<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hypersensitivity pneumonitis and explain in detail? [/INST] Hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis (EAA) is a syndrome caused by the repetitive inhalation of antigens from the environment in susceptible or sensitized people. Common antigens include molds, bacteria, bird droppings, bird feathers, agricultural dusts, bioaerosols and chemicals from paints or plastics. People affected by this type of lung inflammation (pneumonitis) are commonly exposed to the antigens by their occupations, hobbies, the environment and animals. The inhaled antigens produce a hypersensitivity immune reaction causing inflammation of the airspaces (alveoli) and small airways (bronchioles) within the lung. Hypersensitivity pneumonitis may eventually lead to interstitial lung disease.

Signs and symptoms
Hypersensitivity pneumonitis (HP) can be categorized as acute, subacute, and chronic based on the duration of the illness.

Acute
In the acute form of HP dose of antigen exposure tends to be very high but only for a short duration. Symptoms may develop 4–6 hours following heavy exposure to the provoking antigen. Symptoms include fever, chills, malaise, cough, chest tightness, dyspnea, rash, swelling and headache. Symptoms resolve within 12 hours to several days upon cessation of exposure.

Subacute
Patients with subacute HP gradually develop a productive cough, dyspnea, fatigue, anorexia, weight loss, and pleurisy. Symptoms are similar to the acute form of the disease, but are less severe and last longer. Findings may be present in patients who have experienced repeated acute attacks.

Chronic
In chronic HP, dose of the antigen tends to be low volume but for a longer duration. Patients often lack a history of acute episodes. They have an insidious onset of cough, progressive dyspnea, fatigue, and weight loss. This is associated with partial to complete but gradual reversibility. Avoiding any further exposure is recommended. Clubbing is observed in 50% of patients. Tachypnea, respiratory distress, and inspiratory crackles over lower lung fields often are present. In fact, hypersensitivity pneumonitis can often resemble (IPF) in terms of pulmonary fibrosis and that many patients experience hypoxemia.

Epidemiology
Although the prevalence of hypersensitivity pneumonitis is not established it is thought to be low.  Data collection limitations are a result of difficulty in diagnosis, sub-clinical presentations that go undetected and variability in climate, region and proximity to local industries. The most common types are bird fanciers and farmers lung. Interestingly, cigarette smoking appears to be protective against the disease.

Pathophysiology
Hypersensitivity pneumonitis is caused by an exaggerated immune response (hypersensitivity). Type III hypersensitivity and type IV hypersensitivity can both occur depending on the cause. In general, acute HP is suspected to be attributed to a type III hypersensitivity while the subacute and chronic types are suspected to be caused by T cell infiltration and granuloma formation. Because different people react variably to antigen exposure, the exact mechanism is unclear but genetic and host factors are likely at play. The two hit hypothesis is often toted in the literature to explain why some people have a normal reaction to an antigenic exposure without clinical findings while others experience an exaggerated immune response. The "first hit" in the hypothesis is proposed to be genetic susceptibility and surrounding environmental factors and the "second hit" would be the introduction of the antigen into the respiratory system which causes the exaggerated immune response.

Diagnosis
The diagnosis is made through clinical judgement using a combination of findings because there does not exist a single, universal diagnostic criteria for the disease. The diagnosis is most commonly ascertained first with a detailed exposure history followed by a battery of clinical tests including: imaging, histopathology, pulmonary function testing, serology, bronchoscopy, and more. In 2020, official guidelines were published by American Thoracic Society, Japanese Respiratory Society, and Asociación Latinoamericana del Tórax which provides a systematic approach to the diagnosis of HP that relies on high-resolution computed tomography.

Exposure History
A detailed occupational, home and environmental exposure history is the first step in diagnosis. Unfortunately, only 60% of inciting antigens are identified in exposure assessment. Re-exposure to the antigen can help aid in diagnosis. Standardized questionnaires have been created to help in obtaining an exposure history although no official questionnaire has been purported. It has been recommended that the questionnaire administered should be relevant to the region in which the exposure has potentially occurred.Detailed exposure assessments are warranted in the cause of damp indoor environments which have the potential to propagate mold throughout the dwelling. The decision to enlist an industrial hygienist should be made based on the answers to evidence based questions during the environmental assessment. The industrial hygeinst or environmental scientist will make the decision to conduct additional sampling.

Types
Hypersensitivity pneumonitis may also be called many different names, based on the provoking antigen. These include:

Of these types, Farmers Lung and Bird-Breeders Lung are the most common. "Studies document 8-540 cases per 100,000 persons per year for farmers and 6000-21,000 cases per 100,000 persons per year for pigeon breeders. High attack rates are documented in sporadic outbreaks. Prevalence varies by region, climate, and farming practices. HP affects 0.4–7% of the farming population. Reported prevalence among bird fanciers is estimated to be 20-20,000 cases per 100,000 persons at risk."

Imaging
No single imaging finding is singularly definitive of a diagnosis rather clinicians rely on a constellation of findings. Both chest radiographs and high resolution CT scans can be normal.

Chest Radiographs
Acute presentation may reveal poorly defined a micro-nodular interstitial pattern and ground-glass opacities in the lower and mid lung zones. In addition to this, subacute presentations may show reticular nodular opacities in mid-to-lower lung zones. Chronic forms may show fibrotic changes and appear like Idiopathic pulmonary fibrosis.

High-Resolution Computed Tomography
This has become a common diagnostic imaging for the diagnosis and is the modality used in the Official ATS/JRS/ALAT Clinical Practice Guideline. Two forms of hypersensitivity pneumonitis are fibrotic and non-fibrotic findings on chest CT. The two differ in terms of their diagnostic work up and management although there is overall between them. The non-fibrotic form is typically characterized by ground glass opacities, mosaic attenuation, ill-defined centrilobular nodules (<5 mm), and air trapping. The fibrotic form is typically characterized by irregular linear opacities/coarse reticulations, traction bronchiectasis, and honeycombing, patchy ground-glass attenuation, centrilobular nodules, and mosaic attenuation. Three-density pattern (head cheese sign) is radiological sign which shows a region of the lung with three or more different types of attenuation which can be typical for the fibrotic type.

Histopathology
The acute form can be characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells. The subacute, or intermittent, form produces more well-formed noncaseating granulomas, bronchiolitis with or without organizing pneumonia, and interstitial fibrosis. Much like the pathogenesis of idiopathic pulmonary fibrosis (IPF), chronic HP is related to increased expression of Fas antigen and Fas ligand, leading to increased epithelial apoptosis activation in the alveoli. Cholesterol clefts or asteroid bodies are present within or outside granulomas.

Pulmonary Function Testing
Pulmonary function tests (PFTs) can generally reveal a restrictive pattern  however, either a restrictive or obstructive pattern (or both) may emerge on PFTs. PFTs, therefore, are less useful in making a diagnosis but rather tracking improvement or deterioration in lung function following removal or addition of suspected antigens. They may also demonstrate reduced diffusion capacity of lungs for carbon monoxide (DLCO).

Bronchoscopy
Bronchoalveolar lavage (BAL) is a reliable way to detect inflammation in the lung airways. Fluid analysis from the lavage extracted from the airways on bronchoscopy often reveals a total elevation in cell count in addition to an elevation in the percentage of T lymphocytes. This is a good way to help exclude other similar lung diseases like sarcoidosis, infection and Idiopathic pulmonary fibrosis.

Lung biopsy
Lung biopsies can be diagnostic in cases of chronic hypersensitivity pneumonitis, or may help to suggest the diagnosis and trigger or intensify the search for an allergen. The main feature of chronic hypersensitivity pneumonitis on lung biopsies is expansion of the interstitium by lymphocytes accompanied by an occasional multinucleated giant cell or loose granuloma.When fibrosis develops in chronic hypersensitivity pneumonitis, the differential diagnosis in lung biopsies includes the idiopathic interstitial pneumonias. This group of diseases includes usual interstitial pneumonia, non-specific interstitial pneumonia and cryptogenic organizing pneumonia, among others.The prognosis of some idiopathic interstitial pneumonias, e.g. idiopathic usual interstitial pneumonia (i.e. idiopathic pulmonary fibrosis), are very poor and the treatments of little help.  This contrasts the prognosis (and treatment) for hypersensitivity pneumonitis, which is generally fairly good if the allergen is identified and exposures to it significantly reduced or eliminated.  Thus, a lung biopsy, in some cases, may make a decisive difference.

Serum Precipitins
Assays for serum IgGs can aid in identifying possible antigenic exposures and are used as markers of exposure  However, there use is limited in making a definitive diagnosis because serum antibody levels are often elevated in those people who are exposed to an antigen but do not have the disease. Up to 90% of people exposed to the antigen have precipitins but only 50% of similarly exposed people who are asymptomatic have the same precipitins. False negatives are often common with serum precipitins because of lack of testing reagents for many antigens.Precipitating IgG antibodies against fungal or avian antigens can be detected in the laboratory using the traditional Ouchterlony immunodiffusion method wherein precipitin lines form on agar plate. The ImmunoCAP technology has replaced this time-consuming, labor-intensive method with their automated CAP assays and FEIA (Fluorescence enzyme immunoassay) that can detect IgG antibodies against Aspergillus fumigatus (Farmers lung or for ABPA) or avian antigens (Bird Fanciers Lung).

Differential Diagnosis
Organic dust toxic syndrome presents similarly with fevers, chills a few hours after exposure to bioaerosols with toxins from fungi, however this is not a true hypersensitivity reaction because it occurs on initial exposure without a preceding sensitization In chronic disease, HP must be differentiated from very similarly presenting idiopathic pulmonary fibrosis.Although overlapping in many cases, hypersensitivity pneumonitis may be distinguished from occupational asthma in that it is not restricted to only occupational exposure, and that asthma generally is classified as a type I hypersensitivity. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.Similarly, sarcoidosis has noncaseating granuloma formation, however hilar adenopathy is often seen on chest radiographs.

Treatment
The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage and acute disease is often self-limiting </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bruise and explain in detail? [/INST] A bruise, also known as a contusion, is a type of hematoma of tissue, the most common cause being capillaries damaged by trauma, causing localized bleeding that extravasates into the surrounding interstitial tissues. Most bruises are not very deep under the skin so that the bleeding causes a visible discoloration. The bruise then remains visible until the blood is either absorbed by tissues or cleared by immune system action. Bruises which do not blanch under pressure can involve capillaries at the level of skin, subcutaneous tissue, muscle, or bone. Bruises are not to be confused with other similar-looking lesions. (Such lesions include petechia (less than 3 mm (0.12 in), resulting from numerous and diverse etiologies such as adverse reactions from medications such as warfarin, straining, asphyxiation, platelet disorders and diseases such as cytomegalovirus), purpura (3–10 mm (0.12–0.39 in), classified as palpable purpura or non-palpable purpura and indicates various pathologic conditions such as thrombocytopenia),  and ecchymosis (more than 1 cm (0.39 in), caused by blood dissecting through tissue planes and settled in an area remote from the site of trauma or pathology such as periorbital ecchymosis, e.g. "raccoon eyes", arising from a basilar skull fracture or from a neuroblastoma).As a type of hematoma, a bruise is always caused by internal bleeding into the interstitial tissues which does not break through the skin, usually initiated by blunt trauma, which causes damage through physical compression and deceleration forces. Trauma sufficient to cause bruising can occur from a wide variety of situations including accidents, falls, and surgeries. Disease states such as insufficient or malfunctioning platelets, other coagulation deficiencies, or vascular disorders, such as venous blockage associated with severe allergies can lead to the formation of purpura which is not to be confused with trauma-related bruising/contusion. If the trauma is sufficient to break the skin and allow blood to escape the interstitial tissues, the injury is not a bruise but bleeding, a different variety of hemorrhage. Such injuries may be accompanied by bruising elsewhere.

Signs and symptoms
Bruises often induce pain immediately after the trauma that results in their formation, but small bruises are not normally dangerous alone. Sometimes bruises can be serious, leading to other more life-threatening forms of hematoma, such as when associated with serious injuries, including fractures and more severe internal bleeding.  The likelihood and severity of bruising depends on many factors, including type and healthiness of affected tissues. Minor bruises may be easily recognized in people with light skin color by characteristic blue or purple appearance (idiomatically described as "black and blue") in the days following the injury.
Hematomas can be subdivided by size. By definition, ecchymoses are 1 centimetres in size or larger, and are therefore larger than petechiae (less than 3 millimetres in diameter) or purpura (3 to 10 millimetres in diameter). Ecchymoses also have a more diffuse border than other purpura. A broader definition of ecchymosis is the escape of blood into the tissues from ruptured blood vessels. The term also applies to the subcutaneous discoloration resulting from seepage of blood within the injured tissue.
Bruise colors vary from red, blue, or almost black, depending on the severity of broken capillaries or blood vessels within the bruise site. Broken venules or arterioles often result in a deep blue or dark red bruise, respectively. Darker colored bruises may result from a more severe bleeding from both blood vessels. Older bruises may appear yellow, green or brown.

Cause
There are many causes of subcutaneous hematomas including ecchymoses. Coagulopathies such as Hemophilia A may cause ecchymosis formation in children. The medication betamethasone can have the adverse effect of causing ecchymosis.The presence of bruises may be seen in patients with platelet or coagulation disorders, or those who are being treated with an anticoagulant. Unexplained bruising may be a warning sign of child abuse, domestic abuse, or serious medical problems such as leukemia or meningoccocal infection. Unexplained bruising can also indicate internal bleeding or certain types of cancer. Long-term glucocorticoid therapy can cause easy bruising. Bruising present around the navel (belly button) with severe abdominal pain suggests acute pancreatitis. Connective tissue disorders such as Ehlers-Danlos syndrome may cause relatively easy or spontaneous bruising depending on the severity. Spontaneous bruising or bruising with minimal trauma in the absence of other explanations and together with other minor or major criteria suggestive of Vascular Ehlers-Danlos Syndrome (vEDS) suggests genetic testing for the condition.During an autopsy, bruises accompanying abrasions indicate the abrasions occurred while the individual was alive, as opposed to damage incurred post mortem.

Size and shape
Bruise shapes may correspond directly to the instrument of injury or be modified by additional factors. Bruises often become more prominent as time lapses, resulting in additional size and swelling, and may grow to a large size over the course of the hours after the injury that caused the bruise was inflicted.

Condition and type of tissue: In soft tissues, a larger area is bruised than would be in firmer tissue due to ease of blood to invade tissue.
Age: elderly skin and other tissues are often thinner and less elastic and thus more prone to bruising.
Gender: More bruising occurs in females due to increased subcutaneous fat.
Skin tone: Discoloration caused by bruises is more prominent in lighter complexions.
Diseases: Coagulation, platelet and blood vessel diseases or deficiencies can increase bruising due to more bleeding.
Location: More extensive vascularity causes more bleeding. Areas such as the arms, knees, shins and the facial area are especially common bruise sites.
Forces: Greater striking forces cause greater bruising.
Genes: Despite having completely normal coagulation factors, natural redheads have been shown to bruise more, although this may just be due to greater visibility on commonly associated lighter complexion.

Severity
Bruises can be scored on a scale from 0–5 to categorize the severity and danger of the injury.

The harm score is determined by the extent and severity of the injuries to the organs and tissues causing the bruising, in turn depending on multiple factors.  For example, a contracted muscle will bruise more severely, as will tissues crushed against underlying bone.  Capillaries vary in strength, stiffness and toughness, which can also vary by age and medical conditions.
Low levels of damaging forces produce small bruises and generally cause the individual to feel minor pain straight away. Repeated impacts worsen bruises, increasing the harm level. Normally, light bruises heal nearly completely within two weeks, although duration is affected by variation in severity and individual healing processes; generally, more severe or deeper bruises take somewhat longer.
Severe bruising (harm score 2–3) may be dangerous or cause serious complications.  Further bleeding and excess fluid may accumulate causing a hard, fluctuating lump or swelling hematoma.  This has the potential to cause compartment syndrome in which the swelling cuts off blood flow to the tissues.  The trauma that induced the bruise may also have caused other severe and potentially fatal harm to internal organs.  For example, impacts to the head can cause traumatic brain injury: bleeding, bruising and massive swelling of the brain with the potential to cause concussion, coma and death.  Treatment for brain bruising may involve emergency surgery to relieve the pressure on the brain.
Damage that causes bruising can also cause bones to be broken, tendons or muscles to be strained, ligaments to be sprained, or other tissue to be damaged.  The symptoms and signs of these injuries may initially appear to be those of simple bruising. Abdominal bruising or severe injuries that cause difficulty in moving a limb or the feeling of liquid under the skin may indicate life-threatening injury and require the attention of a physician.

Mechanism
Increased distress to tissue causes capillaries to break under the skin, allowing blood to escape and build up. As time progresses, blood seeps into the surrounding tissues, causing the bruise to darken and spread. Nerve endings within the affected tissue detect the increased pressure, which, depending on severity and location, may be perceived as pain or pressure or be asymptomatic. The damaged capillary endothelium releases endothelin, a hormone that causes narrowing of the blood vessel to minimize bleeding. As the endothelium is destroyed, the underlying von Willebrand factor is exposed and initiates coagulation, which creates a temporary clot to plug the wound and eventually leads to restoration of normal tissue.
During this time, larger bruises may change color due to the breakdown of hemoglobin from within escaped red blood cells in the extracellular space. The striking colors of a bruise are caused by the phagocytosis and sequential degradation of hemoglobin to biliverdin to bilirubin to hemosiderin, with hemoglobin itself producing a red-blue color, biliverdin producing a green color, bilirubin producing a yellow color, and hemosiderin producing a golden-brown color. As these products are cleared from the area, the bruise disappears </s>


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

Signs and symptoms
Patients will present with a sudden onset of cramps/abdominal pain or a stitch </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Exophthalmos and explain in detail? [/INST] Exophthalmos (also called exophthalmus, exophthalmia, proptosis, or exorbitism) is a bulging of the eye anteriorly out of the orbit.  Exophthalmos can be either bilateral (as is often seen in Graves disease) or unilateral (as is often seen in an orbital tumor). Complete or partial dislocation from the orbit is also possible from trauma or swelling of surrounding tissue resulting from trauma.
In the case of Graves disease, the displacement of the eye results from abnormal connective tissue deposition in the orbit and extraocular muscles, which can be visualized by CT or MRI.If left untreated, exophthalmos can cause the eyelids to fail to close during sleep, leading to corneal dryness and damage. Another possible complication is a form of redness or irritation called superior limbic keratoconjunctivitis, in which the area above the cornea becomes inflamed as a result of increased friction when blinking. The process that is causing the displacement of the eye may also compress the optic nerve or ophthalmic artery, and lead to blindness.

Causes
Inflammatory/Infection:

Graves ophthalmopathy due to Graves disease, usually causes bilateral proptosis.
Orbital cellulitis – often with unilateral proptosis, severe redness, and moderate to severe pain, sinusitis and an elevated white blood cell count.
Dacryoadenitis
Erdheim–Chester disease
Mucormycosis
Orbital pseudotumor – presents with acute, usually unilateral proptosis with severe pain.
High-altitude cerebral edema
Granulomatosis with polyangiitisNeoplastic:

Leukemias
Meningioma, (of sphenoid wing)
Nasopharyngeal angiofibroma
Hand–Schüller–Christian disease
Hemangioma, cavernousCystic:

Dermoid cystVascular:

Carotid-cavernous fistula
Aortic insufficiency: manifests as a pulsatile pseudoproptosis, described by British cardiothoracic surgeon Hutan Ashrafian in 2006Others:

Orbital fracture: apex, floor, medial wall, zygomatic
Retrobulbar hemorrhage: trauma to the orbit can lead to bleeding behind the eye. The hemorrhage has nowhere to escape and the increased pressure pushes the eye out of the socket, leading to proptosis and can also cause blindness if not treated promptly.
Cushings syndrome (due to fat in the orbital cave)
Some forms of craniosynostosis:
Crouzon syndrome
Pfeiffer syndrome
Pansynostosis

Anatomy
Proptosis is the anterior displacement of the eye from the orbit.  Since the orbit is closed off posteriorly, medially and laterally, any enlargement of structures located within will cause the anterior displacement of the eye.  Swelling or enlargement of the lacrimal gland causes inferior medial and anterior dislocation of the eye.  This is because the lacrimal glands are located superiorly and laterally in the orbit.

Diagnosis
Measurement
Measurement of the degree of exophthalmos is performed using an exophthalmometer.
Most sources define exophthalmos/proptosis as a protrusion of the globe greater than 18 mm.The term exophthalmos is often used when describing proptosis associated with Graves disease.

Animals
Exophthalmos is commonly found in dogs.  It is seen in brachycephalic (short-nosed) dog breeds because of the shallow orbit.  It can lead to keratitis secondary to exposure of the cornea.  Exophthalmos is commonly seen in the pug, Boston terrier, Pekingese, and shih tzu </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Endometrioma and explain in detail? [/INST] Endometrioma is the presence of tissue similar but distinct to the endometrium in and sometimes on the ovary. It is the most common form of endometriosis.  Endometrioma is found in 17–44% patients with endometriosis. More broadly, endometriosis is the presence of tissue similar but distinct to endometrial tissue located outside the uterus. The presence of endometriosis can result in the formation of scar tissue, adhesions and an inflammatory reaction. It usually is a benign growth. An endometrioma is most often found in the ovary. This ovarian endometriosis forms dark, fluid-filled cysts. These fluid-filled sacs can vary greatly in size and are known as endometriomas, also called "chocolate cysts". The fluid inside the cysts is thick, dark, old blood, giving it a chocolate-like appearance. It can also develop in the cul-de-sac (the space behind the uterus), the surface of the uterus, and between the vagina and rectum.

Pathophysiology
Endometrial tissue is the mucous membrane that normally lines the uterus. The endometrium is richly supplied with blood and its growth is regulated by estrogen and progesterone. It consists of glandular and stroma tissue from the lining of the uterus. When the endometrial mucous membrane is found outside of the uterus in places such as the ovaries, it causes chronic pelvic pain with intercourse and menstrual cycles.
Endometriomas can produce a toxic environment by producing estrogen, cytokines, interleukins, and other inflammatory substances, that could damage healthy endometriomal tissue. This toxic fluid content can cause dire alterations to the normal surrounding endometriotic cells, potentially impacting the embryo, the ability of an embryo to implant successfully, and the responsiveness of the endometrium. Endometrioma can potentially lead to premature ovarian failure, decreased ovarian function, or problems with ovulation. Studies have also found that endometriomas occur two times more frequently in the left ovary (67%) than in the right one (33%), possibly due to the presence of the sigmoid colon on the left side.

Risks
Endometriomas can increase the risk of ovarian cancer in reproductive women, decrease normal ovarian function, and cause pain in the pelvis during or after periods or during sexual intercourse. Although most endometriomas are found to be benign, the possibility of malignant tumors still exists, and surgery is needed to confirm malignancy and determine what future treatment must be administered.
Another factor that endometrioma can impact is the ovarian reserve, or the number of quality follicles left in the ovary to produce viable eggs. Ovaries with endometriomas showed significantly less follicular density as compared to healthy ovaries, leading to a decrease in fertility.

Treatment
Medication
Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used first in patients with pelvic pain, particularly if the diagnosis of endometriosis has not been definitively (excision and biopsy) established.  The goal of directed medical treatment is to achieve an anovulatory state. Typically, this is achieved initially using hormonal contraception.  This can also be accomplished with progestational agents (i.e., medroxyprogesterone acetate), danazol, gestrinone, or gonadotropin-releasing hormone agonists (GnRH), as well as other less well-known agents.  These agents are generally used if oral contraceptives and NSAIDs are ineffective. GnRH can be combined with estrogen and progestogen (add-back therapy) without loss of efficacy but with fewer hypoestrogenic symptoms. These medications are often ineffective in treating endometriomas and any relief is short lived while taking the medications. Therapy with these agents has a large number of sometimes permanent side effects, such as hot flushes, loss of bone mass, deepening of voice, weight gain, and facial hair growth.

Surgery
Laparoscopic surgical approaches include excision of ovarian adhesions and of endometriomas. Endometriomas require surgical removal and excision is considered to be superior to cyst vaporization or coagulation in terms of permanent removal of the disease and pain relief. Surgery can sometimes have the effect of improving fertility but can have the adverse effect of leading to increases in cycle day 2 or 3 FSH for many patients. It can also pose the risk of diminishing the ovarian reserve, which could lead to post-surgery infertility </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Autoimmune optic neuropathy and explain in detail? [/INST] Autoimmune optic neuropathy (AON), sometimes called autoimmune optic neuritis, may be a forme fruste of systemic lupus erythematosus (SLE) associated optic neuropathy. AON is more than the presence of any optic neuritis in a patient with an autoimmune process, as it describes a relatively specific clinical syndrome. AON is characterized by chronically progressive or recurrent vision loss associated with serological evidence of autoimmunity. Specifically, this term has been suggested for cases of optic neuritis with serological evidence of vasculitis by positive ANA, despite the lack of meeting criteria for SLE. The clinical manifestations include progressive vision loss that tends to be steroid-responsive and steroid dependent.
Patients with defined SLE that go on to develop optic neuritis should be better identified as lupus optic neuritis.

Signs and symptoms
AON was first described in 1982. It presents with visual loss and signs of optic nerve dysfunction, such as loss of color vision, afferent pupil defect, and sometimes abnormalities of the optic disc. The clinical features of AON can be variable and present in several unilateral or bilateral forms:

Acute anterior or retrobulbar optic neuritis sometimes associated with pain.
Anterior or retrobulbar ischemic optic neuropathy not associated with pain.
Chronic progressive vision loss that mimics a compressive lesion.The main features that differentiate AON from the more common typical demyelinating optic neuritis is the poor recovery of vision and the chronic or recurrent or bilateral course of AON. Furthermore, the workup for multiple sclerosis including MRI, will be negative. Thus, it may be necessary to diagnose AON after a period of observation, noting the problem is not behaving as expected for demyelinative disease.

Pathogenesis
Approximately 1-2% of patients with defined SLE develop an optic neuropathy during the course of their disease. SLE-associated optic neuritis is rarely the presenting sign of the disease. The molecular pathogenesis is hypothesized, based on clinical features and the emerging understanding of mechanisms in SLE </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Iminoglycinuria and explain in detail? [/INST] Iminoglycinuria is an autosomal recessive disorder of renal tubular transport affecting reabsorption of the amino acid glycine, and the imino acids proline and hydroxyproline. This results in excess urinary excretion of all three acids (-uria denotes "in the urine").Iminoglycinuria is a rare and complex disorder, associated with a number of genetic mutations that cause defects in both renal and intestinal transport systems of glycine and imino acids.Imino acids typically contain an imine functional group, instead of the amino group found in amino acids. Proline is considered and usually referred to as an amino acid, but unlike others, it has a secondary amine. This feature, unique to proline, identifies proline also as an imino acid. Hydroxyproline is another imino acid, made from the naturally occurring hydroxylation of proline.

Presentation
The primary characteristic of iminoglycinuria is the presence of glycine and imino acids in the urine. Otherwise, it is thought to be a relatively benign disorder, although symptoms associated with disruptions of proline and glycine metabolism caused by malabsorption may be present with iminoglycinuria. These include encephalopathy, mental retardation, deafness, blindness, kidney stones, hypertension and gyrate atrophy.Gyrate atrophy is an inherited degenerative disorder of the retina and choroid, sometimes accompanying the metabolic condition hyperornithinemia. The presence of gyrate atrophy with iminoglycinuria stems from a deficiency of proline in chorioretinal tissues, while processes behind hyperornithinemia disrupt the metabolic pathway from ornithine to proline, which alters the catabolism of ornithine, and also results in reduced levels of proline. Thus, gyrate atrophy can be found with either disorder, with proline deficiency as an underlying feature.Hyperglycinuria is another disorder affecting reabsorption of glycine and imino acids, similar to iminoglycinuria and considered to be a heterozygous form. When accompanied by a specific type of kidney stone (nephrolithiasis), it is sometimes referred to as "iminoglycinuria, type II".

Genetics
Iminoglycinuria is believed to be inherited in an autosomal recessive manner. This means a defective gene responsible for the disorder is located on an autosome, and inheritance requires two copies of the defective gene—one from each parent. Parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder.A non-inherited cause of excess urinary excretion of proline and glycine, similar to that found in iminoglycinuria, is quite common to newborn infants younger than six months. Sometimes referred to as neonatal iminoglycinuria, it is due to underdevelopment of high-affinity transport mechanisms within the renal circuit, specifically PAT2, SIT1 and SLC6A18. The condition corrects itself with age. In cases where this persists beyond childhood, however, inherited hyperglycinuria or iminoglycinuria may be suspected.

Pathophysiology
Glycine, proline and hydroxyproline share common renal tubular mechanisms of reabsorption, a function specific to the proximal tubule. Both reabsorption or absorption of glycine and imino acids takes place respectively at the proximal tubule or intestinal brush border epithelium. The more selective transport of proline and other imino acids is driven at the molecular level by a mammalian cellular transport mechanism aptly known as system IMINO.

While no single genetic mutation has been established as the cause of iminoglycinuria; several mutations, affecting transport mechanisms shared by glycine, proline and hydroxyproline, as well as those that selectively transport either glycine or imino acids, including the IMINO system, are known to be associated with the disorder. When combined, these factors will result in a variable phenotype for iminoglycinuria depending on which mutations are present. However, despite the role that intestinal malabsorption of glycine and imino acids can play in iminoglycinuria, the primary defect disrupts their renal transport and reabsorption. This is evident, as inherited iminoglycinuria can be clinically present with no intestinal involvement.In mammals, including humans, the transport of amino and imino acids from the lumen (interior) of the intestine or the renal proximal tubule into the cells occurs at the brush border membrane of the epithelium (moist, tightly packed cellular lining of many tissues and organs of the body). Here, cotransporters such as sodium or chloride (part of the system of Na-K-Cl cotransporters) couple with the amino or imino acids on the molecular level and transport them through specific integral membrane proteins that form ion channels, which are located within the cell membrane. From the cells, the absorbed or reabsorbed amino and imino acids eventually reach the blood. Absorption refers to the overall process happening in the intestine in lieu of normal digestive breakdown of proteins, while reabsorption refers to the process occurring in the renal proximal tubule to reclaim amino and imino acids that have been filtered out of the blood via the glomerulus.These forms of transport require energy, as the products being transported are usually moving against a higher concentration gradient. This process, called active transport, get its energy from ATP and other ATP-related cotransport systems that produce energy, like the sodium-potassium pump.

Mechanism
The primary defect associated with iminoglycinuria is a homozygous (recessive) mutation of the SLC36A2 (PAT2) gene. One of several membrane transport proteins in the solute carrier family of amino acid transporters, PAT2 is the high-affinity renal transporter of glycine, proline and hydroxyproline found to be defective in both alleles when iminoglycinuria is present in an individual. This is in contrast to the fact that when only one PAT2 allele is defective, hyperglycinuria will be present instead of iminoglycinuria. These findings delineate iminoglycinuria as the homozygous form of hyperglycinuria, with the former having a higher degree of urinary excretion of glycine and imino acids correlating to mutations in both alleles.Another mutation suspected to convey the iminoglycinuria phenotype may be found in the SLC36A1 (PAT1) gene. Identified as the low-affinity intestinal transporter of glycine and imino acids, PAT1 works in cooperation with the renal sodium-hydrogen exchanger NHE3 (SLC9A3) </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Malonyl-CoA decarboxylase deficiency and explain in detail? [/INST] Malonyl-CoA decarboxylase deficiency (MCD) is an autosomal-recessive metabolic disorder caused by a genetic mutation that disrupts the activity of Malonyl-CoA decarboxylase. This enzyme breaks down Malonyl-CoA (a fatty acid precursor and a fatty acid oxidation blocker) into acetyl-CoA and carbon dioxide.

Signs and symptoms
The signs and symptoms of this disorder typically appear in early childhood. Almost all affected children have delayed development. Additional signs and symptoms can include weak muscle tone (hypotonia), seizures, diarrhea, vomiting, and low blood sugar (hypoglycemia). A heart condition called cardiomyopathy, which weakens and enlarges the heart muscle, is another common feature of malonyl-CoA decarboxylase deficiency.
Some common symptoms in Malonyl-CoA decarboxylase deficiency, such as cardiomyopathy and metabolic acidosis, are triggered by the high concentrations of Malonyl-CoA in the cytoplasm. High levels of Malonyl-CoA will inhibit β-oxidation of fatty acids through deactivating the carrier of fatty acyl group, CPT1, and thus, blocking fatty acids from going into the mitochondrial matrix for oxidation.A research conducted in Netherlands has suggested that carnitine supplements and a low fat diet may help to reduce the level of malonic acid in our body.

Genetics
Malonyl-CoA decarboxylase deficiency is caused by mutations in the MLYCD gene, located on chromosome 16q24. The gene encodes the enzyme malonyl-CoA decarboxylase. Within cells, this enzyme helps regulate the formation and breakdown of a certain group of fats called fatty acids.
Many tissues, including heart muscle, use fatty acids as a major source of energy. Mutations in the MLYCD gene reduce or eliminate the function of malonyl-CoA decarboxylase. A lack of this enzyme disrupts the normal balance of fatty acid formation and breakdown. As a result, fatty acids cannot be converted to energy, which can lead to characteristic features of this disorder, such as low blood sugar and cardiomyopathy. By-products of fatty acid processing build up in tissues, which also contributes to the signs and symptoms of malonyl-CoA decarboxylase deficiency.
Malonyl-CoA decarboxylase deficiency is inherited in an autosomal recessive pattern. This means that the defective gene is located on an autosome (chromosome 16 is an autosome), and two copies of the defective gene - one inherited from each parent - are required to be born with the disorder. The parents of a child with an autosomal recessive disorder both carry one copy of the defective gene, but are usually not affected by the disorder.
Malonyl-CoA decarboxylase deficiency is extremely rare, evidence suggests that it is caused by the abnormality in the protein transcription regulation. Looking at the molecular basis, two distinct homozygous mutations are found to cause Malonyl-CoA  Decarboxylase deficiency in human. The first mutation is the transversion of gene from C to G causing a premature stop signal in the protein </s>


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


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


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Nephronophthisis and explain in detail? [/INST] Nephronophthisis is a genetic disorder of the kidneys which affects children. It is classified as a medullary cystic kidney disease. The disorder is inherited in an autosomal recessive fashion and, although rare, is the most common genetic cause of childhood kidney failure. It is a form of ciliopathy. Its incidence has been estimated to be 0.9 cases per million people in the United States, and 1 in 50,000 births in Canada.

Signs and symptoms
Infantile, juvenile, and adolescent forms of nephronophthisis have been identified. Although the range of characterizations is broad, people affected by nephronophthisis typically present with polyuria (production of a large volume of urine), polydipsia (excessive liquid intake), and after several months to years, end-stage kidney disease, a condition necessitating either dialysis or a kidney transplant in order to survive. Some individuals with nephronophthisis also have so-called "extra-renal symptoms" which can include tapetoretinal degeneration, liver problems, oculomotor apraxia, and cone-shaped epiphysis (Saldino-Mainzer syndrome).

Cause
Nephronophthisis is characterized by fibrosis and the formation of cysts at the cortico-medullary junction, it is an autosomal recessive disorder which eventually leads to terminal kidney failure.

Pathophysiology
Mechanism of nephronophthisis indicates that all proteins mutated in cystic kidney diseases express themselves in primary cilia. NPHP gene mutations cause defects in signaling resulting in flaws of planar cell polarity. The ciliary theory indicates that  multiple organs are involved in NPHP (retinal degeneration, cerebellar hypoplasia, liver fibrosis, and intellectual disability).

Related rare genetic disorders
Nephronophthisis is a ciliopathy.  Other known ciliopathies include primary ciliary dyskinesia, Bardet–Biedl syndrome, polycystic kidney and liver disease, Alström syndrome, Meckel–Gruber syndrome and some forms of retinal degeneration.NPHP2 is infantile type of nephropthisis and sometimes associated with situs inversus this can be explained by its relation with inversin gene. NPHP1, NPHP3, NPHP4, NPHP5, and NPHP6 are sometimes seen with retinitis pigmentosa, this particular association has a name, Senior-Loken syndrome.

Diagnosis
The diagnosis of nephronophthisis can be obtained via a kidney ultrasound, family history and clinical history of the affected individual according to Stockman, et al.

Types
Infantile NPH
Juvenile NPH
Adult NPH

Management
The management of this condition can be done via-improvement of any electrolyte imbalance, as well as, high blood pressure and low red blood cell counts (anemia) treatment as the individuals condition warrants.

Epidemiology
Nephronophthisis occurs equally in both sexes and has an estimate 9 in about 8 million rate in individuals. Nephronophthisis is the leading monogenic cause of end-stage kidney disease.

References
Further reading
Simms, Roslyn J.; Hynes, Ann Marie; Eley, Lorraine; Sayer, John A. (2011). "Nephronophthisis: A Genetically Diverse Ciliopathy". International Journal of Nephrology. 2011: 1–10. doi:10.4061/2011/527137. PMC 3108105. PMID 21660307.
Hildebrandt, Friedhelm; Attanasio, Massimo; Otto, Edgar (2009-01-01). "Nephronophthisis: Disease Mechanisms of a Ciliopathy" </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Familial multiple lipomatosis and explain in detail? [/INST] Familial multiple lipomatosis is a hereditary adipose tissue disorder that is characterized by the formation of multiple lipomas that occur in a particular distribution. The lipomas are well-encapsulated, slow-growing, benign fatty tumors. The distribution is defined as being focused in the trunk of the body and extremities.  Familial Multiple Lipomatosis can be identified when multiple lipomas occur in multiple family members that span different generations. Some people may have hundreds of lipomas present.

Symptoms
The source of this disease is from family history, and symptoms most often arise in middle age. Newly formed lipomas frequently present themselves as a bead-like lump under the skin, and become rubbery and movable. They may be seen throughout the body and in some areas more than others, however, it does not make an appearance on the head or shoulders of the individual. The size of those bumps may vary and could possibly get in the way of an individual living their life peacefully. There are usually no feelings of discomfort or pain unless a lipoma has been aggravated or is directly on a nerve. Lipomas that sit over bony areas such as the ribs and lower back can cause discomfort when lying down or receiving any kind of pressure. The age at which familial multiple lipomatosis begins to make an appearance on the individual’s body varies; for some it may be as early as 5 years of age.

Diagnosis
Familial multiple lipomatosis is usually diagnosed through a physical exam via palpation, medical history and imaging studies such as ultrasound, CT scan, or magnetic resonance imaging (MRI). A CT scan is an imaging method that uses x-rays to create images of cross sections of the body, while an MRI uses powerful magnets and radio waves to create images of lipomas and surrounding tissues. Both tests are useful to establish the diagnosis of multiple symmetric lipomatosis, although magnetic resonance imaging provides more details and may be used when lipomas are large, deep, or have infiltrated muscle fibers or nerves. In some cases, a biopsy of the lipomas may be necessary to confirm the diagnosis.

Differential diagnoses
Liposarcoma
Dercum’s disease
Benign symmetric lipomatosis
Madelung’s disease
Cyst

Causes
The exact cause of FML is not yet known, but there are several theories of different causes:
Hormonal disorder due to the bodys inability to properly metabolize fat
Increase in fat cells (adipocytes)
Enzymatic defect or a change in the surface of the cells that could prevent the breakdown of fat
Poor lymphatic drainage
Defective regulation of mitochondria in brown fat. Brown fat is responsible for causing heat in times of stress or cold. For general callus tissue is stimulated by the sympathetic nervous system and this response is mediated by a substance called norepinephrine. This process occurs in the mitochondria
In most families, the mode of inheritance has not been determined </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hypochondrogenesis and explain in detail? [/INST] Hypochondrogenesis is a severe genetic disorder causing malformations of bone growth. The condition is characterized by a short body and limbs and abnormal bone formation in the spine and pelvis.
Hypochondrogenesis is a subtype of collagenopathy, types II and XI, and is similar to another skeletal disorder, achondrogenesis type 2, although the spinal changes seen in hypochondrogenesis tend to be somewhat milder.

Signs and symptoms
Symptoms of hypochondrogenesis include: edema, limb undergrowth, spondyloepiphyseal dysplasia, short ribs, respiratory failure, short chin, upper limb undergrowth, thoracic hypoplasia, hypertelorism, hydrops fetalis, pulmonary hypoplasia, and a cleft palate.

Pathophysiology
Hypochondrogenesis is one of the most severe conditions in a spectrum of disorders caused by mutations in the COL2A1 gene. The protein made by this gene forms type II collagen, a molecule found mostly in cartilage and in the clear gel that fills the eyeball (the vitreous) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Ependymoma and explain in detail? [/INST] An ependymoma is a tumor that arises from the ependyma, a tissue of the central nervous system. Usually, in pediatric cases the location is intracranial, while in adults it is spinal. The common location of intracranial ependymomas is the fourth ventricle. Rarely, ependymomas can occur in the pelvic cavity.
Syringomyelia can be caused by an ependymoma.
Ependymomas are also seen with neurofibromatosis type II.

Signs and symptoms
Source:
severe headache
visual loss (due to papilledema)
vomiting
bilateral Babinski sign
drowsiness (after several hours of the above symptoms)
gait change (rotation of feet when walking)
impaction/constipation
back flexibility

Morphology
Ependymomas are composed of cells with regular, round to oval nuclei.  There is a variably dense fibrillary background. Tumor cells may form gland-like round or elongated structures that resemble the embryologic ependymal canal, with long, delicate processes extending into the lumen; more frequently present are perivascular pseudorosettes in which tumor cells are arranged around vessels with an intervening zone consisting of thin ependymal processes directed toward the wall of the vessel.It has been suggested that ependymomas are derived from radial glia, despite their name suggesting an ependymal origin.

Ependymoma tumors
Ependymomas make up about 5% of adult intracranial gliomas and up to 10% of childhood tumors of the central nervous system (CNS). Their occurrence seems to peak at age 5 years and then again at age 35. They develop from cells that line both the hollow cavities of the brain and the canal containing the spinal cord, but they usually arise from the floor of the fourth ventricle, situated in the lower back portion of the brain, where they may produce headache, nausea and vomiting by obstructing the flow of cerebrospinal fluid. This obstruction may also cause hydrocephalus. They may also arise in the spinal cord, conus medullaris and supratentorial locations. Other symptoms can include (but are not limited to): loss of appetite, difficulty sleeping, temporary inability to distinguish colors, uncontrollable twitching, seeing vertical or horizontal lines when in bright light, and temporary memory loss.  It should be remembered that these symptoms also are prevalent in many other illnesses not associated with ependymoma.About 10% of ependymomas are benign myxopapillary ependymoma (MPE). MPE is a localized and slow-growing low-grade tumor, which originates almost exclusively from the lumbosacral nervous tissue of young patients. On the other hand, it is the most common tumor of the lumbosacral canal comprising about 90% of all tumoral lesions in this region.Although some ependymomas are of a more anaplastic and malignant type, most of them are not anaplastic </s>


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


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


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