it is less harmful, and to reduce the occurrence of shingles in those who have already had chickenpox by repeated exposure to the virus later in life. In populations that have not been immunized or if immunity is questionable, a clinician may order an enzyme immunoassay. An immunoassay measures the levels of antibodies against the virus that give immunity to a person. If the levels of antibodies are low (low titer) or questionable, reimmunization may be done.

Treatment
Treatment mainly consists of easing the symptoms. As a protective measure, people are usually required to stay at home while they are infectious to avoid spreading the disease to others. Cutting the fingernails short or wearing gloves may prevent scratching and minimize the risk of secondary infections.Although there have been no formal clinical studies evaluating the effectiveness of topical application of calamine lotion (a topical barrier preparation containing zinc oxide, and one of the most commonly used interventions), it has an excellent safety profile. Maintaining good hygiene and daily cleaning of skin with warm water can help to avoid secondary bacterial infection; scratching may increase the risk of secondary infection.Paracetamol (acetaminophen) but not aspirin may be used to reduce fever. Aspirin use by someone with chickenpox may cause serious, sometimes fatal disease of the liver and brain, Reye syndrome. People at risk of developing severe complications who have had significant exposure to the virus may be given intra-muscular varicella zoster immune globulin (VZIG), a preparation containing high titres of antibodies to varicella zoster virus, to ward off the disease.Antivirals are sometimes used.

Children
If aciclovir by mouth is started within 24 hours of rash onset, it decreases symptoms by one day but has no effect on complication rates. Use of aciclovir therefore is not currently recommended for individuals with normal immune function. Children younger than 12 years old and older than one month are not meant to receive antiviral drugs unless they have another medical condition which puts them at risk of developing complications.Treatment of chickenpox in children is aimed at symptoms while the immune system deals with the virus. With children younger than 12 years, cutting fingernails and keeping them clean is an important part of treatment as they are more likely to scratch their blisters more deeply than adults.Aspirin is highly contraindicated in children younger than 16 years, as it has been related to Reye syndrome.

Adults
Infection in otherwise healthy adults tends to be more severe. Treatment with antiviral drugs (e.g. aciclovir or valaciclovir) is generally advised, as long as it is started within 24–48 hours from rash onset. Remedies to ease the symptoms of chickenpox in adults are basically the same as those used for children. Adults are more often prescribed antiviral medication, as it is effective in reducing the severity of the condition and the likelihood of developing complications. Adults are advised to increase water intake to reduce dehydration and to relieve headaches. Painkillers such as paracetamol (acetaminophen) are recommended, as they are effective in relieving itching and other symptoms such as fever or pains. Antihistamines relieve itching and may be used in cases where the itching prevents sleep, because they also act as a sedative. As with children, antiviral medication is considered more useful for those adults who are more prone to develop complications. These include pregnant women or people who have a weakened immune system.

Prognosis
The duration of the visible blistering caused by varicella zoster virus varies in children usually from 4 to 7 days, and the appearance of new blisters begins to subside after the fifth day. Chickenpox infection is milder in young children, and symptomatic treatment, with sodium bicarbonate baths or antihistamine medication may ease itching.
In adults, the disease is more severe, though the incidence is much less common. Infection in adults is associated with greater morbidity and mortality due to pneumonia (either direct viral pneumonia or secondary bacterial pneumonia), bronchitis (either viral bronchitis or secondary bacterial bronchitis), hepatitis, and encephalitis. In particular, up to 10% of pregnant women with chickenpox develop pneumonia, the severity of which increases with onset later in gestation. In England and Wales, 75% of deaths due to chickenpox are in adults. Inflammation of the brain, encephalitis, can occur in immunocompromised individuals, although the risk is higher with herpes zoster. Necrotizing fasciitis is also a rare complication.Varicella can be lethal to individuals with impaired immunity. The number of people in this high-risk group has increased, due to the HIV epidemic and the increased use of immunosuppressive therapies. Varicella is a particular problem in hospitals when there are patients with immune systems weakened by drugs (e.g., high-dose steroids) or HIV.Secondary bacterial infection of skin lesions, manifesting as impetigo, cellulitis, and erysipelas, is the most common complication in healthy children. Disseminated primary varicella infection usually seen in the immunocompromised may have high morbidity. Ninety percent of cases of varicella pneumonia occur in the adult population. Rarer complications of disseminated chickenpox include myocarditis, hepatitis, and glomerulonephritis.Hemorrhagic complications are more common in the immunocompromised or immunosuppressed populations, although healthy children and adults have been affected. Five major clinical syndromes have been described: febrile purpura, malignant chickenpox with purpura, postinfectious purpura, purpura fulminans, and anaphylactoid purpura. These syndromes have variable courses, with febrile purpura being the most benign of the syndromes and having an uncomplicated outcome. In contrast, malignant chickenpox with purpura is a grave clinical condition that has a mortality rate of greater than 70%. The cause of these hemorrhagic chickenpox syndromes is not known.

Epidemiology
Primary varicella occurs in all countries worldwide. In 2015 chickenpox resulted in 6,400 deaths globally – down from 8,900 in 1990. There were 7,000 deaths in 2013. Varicella is highly transmissible, with an infection rate of 90% in close contacts.In temperate countries, chickenpox is primarily a disease of children, with most cases occurring during the winter and spring, most likely due to school contact </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 Acute posthemorrhagic anemia 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 Secondary glaucoma and can you explain it in depth? [/INST] Secondary glaucoma is a collection of progressive optic nerve disorders associated with a rise in intraocular pressure (IOP) which results in the loss of vision. In clinical settings, it is defined as the occurrence of IOP above 21 mmHg requiring the prescription of IOP-managing drugs. It can be broadly divided into two subtypes: secondary open-angle glaucoma and secondary angle-closure glaucoma, depending on the closure of the angle between the cornea and the iris. Principal causes of secondary glaucoma include optic nerve trauma or damage, eye disease, surgery, neovascularization, tumours and use of steroid and sulfa drugs. Risk factors for secondary glaucoma include uveitis, cataract surgery and also intraocular tumours. Common treatments are designed according to the type (open-angle or angle-closure) and the underlying causative condition, in addition to the consequent rise in IOP. These include drug therapy, the use of miotics, surgery or laser therapy.

Pathophysiology
Secondary glaucoma has different forms based on the varying underlying ocular conditions. These conditions result in an increase in IOP that manifests as secondary glaucoma.

Paediatric congenital cataract associated glaucoma
Based on the onset of secondary glaucoma in paediatric patients, it can be classified into early-stage and late-stage glaucoma cases. Early-stage secondary glaucoma, observed as angle-closure glaucoma, results from the blockage and inflammation of the peripheral anterior synechiae structure. However, early-stage secondary glaucoma rarely occurs with the readily available prescription of anti-inflammatory medications. On the other hand, late-stage glaucoma is commonly associated with open-angle glaucoma but the mechanisms are currently unconfirmed. Yet, it is believed to be closely related to the onset of trabeculitis or vitreous toxicity.In paediatric congenital cataract patients under the age of two, cataract surgery is considered and frequently employed as the primary treatment. There are two types of therapeutic combination, primary and secondary lens implantation (IOL). In primary IOL, cataract surgery is performed alongside immediate implantation of IOL. However, in secondary IOL implantation, the patient is prescribed aphakic glasses or contact lenses till the implantation of IOL after a varied period of time between a few months or years. Primary IOL implantation is observed to significantly reduce and avoid the occurrence of secondary glaucoma in paediatric patients under the age of two.

Herpetic anterior uveitis associated glaucoma
In patients diagnosed with herpetic anterior uveitis, elevated IOP and secondary glaucoma are often detected. This is due to two main reasons, the blockage of vitreous flow resulting from inflammation in the structures of the trabecular meshwork, and the sedimentation of inflamed cells. Specifically for viral anterior uveitis, patients with IOP levels above 30 mmHg are often suffer from secondary glaucoma caused by cytomegalovirus.

Other forms of secondary glaucoma
Pigmentary glaucoma: In pigmentary glaucoma, the obstruction of the trabecular meshwork caused by iris pigment release results in increased IOP. This release in iris pigment occurs as a result of the interaction of a flaccid iris with the zonular fibres.Exfoliation syndrome: Exfoliation syndrome is a classic cause of secondary open-angle glaucoma, a common symptom of exfoliation syndrome is a cloudy layer on the anterior lens capsule.Aphakic and pseudophakic glaucoma: Aphakic glaucoma is a common side-effect of cataract surgery which causes an increase in IOP.Corticosteroid-induced glaucoma: Corticosteroids is a risk factor for the development of secondary glaucoma, as there had been increased IOP observed as a drug side-effect.Post-traumatic glaucoma: Trauma to the eye is often observed to cause secondary glaucoma. The incidence is notably higher in populations with increased levels of physical activity.Ghost-cell glaucoma: Ruptured red blood cells will release haemoglobin in the form of Heinz bodies, which are potent in increasing the IOP level.Inflammatory glaucoma: The inflammatory reaction will affect the drainage of aqueous humour in the eye, causing an increase in IOP.Glaucoma associated with ocular tumours: Although each tumour subtype has its own mechanism in causing secondary glaucoma, the general cause is the restriction of the meshwork resulting in the obstruction of aqueous humour flow.Increased episcleral venous pressure: According to the Goldmann equation, the relationship between episcleral venous pressure (EVP) is directly proportional to the IOP. Therefore, an increase in the EVP will result in an increase in IOP.
Neovascular glaucoma: As a consequence of neovascularisation, or the formation of new blood vessels and supporting connective structures, there is blockage of the anterior chamber angle. This leads to elevation of IOP causing neovascular glaucoma.

Epidemiology
The overall prevalence of secondary glaucoma across China between 1990 and 2015 was reported to be 0.15%, lower than the overall estimates for East Asia (0.39%).

Varying forms of secondary glaucoma
Pigmentary glaucoma has lower incidence in Black and Asian populations, due to their characteristically thicker irises that result in a lower likelihood of pigment release, as compared to the White populations. Incidence of exfoliation syndrome-caused secondary glaucoma is estimated to be approximately 10% of the glaucoma patient population in the United States and over 20% of the patient population in Iceland and Finland.In populations above the age of 40, neovascular glaucoma has a prevalence of 0.4% worldwide. The incidence of pigmentary glaucoma decreases with age while in exfoliation syndrome the incidence increases with age. However, given the derived nature of secondary glaucoma, there may be no significant association between age, ethnicity or gender and the prevalence of the condition.Secondary glaucoma indicated after congenital cataract surgery is found between 6 and 24% of the cases noted, whereas, secondary glaucoma caused by primary IOL implantation was observed as 9.5%. Additionally, for patients with aphakia and secondary IOL implantation, 15.1% of the cases were determined. The incidence risk in primary IOL implantation in children with cataract in both eyes is lower than secondary IOL implantation and aphakic condition. However, this difference is not observed in the general population and populations with cataract in one eye.Due to lack of concrete and specific epidemiological evidence, further research is required to accurately estimate the prevalence of secondary glaucoma and its subtypes.

Risk factors
In general, elevated IOP is a major risk factor in the development of secondary glaucoma. However, there are several risk factors contributing to the fluctuation in IOP levels.

Uveitis
Secondary glaucoma is commonly associated with uveitis. Uveitis is the inflammation of the uvea, a middle layer tissue of the eye consisting of the ciliary body, choroid and iris. Various causes have been identified as potential risk factors contributing to the occurrence of secondary glaucoma. These include viral anterior uveitis due to cytomegalovirus infection, and herpetic anterior uveitis caused by herpes simplex virus. The observed pathophysiology of secondary glaucoma in uveitis is found to be linked to the increase and fluctuation of IOP. Inflammation of eye tissues contributes to the blockage of IOP produced in the ciliary body. This results in the accumulation of aqueous and thus elevated IOP, which is a common risk factor for the progression of secondary glaucoma.

Paediatric congenital cataract surgery
Paediatric congenital cataract surgery is also identified as a risk factor for the progression of secondary glaucoma. Cataract is an ocular disease, identified by the progressive clouding of the lens. Surgical procedures are often employed to replace the lens and allow for clear vision. However, there is an increased risk of secondary glaucoma development in children due to the secondary IOL implantation procedure. The increased inflammatory sensitivity in the anterior chamber angle may contribute to the risks of secondary glaucoma.

Intraocular tumour
Intraocular tumours (uveal and retinal tumours) are also found to be closely associated with the development of secondary glaucoma. The pathophysiology of secondary glaucoma in these cases is affected by the type of tumour, location and other tumour-associated factors. Among the many subtypes of uveal tumours, secondary glaucoma is the most prominent among patients with trabecular meshwork iris melanoma. The blockage of vitreous flow due to inflammation in the structures of the trabecular meshwork is also observed in herpetic anterior uveitis patients. In addition to this, angle invasion is a mechanism that is observed to contribute greatly to the development of secondary glaucoma in patients with iris tapioca melanoma, iris lymphoma, choroidal melanoma, and medulloepithelioma.

Treatment and management
Pharmacological interventions
Miotic drugs are a class of cholinergic drugs that are frequently employed in the treatment and management of all types of glaucoma. These drugs stimulate the contraction of the pupil causing the iris to pull away from the trabecular meshwork. Consequently, the normal drainage of the aqueous humour is restored, relieving IOP. In addition to causing a direct effect on IOP, these drugs are applied to reduce pigment release (from the iris pigment epithelium) in the treatment of pigmentary glaucoma. Despite the advantages, the widespread use of miotic drugs is limited by its associated side effects. There is an increased risk of development of posterior synechiae in glaucoma secondary to exfoliation syndrome and ocular trauma. Other side effects include increased risk of miosis-induced headaches, blurred vision, retinal detachment and damage to the blood-aqueous barrier.Alternative drugs which can reduce the synthesis of aqueous humour, called aqueous suppressants, or increase the drainage of aqueous humour emerged as effective first-line treatments. Aqueous suppressants include beta-blockers, alpha-agonists and carbonic anhydrase inhibitors. They are particularly effective in treating corticosteroid, uveitic, aphakic, pseudophakic, ghost-cell and post-traumatic glaucoma. Prostaglandin analogues increase aqueous drainage and are thus used in the reduction of IOP. There are contradictory findings regarding the occurrence of prostaglandin analogue mediated side effects in the treatment of uveitic glaucoma. It was previously identified that the side effects comprise damage to the blood-aqueous barrier, cystoid macular oedema, risk of developing anterior uveitis and recurrence of keratitis caused by herpes simplex virus. However, current scientific evidence only supports the reactivation of herpes simplex keratitis among the other side effects.In uveitic and inflammatory glaucoma, reduction in inflammation is a critical step during the treatment and management process. This is commonly done using corticosteroids coupled with immunosuppressants. Steroidal treatment is also used in management of aphakic, pseudophakic, and post-traumatic glaucoma. Inflammatory glaucoma may further be treated using cycloplegics, a class of drugs that treats pain, ciliary spasm, uveoscleral tract blockage and disrupted blood-aqueous barrier linked with this form of glaucoma. While some studies recommend the use of anti-vascular endothelial growth factor drugs for inhibition of neovascularization in neovascular glaucoma, there is a lack of substantial evidence for the effectiveness of this treatment method.

Laser therapy
Among different laser therapies, laser peripheral iridotomy and laser trabeculoplasty are the most common procedures for secondary glaucoma. Both methods involve creating new outlets for the aqueous humour to flow out of, effectively reducing the IOP. In peripheral laser iridotomy, the opening is created in the iris tissue while in trabeculoplasty, this opening is made in the trabecular meshwork. Further, there are two types of laser trabeculoplasty: argon laser trabeculoplasty and selective laser trabeculoplasty.Laser peripheral iridotomy has high efficacy in the treatment of pigmentary glaucoma </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 Phytobezoar and can you explain it in depth? [/INST] A phytobezoar is a type of bezoar, or trapped mass in the gastrointestinal system, that consists of components of indigestible plant material, such as fibres, skins and seeds. While phytobezoars may be discovered incidentally on barium x-ray or endoscopic testing of the stomach, individuals with phytobezoars may develop symptoms: nausea, vomiting, gastric outlet obstruction, perforation, abdominal pain, and bleeding have been reported. Conditions that lead to decreased motility in the stomach (gastroparesis) and surgeries on the stomach (such as vagotomy or gastric bypass) are associated with the development of phytobezoars.  A specific type of phytobezoar, termed a diospyrobezoar, is associated with ingestion of unripe persimmons, which contain a soluble tannin called shibuol that polymerizes into a coagulative cellulose-protein compound in the acid environment of the stomach, to form the bezoar.  In addition to their presence in human stomachs, phytobezoars have been documented in the stomachs of slaughtered plant-eating animals.

Cause
Gastric phytobezoars are a form of intestinal blockage and are seen in those with poor gastric motility. The preferred treatment of bezoars includes different therapies and/or fragmentation to avoid surgery. Phytobezoars are most common and consist of undigested lignin, cellulose,  tannins, celery, pumpkin skin, grape skins, prunes, raisins, vegetables and fruits. Phytobezoars can form after eating persimmons and pineapples. These are more difficult to treat and are referred to as diospyrobezoars. Phytobezoars are more likely to form due to the ingestion of raw plant foods, even in persons without predisposing factors, as cooking softens them for easier digestion.

Treatment
Several treatments for phytobezoars have been described </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 Trichotillomania and can you explain it in depth? [/INST] Trichotillomania (TTM), also known as hair-pulling disorder or compulsive hair pulling, is a mental disorder characterized by a long-term urge that results in the pulling out of ones own hair. A brief positive feeling may occur as hair is removed. Efforts to stop pulling hair typically fail. Hair removal may occur anywhere; however, the head and around the eyes are most common. The hair pulling is to such a degree that it results in distress and hair loss can be seen.The disorder may run in families. It occurs more commonly in those with obsessive compulsive disorder. Episodes of pulling may be triggered by anxiety. People usually acknowledge that they pull their hair, and broken hairs may be seen on examination. Other conditions that may present similarly include body dysmorphic disorder; however, in that condition people remove hair to try to improve what they see as a problem in how they look.Treatment is typically with cognitive behavioral therapy. The medication clomipramine may also be helpful, as will keeping fingernails clipped. Trichotillomania is estimated to affect one to four percent of people. Trichotillomania most commonly begins in childhood or adolescence. Women are affected about 10 times more often than men. The name was created by François Henri Hallopeau in 1889, from the Greek θριξ/τριχ; thrix (meaning hair), along with τίλλειν; tíllein (meaning to pull), and μανία; mania (meaning madness).

Signs and symptoms
Trichotillomania is usually confined to one or two sites, but can involve multiple sites. The scalp is the most common pulling site, followed by the eyebrows, eyelashes, face, arms, and legs. Some less common areas include the pubic area, underarms, beard, and chest. The classic presentation is the "Friar Tuck" form of vertex and crown alopecia. Children are less likely to pull from areas other than the scalp.People with trichotillomania often pull only one hair at a time and these hair-pulling episodes can last for hours at a time. Trichotillomania can go into remission-like states where the individual may not experience the urge to "pull" for days, weeks, months, or even years.Individuals with trichotillomania exhibit hair of differing lengths; some are broken hairs with blunt ends, some new growth with tapered ends, some broken mid-shaft, or some uneven stubble. Scaling on the scalp is not present, overall hair density is normal, and a hair pull test is negative (the hair does not pull out easily). Hair is often pulled out leaving an unusual shape. Individuals with trichotillomania may be secretive or shameful of the hair pulling behavior.An additional psychological effect can be low self-esteem, often associated with being shunned by peers and the fear of socializing, due to appearance and negative attention they may receive. Some people with trichotillomania wear hats, wigs, false eyelashes, eyebrow pencil, or style their hair in an effort to avoid such attention. There seems to be a strong stress-related component. In low-stress environments, some exhibit no symptoms (known as "pulling") whatsoever. This "pulling" often resumes upon leaving this environment. Some individuals with trichotillomania may feel they are the only person with this problem due to low rates of reporting.For some people, trichotillomania is a mild problem, merely a frustration. But for many, embarrassment about hair pulling causes isolation and results in a great deal of emotional distress, placing them at risk for a co-occurring psychiatric disorder, such as a mood or anxiety disorder. Hair pulling can lead to tension and strained relationships with family members and friends. Family members may need professional help in coping with this problem.Other medical complications include infection, permanent loss of hair, repetitive stress injury, carpal tunnel syndrome, and gastrointestinal obstruction as a result of trichophagia. In trichophagia, people with trichotillomania also ingest the hair that they pull; in extreme (and rare) cases this can lead to a hair ball (trichobezoar). Rapunzel syndrome, an extreme form of trichobezoar in which the "tail" of the hair ball extends into the intestines, can be fatal if misdiagnosed.Environment is a large factor which affects hair pulling. Sedentary activities such as being in a relaxed environment are conducive to hair pulling. A common example of a sedentary activity promoting hair pulling is lying in a bed while trying to rest or fall asleep. An extreme example of automatic trichotillomania is found when some patients have been observed to pull their hair out while asleep. This is called sleep-isolated trichotillomania.

Causes
Anxiety, depression and obsessive–compulsive disorder are more frequently encountered in people with trichotillomania. Trichotillomania has a high overlap with post traumatic stress disorder, and some cases of trichotillomania may be triggered by stress. Another school of thought emphasizes hair pulling as addictive or negatively reinforcing, as it is associated with rising tension beforehand and relief afterward. A neurocognitive model — the notion that the basal ganglia play a role in habit formation and that the frontal lobes are critical for normally suppressing or inhibiting such habits — sees trichotillomania as a habit disorder.Abnormalities in the caudate nucleus are noted in OCD, but there is no evidence to support that these abnormalities can also be linked to trichotillomania. One study has shown that individuals with trichotillomania have decreased cerebellar volume. These findings suggest some differences between OCD and trichotillomania. There is a lack of structural MRI studies on trichotillomania. In several MRI studies that have been conducted, it has been found that people with trichotillomania have more gray matter in their brains than those who do not have the disorder.It is likely that multiple genes confer vulnerability to trichotillomania. One study identified mutations in the SLITRK1 gene.

Diagnosis
Patients may be ashamed or actively attempt to disguise their symptoms. This can make diagnosis difficult as symptoms are not always immediately obvious, or have been deliberately hidden to avoid disclosure. If the patient admits to hair pulling, diagnosis is not difficult; if patients deny hair pulling, a differential diagnosis must be pursued. The differential diagnosis will include evaluation for alopecia areata, iron deficiency, hypothyroidism, tinea capitis, traction alopecia, alopecia mucinosa, thallium poisoning, and loose anagen syndrome. In trichotillomania, a hair pull test is negative.A biopsy can be performed and may be helpful; it reveals traumatized hair follicles with perifollicular hemorrhage, fragmented hair in the dermis, empty follicles, and deformed hair shafts. Multiple catagen hairs are typically seen. An alternative technique to biopsy, particularly for children, is to shave a part of the involved area and observe for regrowth of normal hairs.

Classification
Trichotillomania is defined as a self-induced and recurrent loss of hair. It includes the criterion of an increasing sense of tension before pulling the hair and gratification or relief when pulling the hair. However, some people with trichotillomania do not endorse the inclusion of "rising tension and subsequent pleasure, gratification, or relief" as part of the criteria because many individuals with trichotillomania may not realize they are pulling their hair, and patients presenting for diagnosis may deny the criteria for tension prior to hair pulling or a sense of gratification after hair is pulled.Trichotillomania may lie on the obsessive-compulsive spectrum, also encompassing obsessive-compulsive disorder (OCD), body dysmorphic disorder (BDD), nail biting (onychophagia) and skin picking (dermatillomania), tic disorders and eating disorders. These conditions may share clinical features, genetic contributions, and possibly treatment response; however, differences between trichotillomania and OCD are present in symptoms, neural function and cognitive profile. In the sense that it is associated with irresistible urges to perform unwanted repetitive behavior, trichotillomania is akin to some of these conditions, and rates of trichotillomania among relatives of OCD patients is higher than expected by chance. However, differences between the disorder and OCD have been noted, including: differing peak ages at onset, rates of comorbidity, gender differences, and neural dysfunction and cognitive profile. When it occurs in early childhood, it can be regarded as a distinct clinical entity.Because trichotillomania can be present in multiple age groups, it is helpful in terms of prognosis and treatment to approach three distinct subgroups by age: preschool age children, preadolescents to young adults, and adults.In preschool age children, trichotillomania is considered benign. For these children, hair-pulling is considered either a means of exploration or something done subconsciously, similar to nail-biting and thumb-sucking, and almost never continues into further ages.The most common age of onset of trichotillomania is between ages 9 and 13. In this age range, trichotillomania is usually chronic, and continues into adulthood. Trichiotillomania that begins in adulthood most commonly arises from underlying psychiatric causes.Trichotillomania is often not a focused act, but rather hair pulling occurs in a "trance-like" state; hence, trichotillomania is subdivided into "automatic" versus "focused" hair pulling. Children are more often in the automatic, or unconscious, subtype and may not consciously remember pulling their hair. Other individuals may have focused, or conscious, rituals associated with hair pulling, including seeking specific types of hairs to pull, pulling until the hair feels "just right", or pulling in response to a specific sensation. Knowledge of the subtype is helpful in determining treatment strategies.

Treatment
Treatment is based on a persons age. Most pre-school age children outgrow the condition if it is managed conservatively. In young adults, establishing the diagnosis and raising awareness of the condition is an important reassurance for the family and patient. Non-pharmacological interventions, including behavior modification programs, may be considered; referrals to psychologists or psychiatrists may be considered when other interventions fail. When trichotillomania begins in adulthood, it is often associated with other mental disorders, and referral to a psychologist or psychiatrist for evaluation or treatment is considered best. The hair pulling may resolve when other conditions are treated.

Psychotherapy
Habit reversal training (HRT) has the highest rate of success in treating trichotillomania. HRT has also been shown to be a successful adjunct to medication as a way to treat trichotillomania. With HRT, the individual is trained to learn to recognize their impulse to pull and also teach them to redirect this impulse. In comparisons of behavioral versus pharmacologic treatment, cognitive behavioral therapy (including HRT) have shown significant improvement over medication alone. It has also proven effective in treating children. Biofeedback, cognitive-behavioral methods, and hypnosis may improve symptoms. Acceptance and commitment therapy (ACT) is also demonstrating promise in trichotillomania treatment. A systematic review from 2012 found tentative evidence for "movement decoupling".

Medication
The United States Food and Drug Administration (FDA) has not approved any medications for trichotillomania treatment.However, some medications have been used to treat trichotillomania, with mixed results. Treatment with clomipramine, a tricyclic antidepressant, was shown in a small double-blind study to improve symptoms, but results of other studies on clomipramine for treating trichotillomania have been inconsistent. Naltrexone may be a viable treatment. Fluoxetine and other selective serotonin reuptake inhibitors (SSRIs) have limited usefulness in treating trichotillomania, and can often have significant side effects. Behavioral therapy has proven more effective when compared to fluoxetine. There is little research on the effectiveness of behavioral therapy combined with medication, and robust evidence from high-quality studies is lacking </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 Antepartum bleeding and can you explain it in depth? [/INST] Antepartum bleeding, also known as antepartum haemorrhage (APH) or prepartum hemorrhage, is genital bleeding during pregnancy after the 28th week of pregnancy up to delivery.It can be associated with reduced fetal birth weight. Use of aspirin before 16 weeks of pregnancy to prevent pre-eclampsia also appears effective at preventing antepartum bleeding.In regard to treatment, it should be considered a medical emergency (regardless of whether there is pain), as if it is left untreated it can lead to death of the mother or baby.

Classification
The total amount of blood loss and signs of circulatory shock due to blood determine the severity of the antepartum haemorrhaging. There are 4 degrees of antepartum haemorrhaging:

Causes
Placenta praevia
Placenta praevia refers to when the placenta of a growing foetus is attached abnormally low within the uterus. Intermittent antepartum haemorrhaging occurs in 72% of women living with placenta praevia.  The severity of a patients placenta praevia depends on the location of placental attachment;

Types 1 and 2 are classified as minor placental praevia as these typically result in minor antepartum haemorrhaging. Types 3 and 4 are referred to as major placental praevia due to the risk of heavy haemorrhaging in the case of a rupture due to the location of placental attachment. During the third trimester of pregnancy, thinning of the lower uterine segment or contractions caused by cervical dilation can increase the amount of stress placed on the placental attachment to the uterine wall. In patients with placenta praevia, these stresses can cause detachment of the placenta from the uterine wall causing haemorrhaging. To prevent further haemorrhaging patients with major placental praevia are recommended to have a caesarean delivery.

Abnormal placentation
During pregnancy the layer of endometrium that attaches directly to developing blastocyst becomes the maternal portion of the placenta, also known as the decidua basalis. In the absence of a decidua basalis, trophoblast cells on the developing blastocyst form an abnormally deep attachment to the uterine wall, this is known as abnormal placentation. Abnormal placentation can categorised into 3 types, depending on the depth of infiltration of the chorionic villi into the uterine wall:
In placenta percreta, the chorionic villi have grow entirely through the myometrium and invade into the perimetrium. Placenta percreta results in the most intense haemorrhaging that can be expected caused by abnormal placentation. In the event of placental detachment from the uterine wall, the depth of chorionic villi attachment dictates the amount of haemorrhaging that can be expected. The chance of abnormal placentation increases in subsequent pregnancies, if there is scar tissue present from previous pregnancies. For example, previously undergoing a caesarean or placenta previa increases the likelihood of abnormal placentation, therefore increasing the chances of antepartum haemorrhaging.

Placental abruption
Placental abruption occurs when the placenta detaches from the endometrium. Detachment causes antepartum haemorrhaging at the location of abruption. Depending on the site of detachment, haemorrhaging may or may not be apparent. If abruption occurs behind the placenta where blood cannot escape through the cervix, blood will pool and form a retroplacental clot. Only when the site of detachment occurs on the side facing the cervical opening can the total amount of haemorrhaging be measured by vaginal bleeding. Using vaginal bleeding as a measurement of the severity of the placental abruption is therefore ineffective. The scale of haemorrhaging depends on the degree to which the placenta has separated from the uterine wall. In the case of partial placental separation, haemorrhaging can be minor. However, in the case of total placental separation haemorrhaging will be major and emergency delivery will typically be the course of action. Placental abruption causes blood loss from the mother and loss of oxygen and nutrients to the placenta occasionally leading to preterm labour. Other causes of placental abruption can be abdominal trauma or sudden decompression of amniotic fluid, however it is not uncommon for the cause of placental abruption to be unknown.

Vasa praevia
Vasa praevia is the presence of unprotected foetal blood vessels running along the placenta and over the internal cervical opening. Vasa praevia is a very rare, presenting only 4:10,000 cases from the largest study of the condition. Risks of antepartum bleeding due to vasa praevia greatly increase during the third trimester of pregnancy during cervical dilation or placenta praevia. Vessel rupture is very likely in the event of a membranous rupture as foetal blood vessels arent protected by the umbilical cord of the placenta. In the event of foetal vessel rupture, antepartum haemorrhaging occurs however blood is lost from the foetal blood supply. If the foetus is developed enough caesarean sections are often recommended.

Abnormal placental shape
Circumvallate placentaA circumvallate placenta refers to when the foetal membrane wraps twice around, over the foetal side around the edge of the placenta. This is to compensate for an undersized chorionic plate resulting in a decreased nutritional supply to the foetus. Thickening of the placental edge due to a circumvallate placenta can lead to placental abruption, causing antepartum haemorrhaging.
Bilobed PlacentaA bilobed placenta has a cleavage in the middle dividing it into two lobes with membranous vessels branching in between. The exposed connecting membranous vessels present risk of rupturing due to limited protection from thrombosis and trauma. Bilobing of the placenta can be caused by placental implantation occurring over areas of uterine fibroid scarring, previous surgery, decreased blood supply or implantation occurring over the internal cervical orifice.  Chances of vasa previa and placental abruption increase in the presence of a bilobed placenta due to decreased surface area for attachment to the uterine wall and the exposure of membranous vessels.
Multilobed or Succenturiate PlacentaWhen a placenta has multiple lobes which are distal and not of equal size this is referred to as a succenturiate placenta. Distal lobes are connected by a placental artery and vein extending from the main placenta, which tends to be centrally located and is the largest in mass.  At the time of contraction or delivery the connecting placental arteries and veins may rupture resulting in significant haemorrhaging. Incidences of vasa previa and haemorrhaging in the presence of a succenturiate placenta are highly increased.
Fetal blood (can be distinguished with Apt test)

Minor causes
Cervical ectropion
There are 2 types of epithelial cells present within the cervical canal. In the endocervix the epithelia is columnar glandular which transitions into stratified squamous towards the ectocervix and external cervical orifice. During cervical ectropion the epithelial transitional zone (also called the squamo-columnar junction) migrates from the endocervical canal towards the ectocervix exposing some columnar glandular cells on the external cervical orifice. Unlike stratified squamous epithelial cells, glandular cells are columnar and not used to external stresses such as abrasion </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 Birth trauma 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 Spastic cerebral palsy and can you explain it in depth? [/INST] Spastic cerebral palsy is the type of cerebral palsy characterized by spasticity or high muscle tone often resulting in stiff, jerky movements. Cases of spastic CP are further classified according to the part or parts of the body that are most affected. Such classifications include spastic diplegia, spastic hemiplegia, spastic quadriplegia, and in cases of single limb involvement, spastic monoplegia.Spastic cerebral palsy affects the motor cortex of the brain, a specific portion of the cerebral cortex responsible for the planning and completion of voluntary movement. Spastic CP is the most common type of overall cerebral palsy, representing roughly 80% of cases. Spastic CP is a permanent condition and will affect an individual across the lifespan. The brain injury that causes spastic CP remains stable over time, but the way spasticity affects a person can change. For example, with age they may develop bone deformities from the pull of spastic muscles, muscular deterioration, and loss of range of motion in a joint. Thus, individuals with spastic CP often have different support needs with time.

Signs and symptoms
People with the spastic type of CP typically have muscles that are "tight" or stiff due to high muscle tone. Symptoms of spastic cerebral palsy vary as the disability can affect individuals differently. However, they typically appear in infancy and early childhood and most children are diagnosed in the first two years of life. The main indicator of spastic cerebral palsy is a delay in reaching motor milestones. The following are some common early signs, though the presence of a listed symptom does not definitively mean that a child has spastic CP:Prior to 6 months

Legs crossing when a child is picked up, also called scissoring
Stiffness
Head "lagging" when the child is picked up6–10 months

Fisting one hand
Difficulty rolling
Difficulty bringing hands togetherOlder than 12 months of age

Difficulty crawling
Difficulty standing even with support
Walking with an unsteady, uneven, or stiff gaitSpastic CP is distinguished from other forms of cerebral palsy by its prominent symptom of spasticity or stiff, tight movements and gait patterns such as the scissor gait. However, spasticity as a symptom is also seen in other conditions such as stroke and multiple sclerosis. Thus, the presence of spasticity alone does not warrant a conclusive diagnosis of spastic cerebral palsy.
Changes in spasticity and corresponding postures may also occur with other brain activity, such as excitement, fear or anxiety, or even pain, which increase muscle tension.A person with spastic CP will commonly show, in addition to higher muscle tone, persistent primitive reflexes, greater stretch reflexes, plantar reflex, and ankle clonus.A third of people with cerebral palsy have seizures - this is most common in spastic CP. Audiovisual, cognitive compromise and behavioral disorders can occur.

Cause
Spastic cerebral palsy is caused by malformation of or damage to the parts of the brain that control movement. What exactly makes some children susceptible to such brain damage is often unknown but it is believed that cerebral palsy may be the result of causal pathways, or chains of events that cause or increase the likelihood of brain injury. Most of the time, children are born with the brain damage resulting in spastic cerebral palsy, but a small percentage experience the damage shortly after birth following a stroke, head injury, or infection.The following are types of brain damage that can result in spastic cerebral palsy:

cerebral dysgenesis
periventricular leukomalacia
brain bleeds
Hypoxic ischaemic encephalopathy

Risk factors
The following medical conditions are associated with increased likelihood of spastic cerebral palsy, as well as with other types of cerebral palsy:

Preterm birth/low birthweight
Multiple births
Incompatible blood type between mother and fetus
Exposure to toxins
Complicated labor

Diagnosis
There is no single test to diagnose spastic cerebral palsy. It is typically diagnosed by age 2, though milder cases may go undetected for a longer time. A doctor will typically use a series of tests to assess developmental progress in growth, muscle control, coordination, vision, hearing, and posture. Continuous loss of motor skills likely indicates a condition other than spastic CP such as a genetic muscle disease Some metabolic disorders mimic spastic cerebral palsy and can be ruled out using a Magnetic resonance imaging test (MRI).Some tests to assess a child suspected to have spastic cerebral palsy are:

Cranial ultrasound
CT scan
Magnetic resonance imagingThese tests are imaging techniques used to produce pictures of the brain and to examine them for areas of damage that indicate a diagnosis of spastic cerebral palsy. A child with a spastic CP diagnosis will likely be referred to screening for other conditions associated with spastic cerebral palsy such as epilepsy (seizure disorder), intellectual disability, and visual impairment.

Types
Scientific classifications
The types of spastic cerebral palsy are generally distinguished by the primary areas of the body that are affected.
Spastic hemiplegia Hemiplegia is a type of cerebral palsy affecting one vertical half of the body (such as one arm and one leg). The affected side of the body is opposite the affected area of the brain in hemiplegia. For example, if the right side of the brain is damaged, the person will have weakness or paralysis on the left side of the body. People with hemiplegia typically favor an arm or hand and may keep the weaker hand in a fist. Typically, people that have spastic hemiplegia are the most ambulatory of all the forms, although they generally have dynamic equinus (a limping instability) on the affected side and are primarily prescribed ankle-foot orthoses to prevent said equinus.
Spastic diplegia describes spastic CP in which muscle tightness predominantly occurs in the legs. The arms may be somewhat affected or not affected at all.
Spastic monoplegia is one single limb being affected.
Spastic triplegia is three limbs being affected.
Spastic quadriplegia is all four limbs more or less equally affected.  People with spastic quadriplegia are rarely able to ambulate without assistance and may not stand at all. Among the forms of spastic CP, quad CP is more likely to co-occur with seizures and mild to moderate intellectual disability.In spastic cerebral palsy in children with low birth weights, 25% of children had hemiplegia, 37.5% had quadriplegia, and 37.5% had diplegia. No one person with a particular type of spastic CP presents in exactly the same way.

Treatment
There is no cure for spastic cerebral palsy and no way to reverse the initial brain injury. However, various treatments and assistive devices can help mitigate pain and allow those affected to have a higher quality of life. Different combinations of treatments are right for each individual and are determined by individuals and their care team.Some common interventions are:

Physical therapy- exercises to develop balance and strength and to learn skills such as walking, rolling, or driving a wheelchair.
Occupational therapy- therapy to help an individual develop strategies to complete activities of daily living such as dressing, toileting, and bathing either independently or with a level of assistance that is safe and comfortable.
Orthotics- braces and splints to improve posture and positioning (usually on legs or arms).
Assistive devices- Wheelchairs, crutches, and walkers may help someone with spastic CP navigate safely </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 Chondroid lipoma 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 Wound and can you explain it in depth? [/INST] A wound is a rapid onset of injury that involves lacerated or punctured skin (an open wound), or a contusion (a closed wound) from blunt force trauma or compression. In pathology, a wound is an acute injury that damages the epidermis of the skin.

Classification
According to level of contamination, a wound can be classified as:

Clean wound – made under sterile conditions where there are no organisms present, and the skin is likely to heal without complications.
Contaminated wound – usually resulting from accidental injury; there are pathogenic organisms and foreign bodies in the wound.
Infected wound – the wound has pathogenic organisms present and multiplying, exhibiting clinical signs of infection (yellow appearance, soreness, redness, oozing pus).
Colonized wound – a chronic situation, containing pathogenic organisms, difficult to heal (e.g. bedsore).

Open
Open wounds can be classified according to the object that caused the wound:

Incisions or incised wounds – caused by a clean, sharp-edged object such as a knife, razor, or glass splinter.
Lacerations – irregular tear-like wounds caused by some blunt trauma. Lacerations and incisions may appear linear (regular) or stellate (irregular). The term laceration is commonly misused in reference to incisions.
Abrasions (grazes) – superficial wounds in which the topmost layer of the skin (the epidermis) is scraped off. Abrasions are often caused by a sliding fall onto a rough surface such as asphalt, tree bark or concrete.
Avulsions – injuries in which a body structure is forcibly detached from its normal point of insertion. A type of amputation where the extremity is pulled off rather than cut off. When used in reference to skin avulsions, the term degloving is also sometimes used as a synonym.
Puncture wounds – caused by an object puncturing the skin, such as a splinter, nail or needle.
Penetration wounds – caused by an object such as a knife entering and coming out from the skin.
Gunshot wounds – caused by a bullet or similar projectile driving into or through the body. There may be two wounds, one at the site of entry and one at the site of exit, generally referred to as a "through-and-through."
Critical wounds- Including large burns that have been split. These wounds can cause serious hydroelectrolytic and metabolic alterations including fluid loss, electrolyte imbalances, and increased catabolism

Closed
Closed wounds have fewer categories, but are just as dangerous as open wounds:

Hematomas (or blood tumor) – caused by damage to a blood vessel that in turn causes blood to collect under the skin.
Hematomas that originate from internal blood vessel pathology are petechiae, purpura, and ecchymosis. The different classifications are based on size.
Hematomas that originate from an external source of trauma are contusions, also commonly called bruises.
Crush injury – caused by a great or extreme amount of force applied over a long period of time.

Presentation
Complications
Bacterial infection of wound can impede the healing process and lead to life-threatening complications. Scientists at Sheffield University have used light to rapidly detect the presence of bacteria, by developing a portable kit in which specially designed molecules emit a light signal when bound to bacteria. Current laboratory-based detection of bacteria can take hours or days.

Workup
Wounds that are not healing should be investigated to find the causes; many microbiological agents may be responsible. The basic workup includes evaluating the wound, its extent and severity. Cultures are usually obtained both from the wound site and blood. X-rays are obtained and a tetanus shot may be administered if there is any doubt about prior vaccination.

Chronic
Non-healing wounds of the diabetic foot are considered one of the most significant complications of diabetes, representing a major worldwide medical, social, and economic burden that greatly affects patient quality of life. Almost 24 million Americans—one in every twelve—are diabetic and the disease is causing widespread disability and death at an epidemic pace, according to the Centers for Disease Control and Prevention.  Of those with diabetes, 6.5 million are estimated to have chronic or non-healing wounds. Associated with inadequate circulation, poorly functioning veins, and immobility, non-healing wounds occur most frequently in the elderly and in people with diabetes—populations that are sharply rising as the nation ages and chronic diseases increase.
Although diabetes can ravage the body in many ways, non-healing ulcers on the feet and lower legs are common outward manifestations of the disease. Also, diabetics often experience nerve damage in their feet and legs, allowing small wounds or irritations to develop without awareness. Given the abnormalities of the microvasculature and other side effects of diabetes, these wounds take a long time to heal and require a specialized treatment approach for proper healing.
As many as 75% of diabetic patients will eventually develop foot ulcers, and recurrence within five years is 70%. If not aggressively treated, these wounds can lead to amputations. It is estimated that every 30 seconds a lower limb is amputated somewhere in the world because of a diabetic wound. Amputation often triggers a downward spiral of declining quality of life, frequently leading to disability and death. In fact, only about one third of diabetic amputees will live more than five years, a survival rate equivalent to that of many cancers.
Many of these lower extremity amputations can be prevented through an interdisciplinary approach to treatment involving a variety of advanced therapies and techniques, such as debridement, hyperbaric oxygen treatment therapy, dressing selection, special shoes, and patient education.  When wounds persist, a specialized approach is required for healing.

Pathophysiology
To heal a wound, the body undertakes a series of actions collectively known as the wound healing process.

Diagnosis
A wound may be recorded for follow-up and observing progress of healing with different techniques which include:
Photographs, with subsequent area quantification using computer processing
Wound tracings on acetate sheets
Kundin wound gauge

Management
The overall treatment depends on the type, cause, and depth of the wound, and whether other structures beyond the skin (dermis) are involved. Treatment of recent lacerations involves examining, cleaning, and closing the wound.  Minor wounds, like bruises, will heal on their own, with skin discoloration usually disappearing in 1–2 weeks. Abrasions, which are wounds with intact skin (non-penetration through dermis to subcutaneous fat), usually require no active treatment except keeping the area clean, initially with soap and water. Puncture wounds may be prone to infection depending on the depth of penetration. The entry of puncture wound is left open to allow for bacteria or debris to be removed from inside.

Cleaning
Evidence to support the cleaning of wounds before closure is scant. For simple lacerations, cleaning can be accomplished using a number of different solutions, including tap water and sterile saline solution. Infection rates may be lower with the use of tap water in regions where water quality is high. Cleaning of a wound is also known as wound toilet. It is not clear if delaying a shower following a surgery helps reduce complications related to wound healing.

Wound cleansing solutions
Evidence is insufficient to conclude whether cleaning wounds is beneficial or whether wound cleaning solutions (polyhexamethylene biguanide, aqueous oxygen peroxide, etc.) are better than sterile water or saline solutions to help venous leg ulcers heal. It is also uncertain whether the choice of cleaning solution or method of application makes any difference to venous leg ulcer healing.

Closure
If a person presents to a healthcare center within 6 hours of a laceration they are typically closed immediately after evaluating and cleaning the wound. After this point in time, however, there is a theoretical concern of increased risks of infection if closed immediately. Thus some healthcare providers may delay closure while others may be willing to immediately close up to 24 hours after the injury. Using clean non-sterile gloves is equivalent to using sterile gloves during wound closure.If closure of a wound is decided upon a number of techniques can be used. These include bandages, a cyanoacrylate glue, staples, and sutures.  Absorbable sutures have the benefit over non absorbable sutures of not requiring removal. They are often preferred in children. Buffering the pH of lidocaine makes the injection less painful.
Adhesive glue and sutures have comparable cosmetic outcomes for minor lacerations <5 cm in adults and children. The use of adhesive glue involves considerably less time for the doctor and less pain for the person. The wound opens at a slightly higher rate but there is less redness. The risk for infections (1.1%) is the same for both. Adhesive glue should not be used in areas of high tension or repetitive movements, such as joints or the posterior trunk. Split-thickness skin grafting (STSG) is also a surgical technique that features rapid wound closure, multiple possible donor sites with minimal morbidity.

Dressings
In the case of clean surgical wounds, there is no evidence that the use of topical antibiotics reduces infection rates in comparison with non-antibiotic ointment or no ointment at all </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 Cone dystrophy and can you explain it in depth? [/INST] A cone dystrophy is an inherited ocular disorder characterized by the loss of cone cells, the photoreceptors responsible for both central and color vision.

Presentation
The most common symptoms of cone dystrophy are vision loss (age of onset ranging from the late teens to the sixties), sensitivity to bright lights, and poor color vision.  Therefore, patients see better at dusk.  Visual acuity usually deteriorates gradually, but it can deteriorate rapidly to 20/200; later, in more severe cases, it drops to "counting fingers" vision.  Color vision testing using color test plates (HRR series) reveals many errors on both red-green and blue-yellow plates.

Dystrophy of the rods and cones
Dystrophy of the light-sensing cells of the eye may also occur in the rods as well, or in both the cones and the rods.
A type of rod-cone dystrophy—where rod function decline is typically earlier or more pronounced than cone dystrophy—has been identified as a relatively common characteristic of Bardet–Biedl Syndrome.At least one type of autosomal dominant cone-rod dystrophy is caused by mutations in the guanylate cyclase 2D (not geometrical) gene (GUCY2D) on chromosome 17.

Mechanism
The pathogenesis of cone dystrophy has yet to be elucidated.  It appears that the dystrophy is primary, since subjective and objective abnormalities of cone function are found before ophthalmoscopic changes can be seen.   However, the retinal pigment epithelium (RPE) rapidly becomes involved, leading to a retinal dystrophy primarily involving the macula.  The histological examination of the eyes of one such patient showed that the outer nuclear layer of cones and rods had disappeared completely, whereas the RPE showed pronounced pigment changes.  There was also atrophy of the temporal disc.

Diagnosis
The fundus exam via ophthalmoscopy is essentially normal early on in cone dystrophy, and definite macular changes usually occur well after visual loss.  Fluorescein angiography (FA) is a useful adjunct in the workup of someone suspected to have cone dystrophy, as it may detect early changes in the retina that are too subtle to be seen by ophthalmoscope.  For example, FA may reveal areas of hyperfluorescence, indicating that the RPE has lost some of its integrity, allowing the underlying fluorescence from the choroid to be more visible. These early changes are usually not detected during the ophthalmoscopic exam.
The most common type of macular lesion seen during ophthalmoscopic examination has a bulls-eye appearance and consists of a doughnut-like zone of atrophic pigment epithelium surrounding a central darker area.  In another, less frequent form of cone dystrophy there is rather diffuse atrophy of the posterior pole with spotty pigment clumping in the macular area.  Rarely, atrophy of the choriocapillaris and larger choroidal vessels is seen in patients at an early stage.  The inclusion of fluorescein angiography in the workup of these patients is important since it can help detect many of these characteristic ophthalmoscopic features.  In addition to the retinal findings, temporal pallor of the optic disc is commonly observed.
As expected, visual field testing in cone dystrophy usually reveals a central scotoma.  In cases with the typical bulls-eye appearance, there is often relative central sparing.Because of the wide spectrum of fundus changes and the difficulty in making the diagnosis in the early stages, electroretinography (ERG) remains the best test for making the diagnosis.  Abnormal cone function on the ERG is indicated by a reduced single-flash and flicker response when the test is carried out in a well-lit room (photopic ERG).  The relative sparing of rod function in cone dystrophy is evidenced by a normal scotopic ERG, i.e. when the test is carried out in the dark.  In more severe or longer standing cases, the dystrophy involves a greater proportion of rods with resultant subnormal scotopic records.  Since cone dystrophy is hereditary and can be asymptomatic early on in the disease process, ERG is an invaluable tool in the early diagnosis of patients with positive family histories.
Cone dystrophy in general usually occurs sporadically. Hereditary forms are usually autosomal dominant, and instances of autosomal recessive and X-linked inheritance also occur.
In the differential diagnosis, other macular dystrophies as well as the hereditary optic atrophies must be considered.  Fluorescent angiography, ERG, and color vision tests are important tools to help facilitate diagnosis in early stages.

Treatment
Though there is no treatment for cone dystrophy, certain supplements may help in delaying the progression of the disease.
The beta-carotenoids, lutein and zeaxanthin, have been evidenced to reduce the risk of developing age-related macular degeneration (AMD), and may therefore provide similar benefits to people with cone dystrophy.Consuming omega-3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid) has been correlated with a reduced progression of early AMD, and in conjunction with low glycemic index foods, with reduced progression of advanced AMD, and may therefore delay the progression of cone dystrophy.
Dr. Randall Walker, who has a variation of the condition himself, invented a software to enable low vision people to read with greater ease.<ref>url= https://www.bizjournals.com/twincities/print-edition/2014/06/06/made-at-mayo-mayo-professor-doubles-as-founder-of.html <ref>

Notes
References
Stephen J. Ryan et al., Retina, 3rd ed. (C.V. Mosby, 2001) ISBN 0-323-00804-6
Stephen J. Ryan et al., Retina, 4th ed. (C.V. Mosby, 2005) ISBN 0-323-02598-6
Carpentier S, Knaus M, Suh M (April 2009). "Associations between lutein, zeaxanthin, and age-related macular degeneration: an overview". Crit Rev Food Sci Nutr. 49 (4): 313–26 </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 Lipid storage disorder and can you explain it in depth? [/INST] A lipid storage disorder (or lipidosis) is any one of a group of inherited metabolic disorders in which harmful amounts of fats or lipids accumulate in some body cells and tissues. People with these disorders either do not produce enough of one of the enzymes needed to metabolize and break down lipids or, they produce enzymes that do not work properly. Over time, the buildup of fats may cause permanent cellular and tissue damage, particularly in the brain, peripheral nervous system, liver, spleen, and bone marrow.
Inside cells under normal conditions, lysosomes convert, or metabolize, lipids and proteins into smaller components to provide energy for the body.

Classification
Disorders that store this intracellular material are part of the lysosomal storage diseases family of disorders.

Sphingolipidoses
Many lipid storage disorders can be classified into the subgroup of sphingolipidoses, as they relate to sphingolipid metabolism. Members of this group include Niemann-Pick disease, Fabry disease, Krabbe disease, Gaucher disease, Tay–Sachs disease, metachromatic leukodystrophy, multiple sulfatase deficiency, and Farber disease. They are generally inherited in an autosomal recessive fashion, but Fabry disease is X-linked. Taken together, sphingolipidoses have an incidence of approximately 1 in 10,000. Enzyme replacement therapy is available mainly to treat Fabry disease and Gaucher disease and people with these types of sphingolipidoses may live well into adulthood. Generally, the other types are fatal by age 1 to 5 years for infantile forms, but progression may be mild for juvenile-onset or adult-onset forms.Alternatively, some of the sphingolipidoses may be classified into either GM1 gangliosidoses or GM2 gangliosidoses. Tay–Sachs disease belongs to the latter.

Other
Other lipid storage disorders that generally are not classified as sphingolipidoses include fucosidosis, Schindler disease, and Wolman disease.

Genetics
Lipid storage diseases can be inherited two ways:
Autosomal recessive inheritance occurs when both parents carry and pass on a copy of the faulty gene, but neither parent show signs and symptoms of the condition and is not affected by the disorder </s>