<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Palmoplantar keratoderma and can you explain it in depth? [/INST] Palmoplantar keratodermas are a heterogeneous group of disorders characterized by abnormal thickening of the stratum corneum of the palms and soles.
Autosomal recessive, dominant, X-linked, and acquired forms have all been described.: 505 : 211

Types
Clinically, three distinct patterns of palmoplantar keratoderma may be identified: diffuse, focal, and punctate.: 505

Diffuse
Diffuse palmoplantar keratoderma is a type of palmoplantar keratoderma that is characterized by an even, thick, symmetric hyperkeratosis over the whole of the palm and sole, usually evident at birth or in the first few months of life.: 505   Restated, diffuse palmoplantar keratoderma is an autosomal dominant disorder in which hyperkeratosis is confined to the palms and soles.  The two major types can have a similar clinical appearance:
Diffuse epidermolytic palmoplantar keratoderma (also known as "Palmoplantar keratoderma cum degeneratione granulosa Vörner," "Vörners epidermolytic palmoplantar keratoderma", and "Vörner keratoderma") is one of the most common patterns of palmoplantar keratoderma, an autosomal dominant condition that presents within the first few months of life, characterized by a well-demarcated, symmetric thickening of palms and soles, often with a "dirty" snakeskin appearance due to underlying epidermolysis.: 506
Diffuse nonepidermolytic palmoplantar keratoderma (also known as "Diffuse orthohyperkeratotic keratoderma," "Hereditary palmoplantar keratoderma," "Keratosis extremitatum progrediens," "Keratosis palmoplantaris diffusa circumscripta," "Tylosis," "Unna–Thost disease", and "Unna–Thost keratoderma") is inherited as an autosomal dominant condition and is present from infancy, characterized by a well-demarcated, symmetric, often "waxy" keratoderma involving the whole of the palms and soles.: 506–8 : 213

Focal
Focal palmoplantar keratoderma, a type of palmoplantar keratoderma in which large, compact masses of keratin develop at sites of recurrent friction, principally on the feet, although also on the palms and other sites, a pattern of calluses that may be discoid (nummular) or linear.

 Focal palmoplantar keratoderma with oral mucosal hyperkeratosis (also known as "Focal epidermolytic palmoplantar keratoderma," "Hereditary painful callosities," "Hereditary painful callosity syndrome," "Keratosis follicularis," "Keratosis palmoplantaris nummularis", and "Nummular epidermolytic palmoplantar keratoderma") is an autosomal dominant keratoderma that represents a clinical overlap syndrome with pachyonychia congenita type I but without the classic nail involvement.: 510

Punctate
Punctate palmoplantar keratoderma is a form of palmoplantar keratoderma in which many tiny "raindrop" keratoses involve the palmoplantar surface, skin lesions which may involve the whole of the palmoplantar surface, or may be more restricted in their distribution.: 505
Type 1: Keratosis punctata palmaris et plantaris (also known as "Autosomal-dominant hereditary punctate keratoderma associated with malignancy," "Buschke–Fischer–Brauer disease," "Davis Colley disease," "Keratoderma disseminatum palmaris et plantaris," "Keratosis papulosa," "Keratoderma punctatum," "Keratodermia punctata," "Keratoma hereditarium dissipatum palmare et plantare," "Palmar and plantar seed dermatoses," "Palmar keratoses," "Papulotranslucent acrokeratoderma," "Punctate keratoderma," "Punctate keratoses of the palms and soles," and "Maculosa disseminata") is a skin condition, an autosomal dominant palmoplantar keratoderma with variable penetrance, characterized clinically by multiple, tiny, punctate keratoses over the entire palmoplantar surfaces, beginning over the lateral edge of the digits.: 509 : 212–213  It has been linked to 15q22-q24.
Type 2: Spiny keratoderma (also known as "Porokeratosis punctata palmaris et plantaris," "Punctate keratoderma," and "Punctate porokeratosis of the palms and soles") is an autosomal dominant keratoderma of late onset that develops in patients aged 12 to 50, characterized by multiple tiny keratotic plugs, resembling the spines on a music box, involving the entire palmoplantar surfaces.: 509
Type 3: Focal acral hyperkeratosis (also known as "Acrokeratoelastoidosis lichenoides," and "Degenerative collagenous plaques of the hand") is a late-onset keratoderma, inherited as an autosomal dominant condition, characterized by oval or polygonal crateriform papules developing along the border of the hands, feet, and wrists.: 509  It is considered similar to Costa acrokeratoelastoidosis.

Ungrouped
Palmoplantar keratoderma and spastic paraplegia (also known as "Charcot–Marie–Tooth disease with palmoplantar keratoderma and nail dystrophy") is an autosomal dominant or x-linked dominant condition that begins in early childhood with thick focal keratoderma over the soles and, to a lesser extent, the palms.: 513
Palmoplantar keratoderma of Sybert (also known as "Greither palmoplantar keratoderma," "Greither syndrome," "Keratosis extremitatum hereditaria progrediens," "Keratosis palmoplantaris transgrediens et progrediens" "Sybert keratoderma," and "Transgrediens and progrediens palmoplantar keratoderma") is an extremely rare autosomal dominant keratoderma (a skin condition involving horn-like growths) with symmetric severe involvement of the whole palmoplantar surface in a glove-and-stocking distribution.: 509  It was characterized by Aloys Greither in 1952 </s>


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


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


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Focal and diffuse brain injury and can you explain it in depth? [/INST] Focal and diffuse brain injury are ways to classify brain injury: focal injury occurs in a specific location, while diffuse injury occurs over a more widespread area. It is common for both focal and diffuse damage to occur as a result of the same event; many traumatic brain injuries have aspects of both focal and diffuse injury. Focal injuries are commonly associated with an injury in which the head strikes or is struck by an object; diffuse injuries are more often found in acceleration/deceleration injuries, in which the head does not necessarily contact anything, but brain tissue is damaged because tissue types with varying densities accelerate at different rates.  In addition to physical trauma, other types of brain injury, such as stroke, can also produce focal and diffuse injuries. There may be primary and secondary brain injury processes.

Focal
A focal traumatic injury results from direct mechanical forces (such as occur when the head strikes a windshield in a vehicle accident) and is usually associated with brain tissue damage visible to the naked eye.  A common cause of focal injury is penetrating head injury, in which the skull is perforated, as frequently occurs in auto accidents, blows, and gunshot wounds </s>


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Non scarring hair loss and can you explain it in depth? [/INST] Non scarring hair loss, also known as noncicatricial alopecia is the loss of hair without any scarring being present. There is typically little inflammation and irritation, but hair loss is significant. This is in contrast to scarring hair loss during which hair follicles are replaced with scar tissue as a result of inflammation. Hair loss may be spread throughout the scalp (diffuse) or at certain spots (focal). The loss may be sudden or gradual with accompanying stress.
The most common cause is androgenetic alopecia, also known as male pattern or female pattern hair loss due to the effects of dihydrotestosterone (DHT) on the hair follicles. A variety of factors may lead to this condition such as hormonal effects, age, diet, autoimmunity, emotional stress, physical stress, drug effects, genetics, or infections.
Depending on the cause, treatment options include: topical minoxidil, oral finasteride, anti-fungal medications, steroids, hair transplantation, or platelet rich plasma (PRP) therapy. Alternatives for total hair loss include the use of hairpieces or hair fibers.

Signs and Symptoms
Patients will notice either focal or diffuse loss of hair. This may occur due to thinning or shedding of the hair over a sudden or gradual period of time. Stress may be present, and the emotional impact of hair loss is important as it may cause significant distress. Other signs may point to specific causes of the condition. Poor diet may lead to tiredness, other side effects of chemotherapy drugs may be seen, infection can cause itching, stress may lead to pulling of hair or falling of hair. Hair loss may be present in the family, highlighting genetic causes.

Causes
Causes of noncicatricial alopecia can be separated based on focal or diffuse hair loss:Diffuse:

Androgenetic alopecia: androgenic DHT leads to catagenic miniaturization of hair follicles.
Diffuse alopecia areata: diffuse autoimmune destruction of hair follicles
Alopecia totalis: unknown but thought to be autoimmune
Telogen effluvium: emotional or physiologic stress
Anagen effluvium: cancer treatments such as radiation and alkylating agents
Dermatopathia pigmentosa reticularis: genetic autosomal dominant conditionFocal:

Alopecia areata: autoimmune destruction of hair follicles
Tinea capitis: fungal infection
Traction alopecia: pulling force applied to hair
Trichotillomania (Trichotillosis)

Diagnosis
There are a number of conditions that may cause non scarring hair loss and the first step is to determine the pattern: focal or diffuse. The next step is to identify if the hair loss is scarring or non scarring. A history and physical examination is necessary as this will provide clues to the ultimate diagnosis. It is essential to ask about the onset, observed pattern, hairstyles, family history, diet, and social history.Diffuse:

Androgenetic alopecia: history of gradual thinning of hair and characteristic pattern. Males start to lose hair in the front and temples while females lose hair at the top of the head
Diffuse alopecia areata: exclamation point hairs
Alopecia totalis: concomitant loss of facial and skull hair
Telogen effluvium: history of emotional or physiologic stress
Anagen effluvium: history cancer treatments such as radiation and alkylating agents
Dermatopathia pigmentosa reticularis: genetic autosomal dominant conditionFocal:

Alopecia areata: smooth and round lesions
Tinea capitis: black dots with broken hair strands, may see red, scaly lesions and swollen lymph nodes on the back of head.
Traction alopecia: history of tight hairstyles and marginal hairline
Trichotillomania: history of pulling hair or evidence of traumatic folliclesPull Test
This test is performed to estimate the severity of hair loss and refine the differential diagnosis. A clinician grabs sections of hair and observes for active hair loss. A positive pull test is usually caused by telogen effluvium, androgenetic alopecia, and alopecia areata.Tug Test
A doctor holds the top and bottom of a strand of hair and observes for a break in the middle which may be caused by a hair shaft abnormality.Card Test
A part in the hair is created and a small card is placed to contrast the color of the hair and visualize thin strands of hair (seen in telogen effluvium) vs short broken strands (seen in hair shaft abnormalities).Fungal Culture
Scalp is scraped and the specimen is incubated for fungal growth commonly seen in tinea capitis.Scalp biopsy
If the diagnosis of hair loss is unclear or not responsive to the treatment, a scalp biopsy may be required. Scalp biopsy will show evidence of inflammation, location, and change in the follicles. This will frequently refine the diagnosis.Blood Tests
In the case of suspected iron deficiency, thyroid disease, or androgen excess a blood test may be necessary to rule in these causes.Trichoscopy
A new technique which allows for magnified visualization of the hair and scalp, providing a high definition, detailed look at follicles.

Treatment
Steroids
Steroids may be used for the short-term treatment of autoimmune causes of hair loss such as alopecia areata. Topical or oral preparations may be used for a few weeks to reduce inflammation. Long term use of topical steroids has not shown benefits for growth and the use of long term oral steroids has many risks that typically outweigh the benefits.Immunotherapy
Diphenylcyclopropenone or squaric acid may be used topically for the treatment of alopecia areata as an alternative to steroids. This treatment may cause a local skin reaction.Minoxidil
Minoxidil is a topical treatment that comes in a solution or foam. The foam provides increased delivery of the drug and less irritation. This drug has been shown to decrease telogen and increase anagen phase of hair follicles, increase VEGF expression, and have indirect vasodilation effects. FDA has approved this drug for use in androgenetic alopecia, but frequent offlabel uses include alopecia areata, chemotherapy induced alopecia, telogen effluvium, and traction alopecia.Redensyl
Redensyl is emerging as an alternative hair loss treatment containing a newly discovered molecule called dihydroquercetin-glucoside (DHQG), a compound derived from plant extracts known to target the stem cells in hair follicles and encourages the division of the cells. Still in development stage it has been approved by FDA as many of its medication are available widelyHormone modulating
Androgenetic alopecia is routinely treated with drugs that alter hormonal function, in particular DHTs effects. Male pattern hair loss is treated with oral finasteride which is a 5-alpha reductase inhibitor that blocks the formation of DHT from testosterone. Finasteride may cause sexual dysfunction, but it is typically reversed upon discontinuation of the treatment. Female pattern hair loss is treated with spironolactone or flutamide that block the effects of DHT receptors.Anti-fungal
Topical anti-fungal treatments such as ketoconazole and pyrithione zinc shampoo are sometimes effective for male pattern hair loss. Topical therapy is not usually effective for tinea capitis for which oral therapy with terbinafine, fluconazole, or griseofulvin is superior.PRP
Patients may benefit from injections of plasma into the scalp to promote the delivery of nutrients in the plasma to the hair follicles </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Chylothorax and can you explain it in depth? [/INST] A chylothorax is an abnormal accumulation of chyle, a type of lipid-rich lymph, in the space surrounding the lung.  The lymphatics of the digestive system normally returns lipids absorbed from the small bowel via the thoracic duct, which ascends behind the esophagus to drain into the left brachiocephalic vein.  If normal thoracic duct drainage is disrupted, either due to obstruction or rupture, chyle can leak and accumulate within the negative-pressured pleural space.  In people on a normal diet, this fluid collection can sometimes be identified by its turbid, milky white appearance, since chyle contains emulsified triglycerides.
Chylothorax is a rare but serious condition, as it signals leakage of the thoracic duct or one of its tributaries. There are many treatments, both surgical and conservative. About 2–3% of all fluid collections surrounding the lungs (pleural effusions) are chylothoraces.  It is important to distinguish a chylothorax from a pseudochylothorax (a pleural effusion that happens to be high in cholesterol), which has a similar appearance visually but is caused by more chronic inflammatory processes and requires a different treatment.

Signs and symptoms
The symptoms of a chylothorax depend its size and the underlying cause. A small chylothorax may not cause any symptoms and only be detected on a chest X-ray performed for another reason. A large chylothorax may lead to breathlessness or a feeling of pressure in the chest, caused by fluid restricting the expansion of the lungs, although large chylothoraces may remain asymptomatic if the chylothorax has accumulated slowly, as the lungs may have had time to become used to the pressure. Fever or chest pain are not usually associated with chylothorax, as chyle does not generate inflammation by itself.On examination, chylothorax may lead to reduced breath sounds on the affected side, associated with a dull sound when the chest is tapped or percussed. In cases of postoperative chylothorax, the first sign may be persistent drainage from intercostal drains.  Large chylothoraces may cause signs related to the loss of nutrients, including features of malnutrition or decreased ability to fight infections. Rapidly accumulating chylothoraces can cause a sudden drop in blood volume, leading to low blood pressure.

Causes
There are three main types of chylothorax: traumatic, non-traumatic, and idiopathic. Historically the most common form of chylothorax was non-traumatic, but traumatic chylothoraces now represent the majority of cases, with most arising as postoperative complications of surgery. The most common cause of non-traumatic chylothoraces is cancer. Chylothoraces can also be classified as low- or high-output based on the rate of chyle accumulation: low-output chylothoraces accumulate <500 mL of chyle per 24 hours, while high-output chylothoraces accumulate >1000 mL per 24 hours.

Non-traumatic
Malignancies are the most frequent cause of non-traumatic chylothorax. Cancers like chronic lymphocytic leukemia, lung cancer, lymphoma, Kaposi sarcoma, metastatic carcinoma or esophageal cancer are potential causes of chylothorax. Infectious causes are also observed, most often in developing countries. The most common cause of an infectious chylothorax is a complication of tuberculous lymphadenitis. Other possible causative infections include aortitis, histoplasmosis, and filariasis. Chylothorax can also be congenital, and may co-occur with other lymphatic malformations like lymphangiectasis and lymphangiomatosis. Other conditions like tuberous sclerosis, congenital heart disease, trisomy 21 (Down syndrome), Noonan syndrome, or Turner syndrome (missing X chromosome) are also possible causes of congenital chylothorax. Other, more rare causes of congenital chylothorax include Castlemans disease, yellow nail syndrome, Waldenströms macroglobulinemia, sarcoidosis, venous thrombosis, thoracic radiation, macroglobulinemia, amyloidosis, and a goiter. These diseases cause chylothorax by obstructing or destroying the thoracic duct. Also, parenteral nutrition has been a possible cause; a quick dose of total parenteral nutrition can overwhelm the thoracic duct, causing the chyle to leak into the surrounding pleural space.

Traumatic
Iatrogenic chylothorax after surgery is the most common variety of chylothorax. It is a common and serious complication of a pneumonectomy. It is especially common in surgeries requiring mediastinal dissection. The probability of chylothorax depends on the type of surgery. The surgery with the highest risk of chylothorax is an esophagostomy, with a 5-10% risk of chylothorax. Lung resection and mediastinal node dissection have the second highest risk, with 3-7% risk. Other operations like mediastinal tumor resection, thoracic aneurysm repair, sympathectomy, and any other surgeries that take place in the lower neck or the mediastinum can lead to chylothorax. Chylotharax after trauma but not after surgery has also been described after central line placement, pacemaker implantation, and embolization of a pulmonary arteriovenous malformation. Blunt trauma to the chest region is another cause of chylothorax, which has occurred after blast injuries and even simple injuries from coughing or sneezing.

Mechanism
The main mechanism of chylothorax is the leaking of chyle from the thoracic duct, usually caused by a disturbance affecting the structural integrity of the thoracic duct. For example, placement of a central venous catheter can potentially disrupt drainage of lymph into the subclavian veins, followed by the thoracic duct, resulting in chylothorax. The disturbances cause the pressure in the thoracic duct to increase. Soon, collateral channels form, which eventually drain into the thorax. Trauma affecting the thoracic duct is the most common disturbing mechanism.
Whether a chylothorax occurs in the left or right pleural space is a consequence of the thoracic ducts anatomic location in the body and depends on the level where the duct was injured. If the thoracic duct is injured above the fifth thoracic vertebra, then a left-sided chylothorax results. Conversely, a thoracic duct injury below that level will lead to the formation of a right-sided chylothorax. Chylothoraces most commonly occur in the right pleural space (50% of cases). Left-sided and bilateral chylothoraces are less common and occur in 33% and 17% of cases, respectively.In the case of cancer, invasion into the thoracic duct or collateral lymph channels can obstruct lymph. In the case of mediastinal lymphadenopathy, the enlarged lymph node causes compression of the lymphatic channels and thoracic duct. This impedes the centripetal drainage of the flow of lymph from the edges of the lung parenchyma and pleural surfaces. This causes the chyle to ooze extensively into the pleural cavity, leading to a chylothorax. In the case of yellow nail syndrome, or lymphedema, chylothorax is caused by hypoplasia or dilation of the lymph vessels. In rare cases, like in hepatic chylothorax, chylous ascites crosses the diaphragm into the pleural cavity.  In idiopathic cases like genetic disorders, the mechanism is not known. Up to three liters of chyle can easily drain into the pleural space daily.

Diagnosis
Chest X-rays can detect a chylothorax. It appears as a dense, homogeneous area that obscures the costophrenic and cardiophrenic angles. Ultrasounds can also detect a chylothorax, which appears as an echoic region that is isodense with no septation or loculation. However, neither a normal chest x-ray nor an ultrasound can differentiate a chylothorax from any other type of pleural effusion.

The cisterna chyli can be found in a thoracic MRI, making it possible to confirm chylothorax. However, MRI is not the ideal method to scan the thorax, and so it is rarely used. Another diagnostic technique is conventional lymphangiography. It is rarely used since there are equally sensitive yet less invasive techniques available to identify a chylothorax. Lymphangiography procedures use the contrast dye agent lipiodol, which is injected into the lymphatic vessels. The chylothorax shows up on the images and identifies the source any leak in the thoracic duct.Another, more commonly used type of lymphogram is nuclear lymphoscintigraphy; this procedure requires human pentetic acid labeled Tc99m to be injected into the subcutaneous lesions of both sides of the dorsum of the foot. Then two images, anterior and posterior, are obtained using gamma-ray cameras. This test can be used with an integrated low-dose CT-scan with photon emission to get images that are more precise. Once pleural effusion is detected, a thoracentesis is recommended.The fluid of a chylothorax may appear milky, serous or serosanguineous. If the appearance of the fluid is not milky, that does not exclude a chylothorax from consideration. Since chyle is rich in triglycerides, a pleural effusion that is rich in triglycerides (>110 mg/dL) confirms the presence of a chylothorax; a pleural effusion that is low in triglyceride content (<50 mg/dL) virtually excludes the diagnosis. If a pleural effusion contains triglycerides between 50 and 110 mg/dL, analysis of the lipoprotein content of the pleural effusion to evaluate for chylomicrons is recommended. If that procedure detects chylomicrons in the fluid, that confirms a chylothorax. Chylothoraces are typically exudative and often contain a high number of lymphocytes and have low levels of the enzyme lactate dehydrogenase (LDH). However, atypical chylothoraces can occur and are transudative in 14% of cases. A milky appearance of pleural fluid is insufficient to confirm the diagnosis of chylothorax as pseudochylothoraces and empyemas can mimic this appearance. Conversely, the absence of a milky appearance does not mean a chylothorax is not present as they may instead appear serous or bloody.

Treatment
The treatment for chylothorax depends on the underlying cause but may include dietary modification, medication to prevent chyle formation including somatostatin/octreotide, midodrine and sirolimus, pleurodesis, and surgical treatment including ligation of the thoracic duct, pleurovenous or pleuroperitoneal shunting or thoracic duct embolization.

Initial
The initial treatment of a chylothorax is usually drainage of the fluid from the pleural space. This may be necessary to restore lung function compromised by the pressure exerted by the chyle on the lungs. Those with large chylothoraces may need nutritional support due to the nutrients lost, primarily to correct protein and electrolyte losses. Once the affected person is hemodynamically and nutritionally stable, then specific treatment can begin.

Conservative
A conservative treatment is changing diet to include fewer long-chain fatty acids, in particular free fatty acids. Since chyle is formed from these acids, chyle formation will reduce, allowing the defects to heal spontaneously. However, this can lead to fat deficiency and malnutrition over time. A possible response to this drawback is a venous fat hemorrhage, in which small and medium-chain fatty acids are given by diet, and long-chain fatty acids are given intravenously. Thoracentesis and an indwelling catheter for use at home is generally used to drain the chylothorax. If a malignant neoplastic chylothorax is present, then treatment with radiotherapy and/or chemotherapy is warranted.

Surgical
Surgery is indicated if the case is post-traumatic, iatrogenic, or refractory to other treatments, in which cases surgery reduces mortality by 40%. One invasive surgical intervention called a thoracic duct ligation involves closing off the thoracic ducts. Surgical pleurodesis is another option and can be undertaken if the affected person fails to respond to conservative treatment and is not a candidate for surgical intervention.Another treatment option is pleuroperitoneal shunting (creating a communication channel between the pleural space and peritoneal cavity). Since surgery to close the leak is not reliable, talc pleurodesis is recommended; in a case study of 19 people with refractory malignant chylothorax due to lymphoma, it resulted in success for all affected individuals. Chemical pleurodesis is an option, since the leaking of lymphatic fluids is stopped by irritating the lungs and chest wall, resulting in a sterile inflammation. This causes the lung and the chest wall to fuse together, thus preventing lymphatic fluids from leaking into the pleural space.

Prognosis
The morbidity and mortality rates associated with chylothorax have declined as treatments have improved. Malignant, bilateral, and chronic chylothoraces have an inferior prognosis to other types. Currently, the mortality and morbidity rates are about 10% if treated surgically. If cases are post-operative and treated conservatively, mortality rates approach 50%.

Complications
Complications of chylothorax include malnutrition, immunosuppression, dehydration, and respiratory distress. The severity of the complications depends on how quickly the chylothorax accumulated, its size, and its chronicity.

Epidemiology
Chylothoraces are rare and usually occur as a complication of surgeries in the neck and mediastinum </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hydroa vacciniforme and can you explain it in depth? [/INST] Hydroa vacciniforme (HV) is a very rare, chronic photodermatitis-type skin condition with usual onset in childhood. It was first described in 1862 by Bazin. It is sometimes called "Bazins hydroa vacciniforme". A study published in Scotland in 2000 reviewed the cases of 17 patients and estimated a prevalence of 0.34 cases per 100,000 population.  In this study they reported an average age of onset of 7.9 years. Frequently the rash first appeared in the spring or summer months and involved sun-exposed skin.  The rash starts as a vesicular eruption, later becoming umbilicated, and resulted in vacciniform scarring </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Afterimage and can you explain it in depth? [/INST] An afterimage is an image that continues to appear in the eyes after a period of exposure to the original image. An afterimage may be a normal phenomenon (physiological afterimage) or may be pathological (palinopsia). Illusory palinopsia may be a pathological exaggeration of physiological afterimages. Afterimages occur because photochemical activity in the retina continues even when the eyes are no longer experiencing the original stimulus.The remainder of this article refers to physiological afterimages. A common physiological afterimage is the dim area that seems to float before ones eyes after briefly looking into a light source, such as a camera flash. Palinopsia  is a common symptom of visual snow.

Negative afterimages
Negative afterimages are caused when the eyes photoreceptors, primarily known as rods and cones, adapt to overstimulation and lose sensitivity. Newer evidence suggests there is cortical contribution as well. Normally, the overstimulating image is moved to a fresh area of the retina with small eye movements known as microsaccades. However, if the image is large or the eye remains too steady, these small movements are not enough to keep the image constantly moving to fresh parts of the retina. The photoreceptors that are constantly exposed to the same stimulus will eventually exhaust their supply of photopigment, resulting in a decrease in signal to the brain. This phenomenon can be seen when moving from a bright environment to a dim one, like walking indoors on a bright snowy day. These effects are accompanied by neural adaptations in the occipital lobe of the brain that function similar to color balance adjustments in photography. These adaptations attempt to keep vision consistent in dynamic lighting. Viewing a uniform background while these adaptations are still occurring will allow an individual to see the afterimage because localized areas of vision are still being processed by the brain using adaptations that are no longer needed.
The Young-Helmholtz trichromatic theory of color vision postulated that there were three types of photoreceptors in the eye, each sensitive to a particular range of visible light: short-wavelength cones, medium-wavelength cones, and long-wavelength cones. Trichromatic theory, however, can not explain all afterimage phenomena. Specifically, afterimages are the complementary hue of the adapting stimulus, and trichromatic theory fails to account for this fact.The failure of trichromatic theory to account for afterimages indicates the need for an opponent-process theory such as that articulated by Ewald Hering (1878) and further developed by Hurvich and Jameson (1957). The opponent process theory states that the human visual system interprets color information by processing signals from cones and rods in an antagonistic manner. The opponent color theory suggests that there are three opponent channels: red versus green, blue versus yellow, and black versus white. Responses to one color of an opponent channel are antagonistic to those of the other color. Therefore, a green image will produce a magenta afterimage. The green color fatigues the green photoreceptors, so they produce a weaker signal. Anything resulting in less green, is interpreted as its paired primary color, which is magenta, i.e. an equal mixture of red and blue.Example video which produces a distorted illusion after one watches it and looks away. See motion aftereffect.

Positive afterimages
Positive afterimages, by contrast, appear the same color as the original image. They are often very brief, lasting less than half a second. The cause of positive afterimages is not well known, but possibly reflects persisting activity in the brain when the retinal photoreceptor cells continue to send neural impulses to the occipital lobe.A stimulus which elicits a positive image will usually trigger a negative afterimage quickly via the adaptation process. To experience this phenomenon, one can look at a bright source of light and then look away to a dark area, such as by closing the eyes. At first one should see a fading positive afterimage, likely followed by a negative afterimage that may last for much longer </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Granulomatous mastitis and can you explain it in depth? [/INST] Granulomatous mastitis can be divided into idiopathic granulomatous mastitis (also known as granular lobular mastitis) and granulomatous mastitis occurring as a rare secondary complication of a great variety of other conditions such as tuberculosis and other infections, sarcoidosis and granulomatosis with polyangiitis. Special forms of granulomatous mastitis occur as complication of diabetes. Some cases are due to silicone injection (Silicone-induced granulomatous inflammation) or other foreign body reactions.Idiopathic granulomatous mastitis (IGM) is defined as granulomatous mastitis without any other attributable cause such as those above mentioned. It occurs on average two years and almost exclusively up to six years after pregnancy, usual age range is 17 to 42 years. Some cases have been reported that were related to drug induced hyperprolactinemia. Exceptionally rarely it has been diagnosed during pregnancy and in men.Primary presentation of any of these conditions as mastitis is very rare and in many cases probably predisposed by other breast or systemic conditions. Although granulomatous mastitis is easily confused with cancer it is a completely benign (non-cancerous) condition. Treatment is radically different for idiopathic granulomatous mastitis and other granulomatous lesions of the breast, so the precise diagnosis is therefore very important.

Symptoms
Patients mostly present with a hard lump in one breast without any sign of a systemic disease. Other possible symptoms include nipple retraction, pain, inflammation of the overlying skin, nipple discharge, fistula, enlarged lymph nodes, in rare case peau dorange-like changes. Presentation is mostly unilateral although a significant share of cases is bilateral, also in many cases contralateral or bilateral recurrences were documented. Several cases occurring together with fever, polyarthralgia and erythema nodosum were documented.

Diagnosis
Characteristic for idiopathic granulomatous mastitis are multinucleated giant cells and epithelioid histiocytes forming non-caseating granulomas around lobules. Often minor ductal and periductal inflammation is present. The lesion is in some cases very difficult to distinguish from breast cancer and other causes such as infections (tuberculosis, syphilis, corynebacterial infection, mycotic infection), autoimmune diseases (sarcoidosis, granulomatosis with polyangiitis), foreign body reaction and granulomatous reaction in a carcinoma must be excluded.The condition is diagnosed very rarely. As the diagnosis is a lengthy differential diagnosis of exclusion there is considerable uncertainty about incidence. It has been suspected that some cases diagnosed as IGM in developing countries may have other explanations. On the other hand, IGM is usually diagnosed only after complications and referral to a secondary breast care center so light cases may resolve spontaneously or after symptomatic treatment and thus never be diagnosed as IGM. As a completely pathogen free breast will be exceedingly rare even in completely healthy population there is also uncertainty when to consider pathogens as causative or as mere coincidental finding.

Causes of idiopathic granulomatous mastitis
Causes are not known. The histology is suggestive of an autoimmune reaction. The high rate of relapses as well as relatively high proportion of bilateral cases is highly suggestive of a systemic predisposition. Presently most evidence points towards an important role of elevated prolactin levels or overt hyperprolactinemia with additional triggers such as local trauma or irritation. Alpha 1-antitrypsin deficiency was documented in one case, interferon-alpha therapy in another case. Similar cases of granulomatous mastitis were reported in IgG4-related disease though the exact relationship to IGM remains to be elucidated. Other contributing factors of IGM were investigated such as oral contraceptives usage. Many cases were reported after use of prolactin elevating medications such as antipsychotics.Elevated prolactin levels have the direct effects of increasing secretory activity of breast lobules, maintaining tight junctions of the ductal epithelium, preventing involution of the breast gland after weaning and are known to stimulate the immune system, contributing to both physiological and pathological granulomatous lesions and non-caseating granulomas. PRL is also secreted locally in the breast and local secretion by lymphocytes may be enhanced during inflammatory reactions.
Autoimmune reaction to extravasated fat and protein rich luminal fluid (denaturized milk) resulting from the secretory activity is assumed to be one of the triggers of IGM. Several other hormones can contribute to PRL signaling in the breast gland, high levels of insulin caused for example by peripheral insulin resistance (resulting from pregnancy, gestational diabetes or developing diabetes mellitus type 2) will enhance the galactogenic and antiapoptotic effects of PRL and growth hormone by acting synergistically with IGF-1.

Microbiology
The presence of Corynebacterium in granulomatous mastitis was first reported in 1996. Since then multiple reports have confirmed the presence of this genus in granulomatous mastitis. The most commonly isolated species is Corynebacterium kroppenstedtii </s>


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


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Heart valve dysplasia and can you explain it in depth? [/INST] Heart valve dysplasia is a congenital heart defect which affects the aortic, pulmonary, mitral, and tricuspid heart valves.  Dysplasia of the mitral and tricuspid valves can cause leakage of blood or stenosis.Dysplasia of the mitral and tricuspid valves - also known as the atrioventricular (AV) valves - can appear as thickened, shortened, or notched valves.  The chordae tendinae can be fused or thickened.  The papillary muscles can be enlarged or atrophied </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Uveitis and can you explain it in depth? [/INST] Uveitis () is the inflammation of the uvea, the pigmented layer that lies between the inner retina and the outer fibrous layer composed of the sclera and cornea. The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary body, and choroid. Uveitis is described anatomically, by the part of the eye affected, as anterior, intermediate or posterior, from front to back. In the panuveitic form, all parts are involved. The most common form is the anterior one. Symptoms include pain, floaters and blurred vision, and clinical examination may show redness and an irregular pupil, while ophthalmic examination shows dilated ciliary blood vessels and the presence of cells in the anterior chamber. Uveitis may arise spontaneously and associated with some genetic factors, or be associated with a wide range of conditions including autoimmune disease and infections. While the eye is a relatively protected environment, its immune mechanisms may be overcome resulting in inflammation and tissue destruction associated with T-cell activation. The incidence is approximately 1:4500, most commonly between the ages of 20–60.
Uveitis is an ophthalmic emergency and requires a thorough examination by an ophthalmologist or optometrist, including dilation of the pupil to allow better visualisation. Urgent treatment is required to control the inflammation. Further procedures may be required to identify any underlying disease. Treatment usually involves the use of steroids, most commonly as eye drops. Any underlying disease, for instance herpes zoster (shingles) will also require treatment. While initial treatment is usually successful, complications include other ocular disorders, such as uveitic glaucoma, retinal detachment, optic nerve damage, cataracts, and in some cases, a permanent loss of vision. In the United States uveitis accounts for about 10%-20% of cases of blindness.

Signs and symptoms
The signs and symptoms of uveitis include the following;

Anterior uveitis (Iritis)
Pain in the eye(s)
Redness of the eye(s)
Blurred vision
Photophobia
Irregular pupil
Signs of anterior uveitis include dilated ciliary vessels, presence of cells and flare in the anterior chamber, and keratic precipitates ("KP") on the posterior surface of the cornea. In severe inflammation there may be evidence of a hypopyon. Old episodes of uveitis are identified by pigment deposits on lens, KPs, and festooned pupil on dilation of pupil.
Busacca nodules, inflammatory nodules located on the surface of the iris in granulomatous forms of anterior uveitis such as Fuchs heterochromic iridocyclitis (FHI).
Synechia

Intermediate uveitis
Most common:

Floaters, which are dark spots that float in the visual field
Blurred visionIntermediate uveitis usually affects one eye. Less common is the presence of pain and photophobia.

Posterior uveitis
Inflammation in the back of the eye is commonly characterized by:

Floaters
Blurred vision

Causes
Uveitis is usually an isolated illness, but can be associated with many other medical conditions. In anterior uveitis, no associated condition or syndrome is found in approximately one-half of cases. However, anterior uveitis is often one of the syndromes associated with HLA-B27. Presence of this type of HLA allele has a relative risk of evolving this disease by approximately 15%.The most common form of uveitis is acute anterior uveitis (AAU). It is most commonly associated with HLA-B27, which has important features: HLA-B27 AAU can be associated with ocular inflammation alone or in association with systemic disease. HLA-B27 AAU has characteristic clinical features including male preponderance, unilateral alternating acute onset, a non-granulomatous appearance, and frequent recurrences, whereas HLA-B27 negative AAU has an equivalent male to female onset, bilateral chronic course, and more frequent granulomatous appearance. Rheumatoid arthritis is not uncommon in Asian countries as a significant association of uveitis.

Noninfectious or autoimmune causes
Sympathetic ophthalmia
Behçet disease
Crohns disease
Fuchs heterochromic iridocyclitis
Granulomatosis with polyangiitis
HLA-B27 related uveitis
Spondyloarthritis (especially seen in ankylosing spondylitis)
Juvenile idiopathic arthritis
Sarcoidosis
Tubulointerstitial nephritis and uveitis syndrome

Infectious causes
Uveitis may be an immune response to fight an infection inside the eye. While representing the minority of patients with uveitis, such possible infections include:

brucellosis
herpesviruses (herpes zoster ophthalmicus - shingles of the eye)
leptospirosis
Lyme disease
presumed ocular histoplasmosis syndrome
syphilis
toxocariasis
toxoplasmic chorioretinitis
tuberculosis
Zika fever

Associated with systemic diseases
Systemic disorders that can be associated with uveitis include:
Enthesitis
Ankylosing spondylitis
Juvenile rheumatoid arthritis
psoriatic arthritis
reactive arthritis
Behçets disease
inflammatory bowel disease
Whipples disease
systemic lupus erythematosus
polyarteritis nodosa
Kawasakis disease
chronic granulomatous disease
sarcoidosis
multiple sclerosis
Vogt–Koyanagi–Harada disease

Drug related side effects
Rifabutin, a derivative of Rifampin, has been shown to cause uveitis.
Several reports suggest the use of quinolones, especially Moxifloxacin, may lead to uveitis.

White Dot syndromes
Occasionally, uveitis is not associated with a systemic condition: the inflammation is confined to the eye and has unknown cause. In some of these cases, the presentation in the eye is characteristic of a described syndrome, which are called white dot syndromes, and include the following diagnoses:

acute posterior multifocal placoid pigment epitheliopathy
birdshot chorioretinopathy
multifocal choroiditis and panuveitis
multiple evanescent white dot syndrome
punctate inner choroiditis
serpiginous choroiditis
acute zonal occult outer retinopathy

Masquerade syndromes
Masquerade syndromes are those conditions that include the presence of intraocular cells but are not due to immune-mediated uveitis entities. These may be divided into neoplastic and non-neoplastic conditions.

Non-neoplastic:retinitis pigmentosa
intraocular foreign body
juvenile xanthogranuloma
retinal detachmentNeoplastic:retinoblastoma
lymphoma
malignant melanoma
leukemia
reticulum cell sarcoma

Pathophysiology
Immunologic factors
Onset of uveitis can broadly be described as a failure of the ocular immune system and the disease results from inflammation and tissue destruction. Uveitis is driven by the Th17 T cell sub-population that bear T-cell receptors specific for proteins found in the eye. These are often not deleted centrally whether due to ocular antigen not being presented in the thymus (therefore not negatively selected) or a state of anergy is induced to prevent self targeting.Autoreactive T cells must normally be held in check by the suppressive environment produced by microglia and dendritic cells in the eye. These cells produce large amounts of TGF beta and other suppressive cytokines, including IL-10, to prevent damage to the eye by reducing inflammation and causing T cells to differentiate to inducible T reg cells. Innate immune stimulation by bacteria and cellular stress is normally suppressed by myeloid suppression while inducible Treg cells prevent activation and clonal expansion of the autoreactive Th1 and Th17 cells that possess potential to cause damage to the eye.
Whether through infection or other causes, this balance can be upset and autoreactive T cells allowed to proliferate and migrate to the eye. Upon entry to the eye, these cells may be returned to an inducible Treg state by the presence of IL-10 and TGF-beta from microglia. Failure of this mechanism leads to neutrophil and other leukocyte recruitment from the peripheral blood through IL-17 secretion. Tissue destruction is mediated by non-specific macrophage activation and the resulting cytokine cascades. Serum TNF-α is significantly elevated in cases while IL-6 and IL-8 are present in significantly higher quantities in the aqueous humour in patients with both quiescent and active uveitis. These are inflammatory markers that non-specifically activate local macrophages causing tissue damage.

Genetic factors
The cause of non-infectious uveitis is unknown but there are some strong genetic factors that predispose disease onset including HLA-B27 and the PTPN22 genotype.

Infectious agents
Recent evidence has pointed to reactivation of herpes simplex, varicella zoster and other viruses as important causes of developing what was previously described as idiopathic anterior uveitis. Bacterial infection is another significant contributing factor in developing uveitis.

Diagnosis
Diagnosis includes dilated fundus examination to rule out posterior uveitis, which presents with white spots across the retina along with retinitis and vasculitis.
Laboratory testing is usually used to diagnose specific underlying diseases, including rheumatologic tests (e.g. antinuclear antibody, rheumatoid factor) and serology for infectious diseases (Syphilis, Toxoplasmosis, Tuberculosis).
Major histocompatibility antigen testing may be performed to investigate genetic susceptibility to uveitis. The most common antigens include HLA-B27, HLA-A29 (in birdshot chorioretinopathy) and HLA-B51 (in Behçet disease).Radiology X-ray may be used to show coexisting arthritis and chest X-ray may be helpful in sarcoidosis.

Classification
Uveitis is classified anatomically into anterior, intermediate, posterior, and panuveitic forms—based on the part of the eye primarily affected. Prior to the twentieth century, uveitis was typically referred to in English as "ophthalmia."
Anterior uveitis includes iridocyclitis and iritis.  Iritis is the inflammation of the anterior chamber and iris.  Iridocyclitis is inflammation of the iris and ciliary body with inflammation predominantly confined to ciliary body.  Anywhere from two-thirds to 90% of uveitis cases are anterior in location (iritis).  This condition can occur as a single episode and subside with proper treatment or may take on a recurrent or chronic nature.
Intermediate uveitis, also known as pars planitis, consists of vitritis—which is inflammation of cells in the vitreous cavity, sometimes with snowbanking, or deposition of inflammatory material on the pars plana </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Secondary hypertension and can you explain it in depth? [/INST] Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which by definition is caused by an identifiable underlying primary cause. It is much less common than the other type, called essential hypertension, affecting only 5-10% of hypertensive patients. It has many different causes including endocrine diseases, kidney diseases, and tumors. It also can be a side effect of many medications.

Types
Kidney
Renovascular hypertension
It has two main causes: fibromuscular dysplasia and atherosclerosis of the renal artery resulting in stenosis.
See main article at Renovascular hypertension.

Kidney
Other well known causes include diseases of the kidney. This includes diseases such as polycystic kidney disease which is a cystic genetic disorder of the kidneys, PKD, which is characterized by the presence of multiple cysts (hence, "polycystic") in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain.
It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, chronic kidney disease and kidney pain. Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin–angiotensin system.Also, some renal tumors can cause hypertension.  The differential diagnosis of a renal tumor in a young patient with hypertension includes Juxtaglomerular cell tumor, Wilms tumor, and renal cell carcinoma, all of which may produce renin.

Hypertension secondary to other renal disorders
Chronic kidney disease
Kidney disease / renal artery stenosis –  the normal physiological response to low blood pressure in the renal arteries is to increase cardiac output (CO) to maintain the pressure needed for glomerular filtration.Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated.
Renal segmental hypoplasia (Ask-Upmark kidney)

Hypertension secondary to endocrine disorders
Neurogenic hypertension – excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from chronic high activity of the sympathoadrenal system, the sympathetic nervous system and the adrenal gland. The specific mechanism involved is increased release of the "stress hormones", epinephrine (adrenaline) and norepinephrine which increase blood output from the heart and constrict arteries. People with neurogenic hypertension respond poorly to treatment with diuretics as the underlying cause of their hypertension is not addressed.Pheochromocytoma – a tumor which results in an excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction
Hyperaldosteronism (Conns syndrome)   – idiopathic hyperaldosteronism, liddles syndrome (also called pseudoaldosteronism), glucocorticoid remediable aldosteronism
Cushings syndrome – an excessive secretion of glucocorticoids causes the hypertension
Hyperparathyroidism
Acromegaly
Hyperthyroidism
Hypothyroidism

Adrenal
A variety of adrenal cortical abnormalities can cause hypertension, In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.Congenital adrenal hyperplasia, a group of autosomal recessive disorders of the enzymes responsible for steroid hormone production, can lead to secondary hypertension by creating atypically high levels of mineralocorticoid steroid hormones.  These mineralocorticoids cross-react with the aldosterone receptor, activating it and raising blood pressure.
17 alpha-hydroxylase deficiency causes an inability to produce cortisol.  Instead, extremely high levels of the precursor hormone corticosterone are produced, some of which is converted to 11-Deoxycorticosterone (DOC), a potent mineralocorticoid not normally clinically important in humans.  DOC has blood-pressure raising effects similar to aldosterone, and abnormally high levels result in hypokalemic hypertension.
11β-hydroxylase deficiency, aka apparent mineralocorticoid excess syndrome, involves a defect in the gene for 11β-hydroxysteroid dehydrogenase, an enzyme that normally inactivates circulating cortisol to the less-active metabolite cortisone.   At high concentrations cortisol can cross-react and activate the mineralocorticoid receptor, leading to aldosterone-like effects in the kidney, causing hypertension. This effect can also be produced by prolonged ingestion of liquorice (which can be of potent strength in liquorice candy), by causing inhibition of the 11β-hydroxysteroid dehydrogenase enzyme and likewise leading to secondary apparent mineralocorticoid excess syndrome. Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present. Cortisol induced hypertension cannot be completely explained by the activity of Cortisol on Aldosterone receptors. Experiments show that treatment with Spironolactone (an inhibitor of the aldosterone receptor), does not prevent hypertension with excess cortisol. It seems that inhibition of nitric oxide synthesis may also play a role in cortisol induced hypertension.Yet another related disorder causing hypertension is glucocorticoid remediable aldosteronism, which is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not. GRA appears to be the most common monogenic form of human hypertension.Compare these effects to those seen in Conns disease, an adrenocortical tumor which causes excess release of aldosterone, that leads to hypertension.Another adrenal related cause is Cushings syndrome which is a disorder caused by high levels of cortisol. Cortisol is a hormone secreted by the cortex of the adrenal glands. Cushings syndrome can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH). More than 80% of patients with Cushings syndrome develop hypertension., which is accompanied by distinct symptoms of the syndrome, such as central obesity, lipodystrophy, moon face, sweating, hirsutism and anxiety.Neuroendocrine tumors are also a well known cause of secondary hypertension. Pheochromocytoma (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).

Other secondary hypertension
Hormonal contraceptives
Neurologic disorders
Obstructive sleep apnea
Liquorice (when consumed in excessive amounts)
Scleroderma
Neurofibromatosis
Pregnancy: unclear cause.
Cancers: tumours in the kidney can operate in the same way as kidney disease. More commonly, however, tumors cause inessential hypertension by ectopic secretion of hormones involved in normal physiological control of blood pressure.
Drugs: In particular, alcohol, nasal decongestants with adrenergic effects, NSAIDs, MAOIs, adrenoceptor stimulants, and combined methods of hormonal contraception (those containing ethinylestradiol) can cause hypertension while in use.
Heavy alcohol use
Steroid use
Nicotine use.
Malformed aorta, slow pulse, ischemia: these cause reduced blood flow to the renal arteries, with physiological responses as already outlined.
Coarctation of the aorta
Atherosclerosis
Anemia: unclear cause.
Fever: unclear cause.
White coat hypertension, that is, elevated blood pressure in a clinical setting but not in other settings, probably due to the anxiety some people experience during a clinic visit.
Perioperative hypertension is development of hypertension just before, during or after surgery. It may occur before surgery during the induction of anesthesia; intraoperatively e.g. by pain-induced sympathetic nervous system stimulation; in the early postanesthesia period, e.g. by pain-induced sympathetic stimulation, hypothermia, hypoxia, or hypervolemia from excessive intraoperative fluid therapy; and in the 24 to 48 hours after the postoperative period as fluid is mobilized from the extravascular space </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Vibration white finger and can you explain it in depth? [/INST] Vibration white finger (VWF), also known as hand-arm vibration syndrome (HAVS) or dead finger, is a secondary form of Raynauds syndrome, an industrial injury triggered by continuous use of vibrating hand-held machinery. Use of the term vibration white finger has generally been superseded in professional usage by broader concept of HAVS, although it is still used by the general public. The symptoms of vibration white finger are the vascular component of HAVS.
HAVS is a widespread recognized industrial disease affecting tens of thousands of workers. It is a disorder that affects the blood vessels, nerves, muscles, and joints of the hand, wrist, and arm. Its best known effect is vibration-induced white finger (VWF), a term introduced by the Industrial Injury Advisory Council in 1970. Injury can occur at frequencies between 5 and 2000 Hz but the greatest risk for fingers is between 50 and 300 Hz. The total risk exposure for hand and arm is calculated by the use of ISO 5349-1, which stipulates maximum damage between 8 and 16 Hz and a rapidly declining risk at higher frequencies. The ISO 5349-1 frequency risk assessment has been criticized as corresponding poorly to observational data; more recent research suggests that medium and high frequency vibrations also increase HAVS risk.

Effects
Excessive exposure to hand arm vibrations can result in various patterns of diseases casually known as HAVS or VWF. This can affect nerves, joints, muscles, blood vessels or connective tissues of the hand and forearm:
Tingling whiteness or numbness in the fingers (blood vessels and nerves affected): This may not be noticeable at the end of a working day, and in mild cases may affect only the tips of the fingers. As the condition becomes more severe, the whole finger down to the knuckles may become white. Feeling may also be lost.
Fingers change colour (blood vessels affected): With continued exposure the person may experience periodic attacks in which the fingers change colour when exposed to the cold. Initially the fingers rapidly become pale and feeling is lost. This phase is followed by an intense red flush (sometimes preceded by a dusky bluish phase) signalling the return of blood circulation to the fingers and is usually accompanied by uncomfortable throbbing.
Loss of manual dexterity (nerves and muscles affected): In more severe forms, attacks may occur frequently in cold weather, not only at work, but during leisure activities, such as gardening, car washing or even watching outdoor sports and may last up to an hour causing considerable pain and loss of manual dexterity and reduced grip strength.In extreme cases, the affected person may lose fingers. The effects are cumulative. When symptoms first appear, they may disappear after a short time. If exposure to vibration continues over months or years, the symptoms can worsen and become permanent.

Prevention
The Control of Vibration at Work Regulations 2005, created under the Health and Safety at Work etc. Act 1974.  is the legislation in the UK that governs exposure to vibration and assists with preventing HAVS occurring.
Good practice in industrial health and safety management requires that worker vibration exposure is assessed in terms of acceleration, amplitude, and duration. Using a tool that vibrates slightly for a long time can be as damaging as using a heavily vibrating tool for a short time. The duration of use of the tool is measured as trigger time, the period when the worker actually has their finger on the trigger to make the tool run, and is typically quoted in hours per day. Vibration amplitude is quoted in metres per second squared, and is measured by an accelerometer on the tool or given by the manufacturer. Amplitudes can vary significantly with tool design, condition and style of use, even for the same type of tool.In the UK, Health and Safety Executive gives the example of a hammer drill which can vary from 6 m/s² to 25 m/s². HSE publishes a list of typically observed vibration levels for various tools, and graphs of how long each day a worker can be exposed to particular vibration levels. This makes managing the risk relatively straightforward. Tools are given an Exposure Action Value (EAV, the time which a tool can be used before action needs to be taken to reduce vibration exposure) and an Exposure Limit Value (ELV, the time after which a tool may not be used).In the United States, the National Institute for Occupational Safety and Health published a similar database where values for sound power and vibrations for commonly found tools from large commercial vendors in the United States were surveyed. Further testing is underway for more and newer tools.The effect of legislation in various countries on worker vibration limits has been to oblige equipment providers to develop better-designed, better-maintained tools, and for employers to train workers appropriately. It also drives tool designers to innovate to reduce vibration. Some examples are the  easily manipulated mechanical arm (EMMA) and the suspension mechanism designed into chainsaws.

Anti-vibration gloves
Anti vibration gloves are traditionally made with a thick and soft palm material to insulate from the vibrations. The protection is highly dependent on frequency range; most gloves provide no protection in palm and wrist below ~50 Hz and in fingers below ~400 Hz. Factors such as high grip force, cold hands or vibration forces in shear direction can have a reducing effect and or increase damage to the hands and arms.  Gloves do help to keep hands warm but to get the desired effect, the frequency output from the tool must match the properties of the vibration glove that is selected. Anti-vibration gloves in many cases amplify the vibrations at frequencies lower than those mentioned in the text above.

Reactive monitoring
A simpler system, known as re-active monitoring, may be used by, for example, monitoring rates of usage of consumable items </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Cerebellar stroke syndrome and can you explain it in depth? [/INST] Cerebellar stroke syndrome is a condition in which the circulation to the cerebellum is impaired due to a lesion of the superior cerebellar artery, anterior inferior cerebellar artery or the posterior inferior cerebellar artery.Cardinal signs include vertigo, headache, vomiting, and ataxia.

Cerebellar strokes account for only 2-3% of the 600,000 strokes that occur each year in the United States. They are far less common than strokes which occur in the cerebral hemispheres. In recent years mortality rates have decreased due to advancements in health care which include earlier diagnosis through MRI and CT scanning. Advancements have also been made which allow earlier management for common complications of cerebellar stroke such as brainstem compression and hydrocephalus.Research is still needed in the area of cerebellar stroke management; however, several factors may lead to poor outcomes in individuals who have a cerebellar stroke. These factors include:

Declining levels of consciousness
New signs of brainstem involvement
Progressing Hydrocephalus
Stroke to the midline of the cerebellum (a.k.a. the vermis)

References
Further reading
Macdonell, R.A.; Kalnins, R.M.; Donnan, G.A. (1987). "Cerebellar infarction: Natural history, prognosis, and pathology". Stroke. 18 (5): 849–55. doi:10.1161/01.STR.18.5.849. PMID 3629642.
Edlow, J.A.; Newman-Toker, D.E.; Savitz, S.I. (2008). "Diagnosis and initial management of cerebellar infarction". The Lancet Neurology. 7 (10): 951–64. doi:10.1016/S1474-4422(08)70216-3. PMID 18848314. S2CID 25118582.
Norrving, Bo (2014). Oxford Textbook of Stroke and Cerebrovascular Disease. Oxford University Press. pp. 90–1. ISBN 9780199641208.
Nowe, Tim; Jütter, Eric (2014). "Ch. 17: Critical Care of Cerebellar Stroke".  In Schwab, Stefan; Hanley, Daniel; Mendelow, A. David (eds.). Critical Care of the Stroke Patient. Cambridge University Press </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Electrical burn and can you explain it in depth? [/INST] An electrical burn is a burn that results from electricity passing through the body causing rapid injury. Approximately 1000 deaths per year due to electrical injuries are reported in the United States, with a mortality rate of 3-5%. Electrical burns differ from thermal or chemical burns in that they cause much more subdermal damage. They can exclusively cause surface damage, but more often tissues deeper underneath the skin have been severely damaged. As a result, electrical burns are difficult to accurately diagnose, and many people underestimate the severity of their burn. In extreme cases, electricity can cause shock to the brain, strain to the heart, and injury to other organs.For a burn to be classified as electrical, electricity must be the direct cause. For example, burning a finger on a hot electric steam iron would be thermal, not electrical. According to Joules first law: electricity passing through resistance creates heat, so there is no current entering the body in this type of burn. Likewise, a fire that is ruled to be "electrical" in origin, does not necessarily  mean that any injuries or deaths are due to electrical burns. Unless someone was injured at the exact moment that the fire began, it is unlikely that any electrical burns would occur.

Causes
Electrical burns can be caused by a variety of ways such as touching or grasping electrically live objects, short-circuiting, inserting fingers into electrical sockets, and falling into electrified water. Lightning strikes are also a cause of electrical burns, but this is a less common event.
With the advances in technology, electrical injuries are becoming more common and are the fourth leading cause of work-related traumatic death. One third of all electrical traumas and most high-voltage injuries are job related, and more than 50% of these injuries result from power line contact.Electrical burns can be classified into six categories, and any combination of these categories may be present on an electrical burn victim:

Low-voltage burn. A burn produced by contact with a power source of 500 volts or less is classified as a low-voltage burn. The current at this voltage is not enough to cause tissue damage along its path except at the contact site. This type of burn may be mild, superficial, or severe depending on the contact time.
High voltage burn. This burn is very severe as the victim makes direct contact with the high voltage supply and the damage runs its course throughout the body. Exterior injuries are misleading as most of the damage occurs underneath the skin. In this case, subdermal tissues are severely damaged.
Arc burn. This type of burn occurs when electrical energy passes from a high-resistance area to a low-resistance area. No contact is required with an arc burn as the electricity ionizes air particles to complete the circuit. The heat generated can be as high as 4,000 °C (7,200 °F) — hotter than the boiling points of several metals and certainly hot enough to ignite a victims clothing. A form of explosion dissipates excess energy from the arc. In addition, a high-current arc can produce a pressure wave blast in excess of 1,000 pounds per square inch (6,900 kPa) of pressure. This can throw the victim and cause severe injuries.
Flash burn. Flash burns are caused by electrical arcs that pass over the skin. The intense heat and light of an arc flash can cause severe burns in a fraction of a second. Although the burns can cover a large area of skin, they are largely superficial and the tissues beneath the skin are generally undamaged and unaffected. This typically occurs when the frequency of the AC current is significantly higher than the 50 or 60 Hz used in land-based electrical distribution systems (such as in aircraft).
Flame burn. Flame burns are caused by contact to objects that were ignited by an electrical source when associated with flash and arc burns.
Oral burns. This is caused by biting or sucking on electrical cords, and it most commonly happens to children. Electric current typically passes from one side of the childs mouth to the other, possibly causing deformity.

Pathophysiology
Four electrical factors determine the severity of the damage caused by electrical burns: voltage, current, resistance, and frequency. The severity of the burn also depends on the pathway the current takes through the body. Generally, the pathway of the current will follow the course of the least resistant tissues: firstly blood vessels, nerves, and muscle, then skin, tendon, fat, and bone. Most commonly, electric injuries primarily damage the outer limbs, but more critical portions of the body may be affected as well causing severe complications.As the body comes into contact with an electrical source, it becomes part of the electrical circuit. As such, the current has a point of entry and an exit at two different points on the body. The point of entry tends to be depressed and leathery whereas the exit wound is typically more extensive and explosive. It is hard to accurately diagnose an electrical burn because only the entry and exit wounds are visible and the internal damage is not.

Prevention
Basic electrical safety
The following are some examples of unsafe practices which could lead to electric injury (this list is not exhaustive.):
Using electrical appliances while wet (showering, bathing, etc.) as plumbing is often connected to electrical ground, and wet skin loses much of its resistance. Exception for newer quality appliances intended for the bathroom when not simultaneously showering, bathing, being in a path of water going to plumbing, or touching bare concrete or sheet metal. Standing on a dry carpet or rug is ideal.
All power mains outlets should have a wall cover to avoid accidentally touching the electrified sides between the wall and outlet. This is especially important for children, as their small fingers can easily reach into this gap along the sides.
Using AC electrical appliances around bathtubs, swimming pools, hot tubs, etc. with the risk that the appliance may fall into the water and cause electrocution. Only battery-operated devices are safe.
Failure to use child safety plugs in all outlets, and keeping children away from electrical cords.
Adjusting prongs of an electrical cord that are too wide or narrow them with your fingertips while simultaneously plugging the cord into the power mains. The power plug used in the UK and some Commonwealth countries provides limited protection (Type G, with the lower half of the live prongs insulated), but all others do not.
Not following manufacturer safety instructions for electrical appliances. This includes not using and immediately unplugging any appliance with a damaged electrical cord. If this cannot be done safely (i.e. damage is too close to the plug), the circuit breaker should be turned off beforehand.
Touching metallic areas of an AC electrical appliance while also simultaneously touching faucets, water pipes, another metallic AC appliance, or being even partly immersed in water (including wet feet). This could ground the body through metal or water, with the risk that a faulty appliance is electrically "hot" on its outside cover or chassis.
Not installing Ground Fault Circuit Interrupter (GFCI) outlets or circuit breakers in all areas with plumbing, bare concrete flooring, exposed to the elements, or outdoors by a qualified electrician. (Many newer homes already have these devices pre-installed.) Running an extension cord from non-GFCI areas such as bedrooms and hallways defeats this safety feature. Oral burns (above) cannot be prevented by GFCI.
At poolside, not having a non-metallic fiberglass pole or net on hand to pull someone to safety in case the pool water is electrified, and the victim is still conscious. Furthermore, to not know where the circuit breakers for the pool are located.
Failure to install a "feed-through" type GFCI to all electrical devices that are an integral part of a Swimming pool, or not testing it weekly. This is a particular concern due to the use of electric lights and pumps where persons are immersed in water. The GFCI has the typical "test" and "reset" buttons, but no plug-in outlets. A 12-volt system is safer, though not foolproof, as it is ultimately connected to the 120/240 volt power mains. Most electrocutions come from incorrectly grounded or bonded lights. This can send electric current through a pool light even if it is not turned on.
Using an ordinary vacuum cleaner in wet or damp areas. Only a "wet vac" is suitable for this purpose. Overfilling its collection container is also unsafe.
Not double checking polarity before doing a jump start, or attempting a jump on a frozen battery. Although 12-volt batteries used in vehicles are at a safe voltage, a short circuit can still cause various types of burns and an explosion.
Failure to replace high-risk appliances of decades past with new ones (hand-held corded electric drills, blow dryers, etc.)
Not inquiring about the voltage when traveling abroad for those residing in the Americas, Japan, and Taiwan (countries with 110-125 volts). This includes inter-American travel, as a few countries commonly use 220-240 volts. A matching electrical socket (power mains) does not necessarily mean the voltage is the same as ones home country. The doubling of voltage results in a very dangerous four-fold increase in power and heat. Not checking that dual-voltage small appliances have been adjusted correctly for 220-240 volts is also unsafe.
Going near or under a downed power line, even if theres no direct contact with the wire </s>