<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 Varicose veins and can you explain it in depth? [/INST] Varicose veins, also known as varicoses, are a medical condition in which superficial veins become enlarged and twisted. These veins typically develop in the legs, just under the skin. Varicose veins usually cause few symptoms. However, some individuals may experience fatigue or pain in the area. Complications can include bleeding or superficial thrombophlebitis. Varices in the scrotum are known as a varicocele, while those around the anus are known as hemorrhoids. Due to the various physical, social, and psychological effects of varicose veins, they can negatively affect ones quality of life.Varicose veins have no specific cause. Risk factors include obesity, lack of exercise, leg trauma, and family history of the condition. They also develop more commonly during pregnancy. Occasionally they result from chronic venous insufficiency. Underlying causes include weak or damaged valves in the veins. They are typically diagnosed by examination, including observation by ultrasound.By contrast, spider veins affect the capillaries and are smaller.Treatment may involve lifestyle changes or medical procedures with the goal of improving symptoms and appearance. Lifestyle changes may include wearing compression stockings, exercising, elevating the legs, and weight loss. Possible medical procedures include sclerotherapy, laser surgery, and vein stripping. Reoccurrence is common following treatment.Varicose veins are very common, affecting about 30% of people at some time in their lives. They become more common with age. Women develop varicose veins about twice as often as men. Varicose veins have been described throughout history and have been treated with surgery since at least A.D. 400.

Signs and symptoms
Aching, heavy legs
Appearance of spider veins (telangiectasia) in the affected leg
Ankle swelling
A brownish-yellow shiny skin discoloration near the affected veins
Redness, dryness, and itchiness of areas of skin, termed stasis dermatitis or venous eczema
Muscle cramps when making sudden movements, such as standing
Abnormal bleeding or healing time for injuries in the affected area
Lipodermatosclerosis or shrinking skin near the ankles
Restless legs syndrome appears to be a common overlapping clinical syndrome in people with varicose veins and other chronic venous insufficiency
Atrophie blanche, or white, scar-like formations
Burning or throbbing sensation in the legsPeople with varicose veins might have a positive D-dimer blood test result due to chronic low-level thrombosis within dilated veins (varices).

Complications
Most varicose veins are reasonably benign, but severe varicosities can lead to major complications, due to the poor circulation through the affected limb.

Pain, tenderness, heaviness, inability to walk or stand for long hours
Skin conditions / dermatitis which could predispose skin loss
Skin ulcers especially near the ankle, usually referred to as venous ulcers
Development of carcinoma or sarcoma in longstanding venous ulcers. Over 100 reported cases of malignant transformation have been reported at a rate reported as 0.4% to 1%
Severe bleeding from minor trauma, of particular concern in the elderly
Blood clotting within affected veins, termed superficial thrombophlebitis. These are frequently isolated to the superficial veins, but can extend into deep veins, becoming a more serious problem.
Acute fat necrosis can occur, especially at the ankle of overweight people with varicose veins. Females have a higher tendency of being affected than males

Causes
Varicose veins are more common in women than in men and are linked with heredity. Other related factors are pregnancy, obesity, menopause, aging, prolonged standing, leg injury and abdominal straining. Varicose veins are unlikely to be caused by crossing the legs or ankles. Less commonly, but not exceptionally, varicose veins can be due to other causes, such as post-phlebitic obstruction or incontinence, venous and arteriovenous malformations.Venous reflux is a significant cause. Research has also shown the importance of pelvic vein reflux (PVR) in the development of varicose veins. Varicose veins in the legs could be due to ovarian vein reflux. Both ovarian and internal iliac vein reflux causes leg varicose veins. This condition affects 14% of women with varicose veins or 20% of women who have had vaginal delivery and have leg varicose veins. In addition, evidence suggests that failing to look for and treat pelvic vein reflux can be a cause of recurrent varicose veins.There is increasing evidence for the role of incompetent perforator veins (or "perforators") in the formation of varicose veins. and recurrent varicose veins.Varicose veins could also be caused by hyperhomocysteinemia in the body, which can degrade and inhibit the formation of the three main structural components of the artery: collagen, elastin and the proteoglycans. Homocysteine permanently degrades cysteine disulfide bridges and lysine amino acid residues in proteins, gradually affecting function and structure. Simply put, homocysteine is a corrosive of long-living proteins, i.e. collagen or elastin, or lifelong proteins, i.e. fibrillin. These long-term effects are difficult to establish in clinical trials focusing on groups with existing artery decline. Klippel–Trenaunay syndrome and Parkes Weber syndrome are relevant for differential diagnosis.Another cause is chronic alcohol consumption due to the vasodilatation side effect in relation to gravity and blood viscosity.

Diagnosis
Clinical test
Clinical tests that may be used include:
Trendelenburg test–to determine the site of venous reflux and the nature of the saphenofemoral junction

Investigations
Traditionally, varicose veins were investigated using imaging techniques only if there was a suspicion of deep venous insufficiency, if they were recurrent, or if they involved the saphenopopliteal junction. This practice is now less widely accepted. People with varicose veins should now be investigated using lower limbs venous ultrasonography. The results from a randomised controlled trial on patients with and without routine ultrasound have shown a significant difference in recurrence rate and reoperation rate at 2 and 7 years of follow-up.

Stages
The CEAP (Clinical, Etiological, Anatomical, and Pathophysiological) Classification, developed in 1994 by an international ad hoc committee of the American Venous Forum, outlines these stages
C0 – no visible or palpable signs of venous disease
C1 – telangectasia or reticular veins
C2 – varicose veins
C2r - recurrent varicose veins
C3 – edema
C4- changes in skin and subcutaneous tissue due to Chronic Venous Disease
C4a – pigmentation or eczema
C4b – lipodermatosclerosis or atrophie blanche
C4c- Corona phlebectatica
C5 – healed venous ulcer
C6 – active venous ulcer
C6r- recurrent active ulcerEach clinical class is further characterized by a subscript depending upon whether the patient is symptomatic (S) or asymptomatic (A), e.g. C2S.

Treatment
Treatment can be either active or conservative.

Active
Treatment options include surgery, laser and  radiofrequency ablation, and ultrasound-guided foam sclerotherapy. Newer treatments include cyanoacrylate glue, mechanochemical ablation, and endovenous steam ablation. No real difference could be found between the treatments, except that radiofrequency ablation could have a better long-term benefit.

Conservative
The National Institute for Health and Clinical Excellence (NICE) produced clinical guidelines in July 2013 recommending that all people with symptomatic varicose veins (C2S) and worse should be referred to a vascular service for treatment. Conservative treatments such as support stockings should not be used unless treatment was not possible.
The symptoms of varicose veins can be controlled to an extent with the following:

Elevating the legs often provides temporary symptomatic relief.
Advice about regular exercise sounds sensible but is not supported by any evidence.
The wearing of graduated compression stockings with variable pressure gradients (Class II or III) has been shown to correct the swelling, nutritional exchange, and improve the microcirculation in legs affected by varicose veins. They also often provide relief from the discomfort associated with this disease. Caution should be exercised in their use in patients with concurrent peripheral arterial disease.
The wearing of intermittent pneumatic compression devices have been shown to reduce swelling and pain.
Diosmin/hesperidin and other flavonoids.
Anti-inflammatory medication such as ibuprofen or aspirin can be used as part of treatment for superficial thrombophlebitis along with graduated compression hosiery – but there is a risk of intestinal bleeding. In extensive superficial thrombophlebitis, consideration should be given to anti-coagulation, thrombectomy, or sclerotherapy of the involved vein.
Topical gel application helps in managing symptoms related to varicose veins such as inflammation, pain, swelling, itching, and dryness.

Procedures
Stripping
Stripping consists of removal of all or part the saphenous vein (great/long or lesser/short) main trunk. The complications include deep vein thrombosis (5.3%), pulmonary embolism (0.06%), and wound complications including infection (2.2%). There is evidence for the great saphenous vein regrowing after stripping. For traditional surgery, reported recurrence rates, which have been tracked for 10 years, range from 5% to 60%. In addition, since stripping removes the saphenous main trunks, they are no longer available for use as venous bypass grafts in the future (coronary or leg artery vital disease).

Other
Other surgical treatments are:

CHIVA method (ambulatory conservative haemodynamic correction of venous insufficiency) is a relatively low-invasive surgical technique that incorporates venous hemodynamics and preserves the superficial venous system. The overall effectiveness compared to stripping, radiofrequency ablation treatment, or endovenous laser therapy is not clear and there is no strong evidence to suggest that CHIVA is superior to stripping, radiofrequency ablation, or endovenous laser therapy for recurrence of varicose veins. There is some low-certainty evidence that CHIVA may result in more bruising compared to radiofrequency ablation treatment.
Ambulatory phlebectomy.
Vein ligation is done at the saphenofemoral junction after ligating the tributaries at the sephanofemoral junction without stripping the long saphenous vein provided the perforator veins are competent and absent DVT in the deep veins. With this method, the long saphenous vein is preserved.
Cryosurgery- A cryoprobe is passed down the long saphenous vein following saphenofemoral ligation. Then the probe is cooled with NO2 or CO2 to −85o F. The vein freezes to the probe and can be retrogradely stripped after 5 seconds of freezing. It is a variant of Stripping. The only point of this technique is to avoid a distal incision to remove the stripper.

Sclerotherapy
A commonly performed non-surgical treatment for varicose and "spider leg veins" is sclerotherapy, in which medicine called a sclerosant is injected into the veins to make them shrink. The medicines that are commonly used as sclerosants are polidocanol (POL branded Asclera in the United States, Aethoxysklerol in Australia), sodium tetradecyl sulphate (STS), Sclerodex (Canada), Hypertonic Saline, Glycerin and Chromated Glycerin. STS (branded Fibrovein in Australia) liquids can be mixed at varying concentrations of sclerosant and varying sclerosant/gas proportions, with air or CO2 or O2 to create foams. Foams may allow more veins to be treated per session with comparable efficacy. Their use in contrast to liquid sclerosant is still somewhat controversial and there is no clear evidence that foam are superior. Sclerotherapy has been used in the treatment of varicose veins for over 150 years. Sclerotherapy is often used for telangiectasias (spider veins) and varicose veins that persist or recur after vein stripping. Sclerotherapy can also be performed using foamed sclerosants under ultrasound guidance to treat larger varicose veins, including the great saphenous and small saphenous veins.There is some evidence that sclerotherapy is a safe and may be an effective treatment option for improving the cosmetic appearance, reducing residual varicose veins, improving the quality of life, and reducing symptoms that may be present due to the varicose veins. There is also weak evidence that this treatment option may have a slightly higher risk of deep vein thrombosis. It is not known if sclerotherapy decreases the change that varicose veins return (recurrent varicose veins). It is also not known if the type of liquid, substance, or foam used for the sclerotherapy procedure is the most effective and comes with the lowest risk of complications.Complications of sclerotherapy are rare but can include blood clots and ulceration. Anaphylactic reactions are "extraordinarily rare but can be life-threatening," and doctors should have resuscitation equipment ready. There has been one reported case of stroke after ultrasound-guided sclerotherapy when an unusually large dose of sclerosant foam was injected.

Endovenous thermal ablation
There are three kinds of endovenous thermal ablation treatment possible: laser, radiofrequency, and steam.The Australian Medical Services Advisory Committee (MSAC) in 2008 determined that endovenous laser treatment/ablation (ELA) for varicose veins "appears to be more effective in the short term, and at least as effective overall, as the comparative procedure of junction ligation and vein stripping for the treatment of varicose veins." It also found in its assessment of available literature, that "occurrence rates of more severe complications such as DVT, nerve injury, and paraesthesia, post-operative infections, and haematomas, appears to be greater after ligation and stripping than after EVLT". Complications for ELA include minor skin burns (0.4%) and temporary paresthesia (2.1%). The longest study of endovenous laser ablation is 39 months.Two prospective randomized trials found speedier recovery and fewer complications after radiofrequency ablation (ERA) compared to open surgery. Myers wrote that open surgery for small saphenous vein reflux is obsolete. Myers said these veins should be treated with endovenous techniques, citing high recurrence rates after surgical management, and risk of nerve damage up to 15%. By comparison ERA has been shown to control 80% of cases of small saphenous vein reflux at 4 years, said Myers. Complications for ERA include burns, paraesthesia, clinical phlebitis and slightly higher rates of deep vein thrombosis (0.57%) and pulmonary embolism (0.17%). One 3-year study compared ERA, with a recurrence rate of 33%, to open surgery, which had a recurrence rate of 23%.Steam treatment consists in injection of pulses of steam into the sick vein. This treatment which works with a natural agent (water) has similar results than laser or radiofrequency </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 Squamous cell skin cancer and can you explain it in depth? [/INST] Squamous-cell skin cancer, also known as cutaneous squamous-cell carcinoma (cSCC), is one of the main types of skin cancer along with basal cell cancer and melanoma. It usually presents as a hard lump with a scaly top but can also form an ulcer. Onset is often over months. Squamous-cell skin cancer is more likely to spread to distant areas than basal cell cancer. When confined to the outermost layer of the skin, a precancerous or in situ form of cSCC is known as Bowens disease.The greatest risk factor is high total exposure to ultraviolet radiation from the sun. Other risks include prior scars, chronic wounds, actinic keratosis, lighter skin, Bowens disease, arsenic exposure, radiation therapy, tobacco smoking, poor immune system function, previous basal cell carcinoma, and HPV infection. Risk from UV radiation is related to total exposure, rather than early exposure. Tanning beds are becoming another common source of ultraviolet radiation. Risk is also elevated in certain genetic skin disorders, such as xeroderma pigmentosum and certain forms of epidermolysis bullosa. It begins from squamous cells found within the skin. Diagnosis is often based on skin examination and confirmed by tissue biopsy.New in vivo and in vitro studies have proven that the upregulation of FGFR2, a subset of the fibroblast growth factor receptor (FGFR) immunoglobin family, has a critical role to play in the progression of cSCC cells. Mutation in the TPL2 gene causes overexpression of FGFR2, which activates mTORC1 and AKT pathways in both primary and metastatic cSCC cell lines. Only by using FGFR pan-inhibitor, AZD4547, could cell migration and cell proliferation on cSCC be attenuated Additionally, research has identified common driver mutations in cSCC, with alterations in the NOTCH and p53 pathways occurring at high frequency and mutations in the Hippo and Ras/MAPK/PI3K occurring at lower frequency Decreasing exposure to ultraviolet radiation and the use of sunscreen appear to be effective methods of preventing squamous-cell skin cancer. Treatment is typically by surgical removal. This can be by simple excision if the cancer is small otherwise Mohs surgery is generally recommended. Other options may include application of cold and radiation therapy. In the cases in which distant spread has occurred chemotherapy or biologic therapy may be used.As of 2015, about 2.2 million people have cSCC at any given time. It makes up about 20% of all skin cancer cases. About 12% of males and 7% of females in the United States developed cSCC at some point in time. While prognosis is usually good, if distant spread occurs five-year survival is ~34%. In 2015 it resulted in about 51,900 deaths globally. The usual age at diagnosis is around 66. Following the successful treatment of one case of cSCC people are at high risk of developing further cases.

Signs and symptoms
SCC of the skin begins as a small nodule and as it enlarges the center becomes necrotic and sloughs and the nodule turns into an ulcer, and generally are developed from an actinic keratosis. Once keratinocytes begin to grow uncontrollably, they have the potential to become cancerous and produce squamous cell carcinoma.
The lesion caused by SCC is often asymptomatic
Ulcer or reddish skin plaque that is slow growing
Intermittent bleeding from the tumor, especially on the lip
The clinical appearance is highly variable
Usually the tumor presents as an ulcerated lesion with hard, raised edges
The tumor may be in the form of a hard plaque or a papule, often with an opalescent quality, with tiny blood vessels
The tumor can lie below the level of the surrounding skin, and eventually ulcerates and invades the underlying tissue
The tumor commonly presents on sun-exposed areas (e.g. back of the hand, scalp, lip, and superior surface of pinna)
On the lip, the tumor forms a small ulcer, which fails to heal and bleeds intermittently
Evidence of chronic skin photodamage, as in multiple actinic keratoses (solar keratoses)
The tumor grows relatively slowly

Spread
Unlike basal-cell carcinoma (BCC), squamous cell carcinoma (SCC) has a higher risk of metastasis.
Risk of metastasis is higher clinically in SCC arising in scars, on the lower lips or mucosa, and occurring in immunosuppressed and solid organ transplant patients. Risk of metastasis is also higher in SCC that are >2 cm in diameter, growth into the fat layer and along nerves, thickness >6mm.

Causes
Squamous cell carcinoma is the second-most common cancer of the skin (after basal-cell carcinoma but more common than melanoma). It usually occurs in areas exposed to the sun. Sunlight exposure and immunosuppression are risk factors for SCC of the skin, with chronic sun exposure being the strongest environmental risk factor. There is a risk of metastasis starting more than 10 years after diagnosable appearance of squamous cell carcinoma, but the risk is low, though much higher than with basal-cell carcinoma. Squamous cell cancers of the lip and ears have high rates of local recurrence and distant metastasis. In a recent study, it has also been shown that the deletion or severe down-regulation of a gene titled Tpl2 (tumor progression locus 2) may be involved in the progression of normal keratinocytes into becoming squamous cell carcinoma.SCCs represent about 20% of the non-melanoma skin cancers, but 80-90% of those with metastatic potential are located on the head and neck.Tobacco smoking also increases the risk for cutaneous squamous cell carcinoma.The vast majority of SCCs are those of the skin, and are often the result of ultraviolet exposure. SCCs usually occur on portions of the body commonly exposed to the Sun; the face, ears, neck, hands, or arm. The main symptom is a growing bump that may have a rough, scaly surface and flat reddish patches.
Unlike basal-cell carcinomas, SCCs carry a higher risk of metastasis, and may spread to the regional lymph nodes,Erythroplasia of Queyrat (SCC in situ of the glans or prepuce in males, M: 733 : 656  or the vulvae in females.) may be induced by human papilloma virus. It is reported to occur in the corneoscleral limbus. Erythroplasia of Queyrat may also occur on the anal mucosa or the oral mucosa. Some sources state that this condition is synonymous with Bowens disease, however generally speaking Bowens disease refers to carcinoma in situ of any location on the skin such as the lower leg.
Genetically, SCC tumors harbor high frequencies of NOTCH and p53 mutations as well as less frequent alterations in histone acetyltransferase EP300, subunit of the SWI/SNF chromatin remodeling complex PBRM1, DNA-repair deubiquitinase USP28, and NF-κB signaling regulator CHUK.

Immunosuppression
People who have received solid organ transplants are at a significantly increased risk of developing squamous cell carcinoma due to the use of chronic immunosuppressive medication. While the risk of developing all skin cancers increases with these medications, this effect is particularly severe for SCC, with hazard ratios as high as 250 being reported, versus 40 for basal cell carcinoma. The incidence of SCC development increases with time posttransplant. Heart and lung transplant recipients are at the highest risk of developing SCC due to more intensive immunosuppressive medications used.Squamous cell cancers of the skin in individuals on immunotherapy or who have lymphoproliferative disorders (e.g. leukemia) tend to be much more aggressive, regardless of their location. The risk of SCC, and non-melanoma skin cancers generally, varies with the immunosuppressive drug regimen chosen. The risk is greatest with calcineurin inhibitors like cyclosporine and tacrolimus, and least with mTOR inhibitors, such as sirolimus and everolimus. The antimetabolites azathioprine and mycophenolic acid have an intermediate risk profile.

Diagnosis
Diagnosis is confirmed via biopsy of the tissue or tissues suspected to be affected by SCC.  For the skin, look under skin biopsy.
The pathological appearance of a squamous cell cancer varies with the depth of the biopsy.  For that reason, a biopsy including the subcutaneous tissue and basilar epithelium, to the surface is necessary for correct diagnosis.  The performance of a shave biopsy (see skin biopsy) might not acquire enough information for a diagnosis.  An inadequate biopsy might be read as actinic keratosis with follicular involvement.  A deeper biopsy down to the dermis or subcutaneous tissue might reveal the true cancer.  An excision biopsy is ideal, but not practical in most cases.  An incisional or punch biopsy is preferred.  A shave biopsy is least ideal, especially if only the superficial portion is acquired.

Characteristics
Histopathologically, the epidermis in SCC in situ (Bowens disease) will show hyperkeratosis and parakeratosis. There will also be marked acanthosis with elongation and thickening of the rete ridges. These changes will overly keratinocytic cells which are often highly atypical and may in fact have a more unusual appearance than invasive SCC. The atypia spans the full thickness of the epidermis, with the keratinocytes demonstrating intense mitotic activity, pleomorphism, and greatly enlarged nuclei. They will also show a loss of maturity and polarity, giving the epidermis a disordered or "windblown" appearance.Two types of multinucleated cells may be seen: the first will present as a multinucleated giant cell, and the second will appear as a dyskeratotic cell engulfed in the cytoplasm of a keratinocyte. Occasionally, cells of the upper epidermis will undergo vacuolization, demonstrating an abundant and strongly eosinophilic cytoplasm. There may be a mild to moderate lymphohistiocytic infiltrate detected in the upper dermis.

In situ disease
Bowens disease is essentially equivalent to and used interchangeably with SCC in situ, when not having invaded through the basement membrane. Depending on source, it is classified as precancerous or SCC in situ (technically cancerous but non-invasive). In SCC in situ (Bowens disease), atypical squamous cells proliferate through the whole thickness of the epidermis. The entire tumor is confined to the epidermis and does not invade into the dermis. The cells are often highly atypical under the microscope, and may in fact look more unusual than the cells of some invasive squamous cell carcinomas.

Erythroplasia of Queyrat is a particular type of Bowens disease that can arise on the glans or prepuce in males,: 733 : 656  and the vulvae in females. It mainly occurs in uncircumcised males, over the age of 40. It is named for French dermatologist Louis Queyrat (1856–1933),  who was head of the dermatology service of lHôpital Ricord, a venereal hospital in Paris, now Hôpital Cochin.

Invasive disease
In invasive SCC, tumor cells infiltrate through the basement membrane. The infiltrate can be somewhat difficult to detect in the early stages of invasion: however, additional indicators such as full thickness epidermal atypia and the involvement of hair follicles can be used to facilitate the diagnosis. Later stages of invasion are characterized by the formation of nests of atypical tumor cells in the dermis, often with a corresponding inflammatory infiltrate.

Degree of differentiation
Prevention
Appropriate sun-protective clothing, use of broad-spectrum (UVA/UVB) sunscreen with at least SPF 50, and avoidance of intense sun exposure may prevent skin cancer. A 2016 review of sunscreen for preventing squamous cell skin cancer found insufficient evidence to demonstrate whether it was effective.

Management
Most squamous cell carcinomas are removed with surgery. A few selected cases are treated with topical medication. Surgical excision with a free margin of healthy tissue is a frequent treatment modality. Radiotherapy, given as external beam radiotherapy or as brachytherapy (internal radiotherapy), can also be used to treat squamous cell carcinomas. There is little evidence comparing the effectiveness of different treatments for non-metastatic SCC of the skin.Mohs surgery is frequently utilized; considered the treatment of choice for squamous cell carcinoma of the skin, physicians have also utilized the method for the treatment of squamous cell carcinoma of the mouth, throat, and neck.  An equivalent method of the CCPDMA standards can be utilized by a pathologist in the absence of a Mohs-trained physician. Radiation therapy is often used afterward in high risk cancer or patient types.  Radiation or radiotherapy can also be a standalone option in treating SCCs. As a non invasive option brachytherapy serves a painless possibility to treat in particular but not only difficult to operate areas like the earlobes or genitals. An example of this kind of therapy is the High dose brachytherapy Rhenium-SCT which makes use of the beta rays emitting property of Rhenium-188. The radiation source is enclosed in a compound which is applied to a thin protection foile directly over the lesion. This way the radiation source can be applied to complex locations and minimize radiation to healthy tissue.After removal of the cancer, closure of the skin for patients with a decreased amount of skin laxity involves a split-thickness skin graft. A donor site is chosen and enough skin is removed so that the donor site can heal on its own. Only the epidermis and a partial amount of dermis is taken from the donor site which allows the donor site to heal. Skin can be harvested using either a mechanical dermatome or Humby knife.Electrodessication and curettage (EDC) can be done on selected squamous cell carcinoma of the skin.  In areas where SCCs are known to be non-aggressive, and where the patient is not immunosuppressed, EDC can be performed with good to adequate cure rate.Treatment options for SCC in situ (Bowens disease) include photodynamic therapy with 5-aminolevulinic acid, cryotherapy, topical 5-fluorouracil or imiquimod, and excision. A meta-analysis showed evidence that PDT is more effective than cryotherapy and has better cosmetic outcomes. There is generally a lack of evidence comparing the effectiveness of all treatment options.High-risk squamous cell carcinoma, as defined by those occurring around the eye, ear, or nose, is of large size, is poorly differentiated, and grows rapidly, requires more aggressive, multidisciplinary management.
Nodal spread:

Surgical block dissection if palpable nodes or in cases of Marjolins ulcers but the benefit of prophylactic block lymph node dissection with Marjolins ulcers is not proven.
Radiotherapy
Adjuvant therapy may be considered in those with high-risk SCC even in the absence of evidence for local metastasis. Imiquimod (Aldara) has been used with success for squamous cell carcinoma in situ of the skin and the penis, but the morbidity and discomfort of the treatment is severe.  An advantage is the cosmetic result: after treatment, the skin resembles normal skin without the usual scarring and morbidity associated with standard excision.  Imiquimod is not FDA-approved for any squamous cell carcinoma.In general, squamous cell carcinomas have a high risk of local recurrence, and up to 50% do recur. Frequent skin exams with a dermatologist is recommended after treatment.

Prognosis
The long-term outcome of squamous cell carcinomas is dependent upon several factors: the sub-type of the carcinoma, available treatments, location and severity, and various patient health-related variables (accompanying diseases, age, etc.). Generally, the long-term outcome is positive, as less than 4% of Squamous cell carcinoma cases are at risk of metastasis </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 Brief psychotic disorder and can you explain it in depth? [/INST] Brief psychotic disorder — according to the classifications of mental disorders DSM-IV-TR and DSM-5 — is a psychotic condition involving the sudden onset of at least one psychotic symptom (such as disorganized thought/speech, delusions, hallucinations, or grossly disorganized or catatonic behavior) lasting 1 day to 1 month, often accompanied by emotional turmoil. Remission of all symptoms is complete with patients returning to the previous level of functioning. It may follow a period of extreme stress including the loss of a loved one.  Most patients with this condition under DSM-5 would be classified as having acute and transient psychotic disorders under ICD-10.  Prior to DSM-IV, this condition was called "brief reactive psychosis." This condition may or may not be recurrent, and it should not be caused by another condition.
The term bouffée délirante describes an acute non-affective and non-schizophrenic psychotic disorder, which is largely similar to DSM-III-R and DSM-IV brief psychotic and schizophreniform disorders.

Presentation
BPD is characterized by a sudden onset of psychotic symptoms, which may include delusions, hallucinations, disorganized speech or behavior, or catatonic behavior.Symptoms generally last at least a day, but not more than a month, and there is an eventual return to full baseline functioning. BPD may occur in response to a significant stressor in ones life, or in other situations where a stressor is not apparent, including in the weeks following birth.In diagnosis, a careful distinction is considered for culturally appropriate behaviors, such as religious beliefs and activities. It is believed to be connected to or synonymous with a variety of culture-specific phenomena such as latah, koro, and amok.

Classification
There are three forms of brief psychotic disorder:
BPD with a marked stressor (a.k.a. brief reactive psychosis): if BPD symptoms occur in following personal events (single or multiple) that would be expected to cause significant stress to an average individual.
BPD without a marked stressor: if BPD symptoms do not occur in following personal events (single or multiple) that would be expected to cause significant stress to an average individual.
BPD with postpartum onset: if onset of BPD symptoms is during pregnancy or within 4 weeks after birth.

BPD with a marked stressor (brief reactive psychosis)
Brief reactive psychosis (designated since the DSM IV-TR as "brief psychotic disorder with marked stressor(s), BRP"), is the psychiatric term for psychosis which can be triggered by an extremely stressful event in the life of an individual and eventually yielding to a return to normal functioning.Brief reactive psychosis generally follows a recognisably traumatic life event like divorce or homelessness, but may be triggered by any subjective experience which appears catastrophic to the person affected. Among such stressors are the death of a loved one, professional loss such as unexpectedly losing ones job or otherwise becoming unemployed, or serious adverse changes in the patients personal life, such as the breakdown of their family through divorce, etc. It must be emphasised that this is by no means an exhaustive list of stressful life events, because the events which trigger brief reactive psychosis tend, due to the individualistic nature of human psychology, to be extremely personalized. BRP may be the first breakdown for someone with a chronic psychiatric disorder but only time will tell whether the disorder will be brief or lifelong, whether BRP or a chronic condition that is controlled well enough by medication that symptoms do not return.The condition usually resolves spontaneously within a time span of weeks to months, with the severity of the symptoms reducing continuously over the period in question. A primary goal of treatment is to prevent patients who are either suicidal or homicidal from harming themselves or others during the episode.

Cause/pathophysiology
The exact cause of brief psychotic disorder is not known. One theory suggests a genetic link, because the disorder is more common in people who have family members with mood disorders, such as depression or bipolar disorder. Another theory suggests that the disorder is caused by poor coping skills, as a defense against or escape from a particularly frightening or stressful situation. These factors may create a vulnerability to develop brief psychotic disorder </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 Gestational hypertension and can you explain it in depth? [/INST] Gestational hypertension or pregnancy-induced hypertension (PIH) is the development of new hypertension in a pregnant woman after 20 weeks gestation without the presence of protein in the urine or other signs of pre-eclampsia. Gestational hypertension is defined as having a blood pressure
greater than 140/90 on two occasions at least 6 hours apart.

Signs and symptoms
No single diagnostic test currently exists to predict the likelihood of developing gestational hypertension. High blood pressure is the major sign in diagnosing gestational hypertension. Some women with gestational hypertension may present asymptomatic, but a number of symptoms are associated with the condition.[1]
Symptoms

Edema
Sudden weight gain
Blurred vision or sensitivity to light
Nausea and vomiting
Persistent headaches
Increased blood pressure

Risk factors
Maternal causes

Obesity
Mothers under 20 or over 40 years old
Past history of diabetes mellitus, hypertension (particularly gestational hypertension) and renal disease
Pre-existing hypertension
Thrombophilias (anti-phospholipid syndrome, protein C/S deficiency, factor V Leiden)
Having donated a kidneyPregnancy

Multiple gestation (twins or triplets, etc.)
Placental abnormalities:
Hyperplacentosis: Excessive exposure to chorionic villi
Placental ischemiaFamily history

Family history of pre-eclampsia

Diagnosis
Conditions
There exist several hypertensive states of pregnancy:

Gestational hypertension
Gestational hypertension is usually defined as having a blood pressure higher than 140/90 measured on two separate occasions, more than 6 hours apart, without the presence of protein in the urine and diagnosed after 20 weeks of gestation.
Pre-eclampsia
Pre-eclampsia is gestational hypertension plus proteinuria (>300 mg of protein in a 24-hour urine sample). Severe pre-eclampsia involves a blood pressure greater than 160/110, with additional medical signs and symptoms. HELLP syndrome is a type of pre-eclampsia. It is a combination of three medical conditions: hemolytic anemia, elevated liver enzymes and low platelet count.
Eclampsia
This is when tonic-clonic seizures appear in a pregnant woman with high blood pressure and proteinuria.Pre-eclampsia and eclampsia are sometimes treated as components of a common syndrome.

Treatment
There is no specific treatment, but is monitored closely to rapidly identify pre-eclampsia and its life-threatening complications (HELLP syndrome and eclampsia).Drug treatment options are limited, as many antihypertensives may negatively affect the fetus. Methyldopa, hydralazine, and labetalol are most commonly used for severe pregnancy hypertension.The fetus is at increased risk for a variety of life-threatening conditions, including pulmonary hypoplasia (immature lungs).  If the dangerous complications appear after the fetus has reached a point of viability, even though still immature, then an early delivery may be warranted to save the lives of both mother and baby. An appropriate plan for labor and delivery includes selection of a hospital with provisions for advanced life support of newborn babies.

Evolutionary considerations
Humans
Gestational hypertension is one of the most common disorders seen in human pregnancies. Though relatively benign on its own, in roughly half of the cases of gestational hypertension the disorder progresses into pre-eclampsia, a dangerous condition that can prove fatal to expectant mothers.  However, gestational hypertension is a condition that is fairly rare to see in other animals.  For years, it has been the belief of the scientific community that gestational hypertension and pre-eclampsia were relatively unique to humans, although there has been some recent evidence that other primates can also develop similar conditions, albeit due to different underlying mechanisms. The underlying cause of gestational hypertension in humans is commonly believed to be an improperly implanted placenta.  Humans have evolved to have a very invasive placenta to facilitate better oxygen transfer from the mother to the fetus, to support the growth of its large brain.

Origins of the placenta
The origins of gestational hypertension may lie with the development of humans hemochorial placenta.  A hemochorial placenta optimizes the amount of oxygen and nutrients that can be absorbed into the fetal blood supply, while at the same time ensuring rapid diffusion of wastes away from the fetus.  This hemochorial placenta differs from lower primates epitheliochorial placentae in the way that it allows the fetal tissues to interact directly with the mothers blood.  The hemochorial placenta thereby promotes more rapid diffusion to and from the fetal blood supply.In animals with epitheliochorial placentae such as horses and pigs, the greatest resistance to maternal blood flow in the vascular system was found within the placenta.  However, in animals with hemochorial placental structures such as rodents and primates, the vascular resistance in the placenta was low, leading scientists to the conclusion that the greatest resistance to maternal blood flow is found elsewhere in the maternal vascular system.  The high vascular resistance outside of the placenta leads to higher maternal blood pressure throughout the body.The fetal cells that implant into the uterine wall are known as the trophoblast.  The hemochorial placenta bathes the fetal trophoblast in maternal blood by forming lacunae, or lakes, of the mothers blood that surround fetal tissue.  The lacunae are filled by the spiral arteries, which means that the mothers blood pressure is the driving force behind the introduction of new blood, which contains both oxygen and food for the fetus, to the system.  It is thought that humans need the increased diffusion provided by the hemochorial placenta in order to grow the large brains compared to their body size that distinguish them from other primates.

Incorrect placental implantation
It is thought that "failings" in normal hemochorial placental structure lead to pre-eclampsia and gestational hypertension.  The human placenta implants "earlier, deeper, and more extensively" into the uterine wall, which can potentially lead to many problems that are found in human pregnancies, but not as much in other animals.  Miscarriage and pre-eclampsia are both very rare in other species, but are two of the most common pregnancy-related diseases in humans. The genetic roots of gestational hypertension and pre-eclampsia are certain, as women with a family history of the condition are three times more likely to develop it when they are pregnant.One of the potential causes of gestational hypertension and pre-eclampsia is when the trophoblast does not invade far enough into the uterine lining.  When the fetuss trophoblast does not fully extend into the uterine wall, the spiral arteries do not become fully converted into low-resistance channels.  It has been found that this incomplete conversion of spiral arteries increases the resistance to uterine blood flow during pregnancy, and that this occurrence was associated with gestational hypertension.  One potential cause of this incomplete breach of the spiral arteries that leads to gestational hypertension is a mistaken immune response by the maternal tissue, reaction to the alien fetal tissue.  Therefore, it is clear that the complication of gestational hypertension has roots in the early implantation of the fetus in the uterine wall, an implantation technique that is unique to humans.The highly invasive placenta that is found in humans is thought to be linked to humans high circulating levels of the hormones CG and hCG. It has been shown that the higher the levels of these hormones, the deeper the trophoblasts invasion into the uterine wall.  Instances of gestational hypertension and pre-eclampsia have been shown to occur when the invasion of the uterine wall is not deep enough, because of lower CG and hCG levels in the mother.

Evolutionary tradeoff
Despite these risks for gestational hypertension, the hemochorial placenta has been favored because of its advantages in the way that it aids in diffusion from mother to fetus later in pregnancy.  The bipedal posture that has allowed humans to walk upright has also led to a reduced cardiac output, and it has been suggested that this is what necessitated humans aggressive early placental structures.  Increased maternal blood pressure can attempt to make up for lower cardiac output, ensuring that the fetuss growing brain receives enough oxygen and nutrients </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 Essential thrombocythemia and can you explain it in depth? [/INST] Essential thrombocythemia (ET) is a rare chronic blood cancer (myeloproliferative neoplasm) characterised by the overproduction of platelets (thrombocytes) by megakaryocytes in the bone marrow. It may, albeit rarely, develop into acute myeloid leukemia or myelofibrosis. It is a type of myeloproliferative neoplasm (blood cancers) wherein the body makes too many white or red blood cells, or platelets).

Signs and symptoms
Most people with essential thrombocythemia are without symptoms at the time of diagnosis, which is usually made after noting an elevated platelet level on a routine complete blood count (CBC). The most common symptoms are bleeding (due to dysfunctional platelets), blood clots (e.g., deep vein thrombosis or pulmonary embolism), fatigue, headache, nausea, vomiting, abdominal pain, visual disturbances, dizziness, fainting, and numbness in the extremities; the most common signs are increased white blood cell count, reduced red blood cell count, and an enlarged spleen.

Cause
In ET, megakaryocytes are more sensitive to growth factors. Platelets derived from the abnormal megakaryocytes are activated, which, along with the elevated platelet count, contributes to the likelihood of forming blood clots. The increased possibility of bleeding when the platelet count is over 1 million is due to von Willebrand factor (vWF) sequestration by the increased mass of platelets, leaving insufficient vWF for platelet adhesion. A mutation in the JAK2 kinase (V617F) is present in 40–50% of cases and is diagnostic if present. JAK2 is a member of the Janus kinase family.In 2013, two groups detected calreticulin mutations in a majority of JAK2-negative/MPL-negative patients with essential thrombocythemia and primary myelofibrosis, which makes CALR mutations the second most common in myeloproliferative neoplasms. All mutations (insertions or deletions) affected the last exon, generating a reading frame shift of the resulting protein, that creates a novel terminal peptide and causes a loss of endoplasmic reticulum KDEL retention signal.

Diagnosis
The following revised diagnostic criteria for essential thrombocythemia were proposed in 2005. The diagnosis requires the presence of both A criteria together with B3 to B6, or of criterion A1 together with B1 to B6. The criteria are as follows:
A1. Platelet count > 400 × 103/µL for at least 2 months.
A2. Acquired V617F JAK2 mutation present
B1. No cause for a reactive thrombocytosis
normal inflammatory indices
B2. No evidence of iron deficiency
stainable iron in the bone marrow or normal red cell mean corpuscular volume
B3. No evidence of polycythemia vera
hematocrit < midpoint of normal range or normal red cell mass in presence of normal iron stores
B4. No evidence of chronic myeloid leukemia
But the Philadelphia chromosome may be present in up to 10% of cases. Patients with the Philadelphia chromosome have a potential for the development of acute leukemia, especially acute lymphocytic leukemia.
B5. No evidence of myelofibrosis
no collagen fibrosis and ≤ grade 2 reticulin fibrosis (using 0–4 scale)
B6. No evidence of a myelodysplastic syndrome
no significant dysplasia
no cytogenetic abnormalities suggestive of myelodysplasia

Treatment
Indications
Not all those affected will require treatment at presentation. People are usually split up into low and high risk for bleeding/blood clotting groups (based on their age, their medical history, their blood counts and their lifestyles), low risk individuals are usually treated with aspirin, whereas those at high risk are given hydroxycarbamide and/or other treatments that reduce platelet count (such as interferon-α and anagrelide).

Agents
Hydroxycarbamide, interferon-α and anagrelide can lower the platelet count. Low-dose aspirin is used to reduce the risk of blood clot formation unless the platelet count is very high, where there is a risk of bleeding from the disease, and hence this measure would be counter-productive as aspirin-use increases the risk of bleeding.The PT1 study compared hydroxyurea plus aspirin to anagrelide plus aspirin as initial therapy for ET.  Hydroxyurea treated patients had a lower incidence of arterial thrombosis, lower incidence of severe bleeding and lower incidence of transformation to myelofibrosis, but the risk of venous thrombosis was higher with hydroxycarbamide than with anagrelide. It is unknown whether the results are applicable to all ET patients </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 Transient synovitis and can you explain it in depth? [/INST] Transient synovitis of  hip (also called toxic synovitis; see below for more synonyms) is a self-limiting condition in which there is an inflammation of the inner lining (the synovium) of the capsule of the hip joint. The term irritable hip refers to the syndrome of acute hip pain, joint stiffness, limp or non-weightbearing, indicative of an underlying condition such as transient synovitis or orthopedic infections (like septic arthritis or osteomyelitis). In everyday clinical practice however, irritable hip is commonly used as a synonym for transient synovitis.  It should not be confused with sciatica, a condition describing hip and lower back pain much more common to adults than transient synovitis but with similar signs and symptoms.
Transient synovitis usually affects children between three and ten years old (but it has been reported in a 3-month-old infant and in some adults). It is the most common cause of sudden hip pain and limp in young children. Boys are affected two to four times as often as girls. The exact cause is unknown. A recent viral infection (most commonly an upper respiratory tract infection) or a trauma have been postulated as precipitating events, although these are reported only in 30% and 5% of cases, respectively.Transient synovitis is a diagnosis of exclusion. The diagnosis can be made in the typical setting of pain or limp in a young child who is not generally unwell and has no recent trauma. There is a limited range of motion of the hip joint. Nevertheless, children with transient synovitis of the hip can usually weight bear. This is an important clinical differentiating sign from septic arthritis.  Blood tests may show mild inflammation. An ultrasound scan of the hip joint can show a fluid collection (effusion). Treatment is with nonsteroidal anti-inflammatory drugs and limited weight-bearing. The condition usually clears by itself within seven to ten days, but a small group of patients will continue to have symptoms for several weeks. The recurrence rate is 4–17%, most of which is in the first six months.

Symptoms and signs
Transient synovitis causes pain in the hip, thigh, groin or knee on the affected side. However, children with transient synovitis of the hip can usually weight bear with varying degrees of limping. There may be a limp (or abnormal crawling in infants) with or without pain. In small infants, the presenting complaint can be unexplained crying (for example, when changing a diaper). The condition is nearly always limited to one side. The pain and limp can range from mild to severe.Some children may have a slightly raised temperature; high fever and general malaise point to other, more serious conditions. On clinical examination, the child typically holds the hip slightly bent, turned outwards and away from the middle line (flexion, external rotation and abduction). Active and passive movements may be limited because of pain, especially abduction and internal rotation. The hip can be tender to palpation. The log roll test involves gently rotating the entire lower limb inwards and outwards with the patient on his back, to check when muscle guarding occurs. The unaffected hip and the knees, ankles, feet and spine are found to be normal.

Complications
In the past, there have been speculations about possible complications after transient synovitis. The current consensus however is that there is no proof of an increased risk of complications after transient synovitis.One such previously suspected complication was coxa magna, which is an overgrowth of the femoral head and broadening of the femoral neck, accompanied by changes in the acetabulum, which may lead to subluxation of the femur. There was also some controversy about whether continuous high intra-articular pressure in transient synovitis could cause avascular necrosis of the femoral head (Legg-Calvé-Perthes disease), but further studies did not confirm any link between the two conditions.

Diagnosis
There are no set standards for the diagnosis of suspected transient synovitis, so the amount of investigations will depend on the need to exclude other, more serious diseases. It is of great importance to exclude the diagnosis of septic arthritis. This is because if septic arthritis is missed in children, grave complications can occur. The exclusion of septic arthritis is mainly built upon the physicians clinical expertise and is supplemented by basic laboratory test and relevant imaging modalities. Additionally, beware to exclude the diagnosis of acute osteomyelitis, because it not uncommonly cooccurs with septic arthritis of the hip in children.Inflammatory parameters in the blood may be slightly raised (these include erythrocyte sedimentation rate, C-reactive protein and white blood cell count), but raised inflammatory markers are strong predictors of other more serious conditions such as septic arthritis.X-ray imaging of the hip is most often unremarkable. Subtle radiographic signs include an accentuated pericapsular shadow, widening of the medial joint space, lateral displacement of the femoral epiphyses with surface flattening (Waldenström sign), prominent obturator shadow, diminution of soft tissue planes around the hip joint or slight demineralisation of the proximal femur. The main reason for radiographic examination is to exclude bony lesions such as occult fractures, slipped upper femoral epiphysis or bone tumours (such as osteoid osteoma). An anteroposterior and frog lateral (Lauenstein) view of the pelvis and both hips is advisable.An ultrasound scan of the hip can easily demonstrate fluid inside the joint capsule (Fabella sign), although this is not always present in transient synovitis. However, it cannot reliably distinguish between septic arthritis and transient synovitis. If septic arthritis needs to be ruled out, needle aspiration of the fluid can be performed under ultrasound guidance. In transient synovitis, the joint fluid will be clear. In septic arthritis, there will be pus in the joint, which can be sent for bacterial culture and antibiotic sensitivity testing.
More advanced imaging techniques can be used if the clinical picture is unclear; the exact role of different imaging modalities remains uncertain. Some studies have demonstrated findings on magnetic resonance imaging (MRI scan) that can differentiate between septic arthritis and transient synovitis (for example, signal intensity of adjacent bone marrow). Skeletal scintigraphy can be entirely normal in transient synovitis, and scintigraphic findings do not distinguish transient synovitis from other joint conditions in children. CT scanning does not appear helpful.

Differential diagnosis
Pain in or around the hip and/or limp in children can be due to a large number of conditions. Septic arthritis (a bacterial infection of the joint) is the most important differential diagnosis, because it can quickly cause irreversible damage to the hip joint. Fever, raised inflammatory markers on blood tests and severe symptoms (inability to bear weight, pronounced muscle guarding) all point to septic arthritis, but a high index of suspicion remains necessary even if these are not present. Osteomyelitis (infection of the bone tissue) can also cause pain and limp.Bone fractures, such as a toddlers fracture (spiral fracture of the shin bone), can also cause pain and limp, but are uncommon around the hip joint. Soft tissue injuries can be evident when bruises are present. Muscle or ligament injuries can be contracted during heavy physical activity —however, it is important not to miss a slipped upper femoral epiphysis. Avascular necrosis of the femoral head (Legg-Calvé-Perthes disease) typically occurs in children aged 4–8, and is also more common in boys </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 Intestinal malrotation and can you explain it in depth? [/INST] Intestinal malrotation is a congenital anomaly of rotation of the midgut. It occurs during the first trimester as the fetal gut undergoes a complex series of growth and development. Malrotation can lead to a dangerous complication called volvulus. Malrotation can refer to a spectrum of abnormal intestinal positioning, often including:
The small intestine found predominantly on the right side of the abdomen
The cecum displaced from its usual position in the right lower quadrant into the epigastrium or right hypochondrium
An absent or displaced ligament of Treitz
Fibrous peritoneal bands called bands of Ladd running across the vertical portion of the duodenum
An unusually narrow, stalk-like mesenteryThe position of the intestines, narrow mesentery and Ladds bands can contribute to several severe gastrointestinal conditions. The narrow mesentery predisposes some cases of malrotation to midgut volvulus, a twisting of the entire small bowel that can obstruct the mesenteric blood vessels leading to intestinal ischemia, necrosis, and death if not promptly treated. The fibrous Ladds bands can constrict the duodenum, leading to intestinal obstruction.

Signs and symptoms
Signs and symptoms of malrotation vary depending on if the patient is suffering from an acute volvulus or experiencing chronic symptoms.
If the patient, most often an infant, presents acutely with midgut volvulus, it is usually manifested by bilious vomiting, crampy abdominal pain, abdominal distention, and in late cases, the passage of blood and mucus in their stools.
Patients with chronic, uncorrected or undiagnosed malrotation can have recurrent abdominal pain and vomiting.
Malrotation may be asymptomatic.

Complications
Intestinal malrotation can lead to a number of disease manifestations and complications such as:
Acute midgut volvulus
Chronic midgut volvulus
Acute duodenal obstruction
Chronic duodenal obstruction
Short bowel syndrome, in cases of volvulus with intestinal necrosis
Death, in cases of volvulus with pan-necrosis of the bowel, severe septic shock or hypovolemic shock
Malabsorption
Chronic motility issues
Internal herniation
Superior mesenteric artery syndrome

Causes
The exact cause of intestinal malrotation is unknown. It is not definitively associated with a particular gene, but there is some evidence of recurrence in families.

Diagnosis
Malrotation is most often diagnosed during infancy, however, some cases are not discovered until later in childhood or even adulthood.With acutely ill patients, consider emergency surgery laparotomy if there is a high index of suspicion.In cases of volvulus, plain radiography may demonstrate signs of duodenal obstruction with dilatation of the proximal duodenum and stomach but it is often non-specific. Ultrasonography may be useful in some cases of volvulus, depicting a "whirlpool sign" where the superior mesenteric artery and superior mesenteric vein have twisted.Upper gastrointestinal series is the modality of choice for the evaluation of malrotation, as it will often show an abnormal position of the duodenum and duodeno-jejunal flexure (ligament of Treitz) </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 Iliotibial band syndrome and can you explain it in depth? [/INST] Iliotibial band syndrome (ITBS) is the second most common knee injury, and is caused by inflammation located on the lateral aspect of the knee due to friction between the iliotibial band and the lateral epicondyle of the femur. Pain is felt most commonly on the lateral aspect of the knee and is most intensive at 30 degrees of knee flexion. Risk factors in women include increased hip adduction, knee internal rotation. Risk factors seen in men are increased hip internal rotation and knee adduction. ITB syndrome is most associated with long-distance running, cycling, weight-lifting, and with military training.

Signs and symptoms
ITBS symptoms range from a stinging sensation just above the knee and outside of the knee (lateral side of the knee) joint, to swelling or thickening of the tissue in the area where the band moves over the femur. The stinging sensation just above the knee joint is felt on the outside of the knee or along the entire length of the iliotibial band. Pain may not occur immediately during activity, but may intensify over time. Pain is most commonly felt when the foot strikes the ground, and pain might persist after activity. Pain may also be present above and below the knee, where the ITB attaches to the tibia.

Causes
ITBS can result from one or more of the following: training habits, anatomical abnormalities, or muscular imbalances:

Anatomical mechanism
Iliotibial band syndrome is one of the leading causes of lateral knee pain in runners. The iliotibial band is a thick band of fascia on the lateral aspect of the knee, extending from the outside of the pelvis, over the hip and knee, and inserting just below the knee. The band is crucial to stabilizing the knee during running, as it moves from behind the femur to the front of the femur during activity. The continual rubbing of the band over the lateral femoral epicondyle, combined with the repeated flexion and extension of the knee during running may cause the area to become inflamed.

Diagnosis
Diagnosis of iliotibial band syndrome is based on history and physical exam findings, including tenderness at the lateral femoral epicondyle, where the iliotibial band passes over the bone.

Treatment
Conservative treatments
While ITBS pain can be acute, the iliotibial band can be rested, iced, compressed and elevated (RICE) to reduce pain and inflammation, followed by stretching. Utilization of corticosteroid injections and the use of anti-inflammatory medication on the painful area are possible treatments for ITB syndrome. Corticosteroid injections have been shown to decrease running pains significantly 7 days after the initial treatment. Similar results can be found with the use of anti-inflammatory medication, analgesic/anti-inflammatory medication, specifically. Other non-invasive treatments include things such as, flexibility and strength training, neuromuscular/gait training, manual therapy, training volume reduction, or changes in running shoe.  Muscular training of the gluteus maximus and hip external rotators is stressed highly as those muscles are associated with many of the risk factors of ITBS. For runners specifically, neuromuscular/gait training may be needed for success in muscular training interventions to ensure that those trained muscles are used properly in the mechanics of running. Strength training alone will not result in decrease in pain due to ITBS, however, gait training, on its own can result in running form modification that reduces the prevalence of risk factors.

Surgical treatments
Treatments as intensive and invasive as surgery are utilized if several conservative approaches fail to produce results. 6 months should be given for conservative treatments to work before surgical intervention as used.

Epidemiology
Occupation
Significant association between the diagnosis of ITBS and occupational background of the patients has been thoroughly determined. Occupations that require extensive use of iliotibial band are more susceptible to develop ITBS due to continuum of their iliotibial band repeatedly abrading against lateral epicondyle prominence, thereby inducing inflammatory response. Professional or amateur runners are at high clinical risk of ITBS in which shows particularly greater risk in long-distance. Study suggests ITBS alone makes up 12% of all running-related injuries and 1.6% to 12% of runners are affected by ITBS.The relationship between ITBS and mortality/morbidity is claimed to be absent. A study showed that coordination variability did not vary significantly between runners with no injury and runners with ITBS. This result elucidates that the runners ability to coordinate themselves toward direction of their intention (motor coordination) is not, or very minorly affected by the pain of ITBS.Additionally, military trainee in marine boot camps displayed high incidence rate of ITBS. Varying incidence rate of 5.3–22% in basic training was reported in a case study. A report from the U.S. Marine Corps announces that running/overuse-related injuries accounted for >12% of all injuries.In contrast, studies suggested antithesis of conventional perception that racial, gender or age difference manifests in different incidence rate of ITBS diagnosis. No meaningful statistical data successfully provides significant correlation between ITBS and gender, age, or race. Although, there had been a claim that females are more prone to ITBS due to their anatomical difference in pelvis and lower extremity. Males with larger lateral epicondyle prominence may also be more susceptible to ITBS.  Higher incidence rate of ITBS has been reported at age of 15–50, in which generally includes most of active athletes.Other professions that had noticeable association with ITBS include cyclists, heavy weightlifters, et cetera </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 Constipation in children and can you explain it in depth? [/INST] Constipation in children refers to the medical condition of constipation in children. It is a functional gastrointestinal disorder.

Presentation
Children have different bowel movement patterns than adults. In addition, there is a wide spectrum of normalcy when considering childrens bowel habits. On average, infants have 3-4 bowel movements/day, and toddlers have 2-3 bowel movements per day. At around age 4, children develop an adult-like pattern of bowel movements (1-2 stools/day). Children benefit from scheduled toilet breaks, once early in the morning and 30 minutes after meals. The Rome III Criteria for constipation in children helps to define constipation for various age groups.

Causes
While it is difficult to assess an exact age at which constipation most commonly arises, children frequently experience constipation in conjunction with life-changes. Examples include: toilet training, starting or transferring to a new school, and changes in diet. Especially in infants, changes in formula or transitioning from breast milk to formula can cause constipation. Fortunately, the majority of constipation cases are not tied to a medical disease, and treatment can be focused on simply relieving the symptoms.

Congenital causes
A number of diseases present at birth can result in constipation. They are as a group uncommon with Hirschsprungs disease (HD) being the most common. HD is more common in males than females, affecting 1 out of 5000 babies. In people with HD, specific types of cells called neural crest cells fail to migrate to parts of the colon. This causes the affected portion of the colon to be unable to contract and relax to help push out a bowel movement. The affected portion of the colon remains contracted, making it difficult for stool to pass through. Concern for HD should be raised in a child who has not passed stool during the first 48 hours of life. Milder forms of HD, in which only a small portion of the colon is affected, can present later in childhood as constipation, abdominal pain, and bloating. Similar disorders to HD include anal achalasia and hypoganglionosis. In hypoganglionosis, there is a low number of neural crest cells, so the colon remains contracted. In anal achalasia, the internal anal sphincter remains contracted, making it difficult for stool to pass. However, there is a normal number of neural crest cells present.There are also congenital structural anomalies that can lead to constipation, including anterior displacement of the anus, imperforate anus, strictures, and small left colon syndrome. Anterior displacement of the anus can be diagnosed on physical exam. The disease causes constipation because the inappropriate positioning of the anus which make it difficult to pass a bowel movement. Imperforate anus is an anus that ends in a blind pouch and does not connect to the rest of the persons intestines. Small left colon syndrome is a rare disease in which the left side of the babies colon has a small diameter, which makes it difficult for stool to pass. A risk factor for small left colon syndrome is having a mother with diabetes.Some symptoms that may indicate an underlying disease include:
Bowel movements that contain blood.
Severe abdominal bloating.
Peri-anal fistula
Absent anal wink reflex
Sacral dimple
Failure to thrive

Diagnosis
The Rome process suggests a diagnosis of constipation in children fewer than 4 years old when the child has 2 or more of the following complaints for at least 1 month </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 Corneal abrasion and can you explain it in depth? [/INST] Corneal abrasion is a scratch to the surface of the cornea of the eye. Symptoms include pain, redness, light sensitivity, and a feeling like a foreign body is in the eye. Most people recover completely within three days.Most cases are due to minor trauma to the eye such as that which can occur with contact lens use or from fingernails. About 25% of cases occur at work. Diagnosis is often by slit lamp examination after fluorescein dye has been applied. More significant injuries like a corneal ulcer, globe rupture, recurrent erosion syndrome, and a foreign body within the eye should be ruled out.Prevention includes the use of eye protection. Treatment is typically with antibiotic ointment. In those who wear contact lenses a fluoroquinolone antibiotic is often recommended. Paracetamol (acetaminophen), NSAIDs, and eye drops such as cyclopentolate that paralyse the pupil can help with pain. Evidence does not support the usefulness of eye patching for those with simple abrasions.About 3 per 1,000 people are affected a year in the United States. Males are more often affected than females. The typical age group affected is those in their 20s and 30s. Complications can include bacterial keratitis, corneal ulcer, and iritis. Complications may occur in up to 8% of people.

Signs and symptoms
Signs and symptoms of corneal abrasion include pain, trouble with bright lights, a foreign-body sensation, excessive squinting, and reflex production of tears. Signs include epithelial defects and edema, and often redness of the eye. The vision may be blurred, both from any swelling of the cornea and from excess tears. Crusty buildup from excess tears may also be present.

Complications
Complications are the exception rather than the rule from simple corneal abrasions. It is important that any foreign body be identified and removed, especially if containing iron as rusting will occur.Occasionally the healed epithelium may be poorly adherent to the underlying basement membrane in which case it may detach at intervals giving rise to recurrent corneal erosions.

Causes
Corneal abrasions are generally a result of trauma to the surface of the eye. Common causes include being poked by a finger, walking into a tree branch, and wearing old contact lenses.  A foreign body in the eye may also cause a scratch if the eye is rubbed.Injuries can also be incurred by "hard" or "soft" contact lenses that have been left in too long.  Damage may result when the lenses are removed, rather than when the lens is still in contact with the eye. In addition, if the cornea becomes excessively dry, it may become more brittle and easily damaged by movement across the surface.  Soft contact lens wear overnight has been extensively linked to gram negative keratitis (infection of the cornea) particularly by a bacterium known as Pseudomonas aeruginosa which forms in the eyes biofilm as a result of extended soft contact lens wear.  When a corneal abrasion occurs either from the contact lens itself or another source, the injured cornea is much more susceptible to this type of bacterial infection than a non-contact lens users would be.  This is an optical emergency as it is sight- (in some cases eye-) threatening.  Contact lens wearers who present with corneal abrasions should never be pressure patched because it has been shown through clinical studies that patching creates a warm, moist dark environment that can cause the cornea to become infected or cause an existing infection to be greatly accelerated on its destructive path.Corneal abrasions are also a common and recurrent feature in people with specific types of corneal dystrophy, such as lattice corneal dystrophy. Lattice dystrophy gets its name from an accumulation of amyloid deposits, or abnormal protein fibers, throughout the middle and anterior stroma. During an eye examination, the doctor sees these deposits in the stroma as clear, comma-shaped overlapping dots and branching filaments, creating a lattice effect. Over time, the lattice lines will grow opaque and involve more of the stroma. They will also gradually converge, giving the cornea a cloudiness that may also reduce vision. In some people, these abnormal protein fibers can accumulate under the corneas outer layer—the epithelium. This can cause erosion of the epithelium. This condition is known as recurrent epithelial erosion. These erosions: (1) Alter the corneas normal curvature, resulting in temporary vision problems; and (2) Expose the nerves that line the cornea, causing severe pain. Even the involuntary act of blinking can be painful.

Diagnosis
Although corneal abrasions may be seen with ophthalmoscopes, slit lamp microscopes provide higher magnification which allow for a more thorough evaluation. To aid in viewing, a fluorescein stain that fills in the corneal defect and glows with a cobalt blue-light is generally instilled first.A careful search should be made for any foreign body, in particular looking under the eyelids. Injury following use of hammers or power-tools should always raise the possibility of a penetrating foreign body into the eye, for which urgent ophthalmology opinion should be sought.

Prevention
Prevention is the best method to avoid recurrence of corneal abrasions. Protective eyewear should be worn by people who work with hazardous machinery, metal, wood, or chemicals, as well as those who perform yard work or participate in certain contact sports. The appropriate type of protective eyewear depends on the specific circumstances, but all should provide shielding, good visibility, and a comfortable fit. Some examples include polycarbonate glasses or goggles, plastic safety glasses, face shields, and welding helmets. Specifically, welders should use a helmet with a lens that blocks UV light to avoid UV keratitis. It is important to notice that people with one eye are especially vulnerable to potentially blinding injuries, and should pay special attention to protecting their eyes. In these cases, protective eyewear can ensure some degree of safety while also allowing people to participate in their normal day-to-day activities.Ensuring both a proper contact lens fit and the compliance of the person with care measures can prevent contact lens-related complications. As it has been stated previously, these can cause both mechanic damage to the cornea and be a risk factor for the development of microbial keratitis. Thus, an emphasis should be placed on reducing lens contamination by using effective disinfecting solutions, as well as antimicrobial contact lenses and cases. It is important to avoid swimming with contact lenses, because this increases the frequency of bacterial infections, primarily from Staphylococcus epidermidis and other organisms found in contaminated water. Finally, people who use contact lenses can also avoid both mechanical and infectious trauma by not using contacts beyond the length of their intended use.

Treatment
The treatment of corneal abrasions aims to prevent bacterial superinfection, speed healing, and provide symptomatic relief. If a foreign body is found, it needs to be removed.

Foreign body
Positioning: The person is laid in a comfortable position with the affected eye closest to the physician. Loupes can be used if available and the eye can be illuminated with a medical light or, alternatively, with an ophtalmoscope held in the non-dominant hand. The person is then asked to focus on a particular point on the ceiling so that the foreign body sits as centrally between the eyelids as possible. This accounts for a more sterile procedure by keeping the eyelashes as far as possible, and reduces the chance of eliciting a blink reflex. If necessary, the eyelids can be kept open using an eyelid speculum, the examiners fingertips, a cotton tip or an assistant.
Anaesthetic and pupil dilator: Local anaesthetic is instilled into both eyes in order to reduce blepharospasm. Topical oxybuprocaine 0.4% is the preferred choice as it has an onset of action of 20 seconds and a half-life of 20 minutes. A drop of topical pupil dilator such a cyclopentolate 1%, if available, can be helpful to reduce ciliary spasm after removal of the foreign body. Atropine is generally avoided due to its long-lasting mydriatic effects.
Removal techniques: There are mainly two types of techniques, the choice of which will depend on the nature of the foreign body. The first technique is the cotton tip removal, which is indicated in superficial foreign bodies with no surrounding corneal reaction, and the second is the hypodermic needle or nº15 blade removal with which the complete foreign body and any surrounding rust ring can be removed.
Irrigation of the ocular surface and upper and lower fornices can be performed after the procedure to wash out any residual loose foreign body material. A 10 mL ampoule of sterile saline is usually sufficient.

Medications
Current recommendations stress the need to use topical and/or oral analgesia and topical antibiotics. One review has found that eye drops to numb the surface of the eye such as tetracaine improve pain; however, their safety is unclear. Another review did not find evidence of benefit and concluded there was not enough data on safety. Topical nonsteroidal anti-inflammatory drugs (NSAIDs) are useful to reduce the pain caused by corneal abrasions </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 Pneumoconiosis and can you explain it in depth? [/INST] Pneumoconiosis is the general term for a class of interstitial lung diseases where inhalation of dust has caused interstitial fibrosis. The three most common types are asbestosis, silicosis, and coal miners lung. Pneumoconiosis often causes restrictive impairment, although diagnosable pneumoconiosis can occur without measurable impairment of lung function. Depending on extent and severity, it may cause death within months or years, or it may never produce symptoms. It is usually an occupational lung disease, typically from years of dust exposure during work in mining; textile milling; shipbuilding, ship repairing, and/or shipbreaking; sandblasting; industrial tasks; rock drilling (subways or building pilings); or agriculture. It is one of the most common occupational diseases in the world.

Types
Depending upon the type of dust, the disease is given different names:

Coalworkers pneumoconiosis (also known as coal miners lung, black lung or anthracosis) – coal, carbon
Aluminosis – Aluminium
Asbestosis – asbestos
Silicosis (also known as "grinders disease" or Potters rot) – crystalline silica dust
Bauxite fibrosis – bauxite
Berylliosis – beryllium
Siderosis – iron
Byssinosis –  Byssinosis is caused by cotton dust inhalation and typically demonstrates a different pattern of lung abnormalities than most other pneumoconiosis.
Chalicosis – fine dust from stonecutting
Silicosiderosis (also sometimes called iron miners lung) – mixed dust containing silica and iron
Labrador lung (found in miners in Labrador, Canada) – mixed dust containing iron, silica and anthophyllite, a type of asbestos
Stannosis – tin oxide
Talcosis – talc
Baritosis - a benign type of pneumoconiosis caused by barium inhalation; it typically causes little  or no overgrowth, hardening, and/or fibrosis.
Mixed-dust pneumoconiosis

Pathogenesis
The reaction of the lung to mineral dusts depends on many variables, including size, shape, solubility, and reactivity of the particles. For example, particles greater than 5 to 10 μm are unlikely to reach distal airways, whereas particles smaller than 0.5 μm move into and out of alveoli, often without substantial deposition and injury. Particles that are 1 to 5 μm in diameter are the most dangerous, because they get lodged at the bifurcation of the distal airways. Coal dust is relatively inert, and large amounts must be deposited in the lungs before lung disease is clinically detectable. Silica, asbestos, and beryllium are more reactive than coal dust, resulting in fibrotic reactions at lower concentrations. Most inhaled dust is entrapped in the mucus blanket and rapidly removed from the lung by ciliary movement. However, some of the particles become impacted at alveolar duct bifurcations, where macrophages accumulate and engulf the trapped particulates. The pulmonary alveolar macrophage is a key cellular element in the initiation and perpetuation of lung injury and fibrosis. Many particles activate the inflammasome and induce IL-1 production. The more reactive particles trigger the macrophages to release a number of products that mediate an inflammatory response and initiate fibroblast proliferation and collagen deposition. Some of the inhaled particles may reach the lymphatics either by direct drainage or within migrating macrophages and thereby initiate an immune response to components of the particulates and/or to self-proteins that are modified by the particles. This then leads to an amplification and extension of the local reaction. Tobacco smoking worsens the effects of all inhaled mineral dusts, more so with asbestos than with any other particle.

Diagnosis
Typical indications on patient assessment include:
Cough
Shortness of breath
Chest tightness
Chest X-ray may show a characteristic patchy, subpleural, bibasilar interstitial infiltrates or small cystic radiolucencies called honeycombing, particularly in advanced disease.Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplans syndrome.

Epidemiology
The prevalence as of 2021 of pneumoconiosis is around 527,500 cases, with over 60,000 new patients reported globally in 2017. Prevalence has trended somewhat downward since 2015. The mortality of pneumoconiosis patients remained at a high level in recent years, with over 21,000 deaths each year since 2015. It is likely that pneumoconiosis is under-diagnosed and under-reported, especially in countries without highly developed healthcare systems.

Treatment and Prognosis
Lung damage due to pneumoconiosis cannot be reversed. However, some steps can slow down disease progression and relieve symptoms. These include the prescription of medications and breathing treatments to open airways and reduce inflammation. Pulmonary rehabilitation and supplemental oxygen may also be recommended. A lung transplant may be needed in cases of serious diseases. If the patient smokes, smoking cessation is also important. Regular testing, such as X-rays or lung function tests, may be indicated to monitor disease progression.

Prevention
To reduce the likelihood of developing pneumoconiosis, individuals working in affected industries should wear a mask, wash skin that comes in contact with dust, remove dust from clothing and wash the face and hands before eating or drinking. In addition, governments often regulate industry, especially mines, to limit how much dust is in the air. In the United States, coal miners injured by pneumoconiosis and their families may receive monthly payments and medical benefits under the Black Lung Benefits Act.

See also
Aluminosis
Black Lung Benefits Act of 1972
Chalicosis
Philip DArcy Hart
Pneumonoultramicroscopicsilicovolcanoconiosis
Popcorn workers lung disease — diacetyl emissions and airborne dust from butter flavorings used in microwave popcorn production

References
Further reading
Cochrane, A.L.; Blythe, M. (1989). One Mans Medicine, an autobiography of Professor Archie Cochrane. London: BMJ Books. ISBN 0727902776. (Paperback ed. (2009) Cardiff University ISBN 0954088433.

External links

"Pneumoconioses". NIOSH Safety and Health Topic. Center for Disease Control. 30 March 2022.
"Black Lung Benefits Act" </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 Bartholins cyst and can you explain it in depth? [/INST] A Bartholins cyst occurs when a Bartholins gland within the labia becomes blocked. Small cysts may result in minimal or no symptoms. Larger cysts may result in swelling on one side of the vagina, as well as pain during sex or walking. If the cyst becomes infected, an abscess can occur, which is typically red and very painful. If there are no symptoms, no treatment is needed. Bartholins cysts affect about 2% of women at some point in their life. They most commonly occur during childbearing years.When the cyst becomes uncomfortable or painful, drainage is recommended. The preferred method is the insertion of a Word catheter for four weeks, as recurrence following simple incision and drainage is common. A surgical procedure known as marsupialization may be used or, if the problems persist, the entire gland may be removed. Removal is sometimes recommended in those older than 40 to ensure cancer is not present. Antibiotics are not generally needed to treat a Bartholins cyst.The cause of a Bartholins cyst is unknown. An abscess results from a bacterial infection, but it is not usually a sexually transmitted infection (STI). Rarely, gonorrhea may be involved. Diagnosis is typically based on symptoms and examination. In women over the age of 40, a tissue biopsy is often recommended to rule out cancer.The cyst is named after Caspar Bartholin who accurately described the glands in 1677. The underlying mechanism of the cyst was determined in 1967 by 20th Century obstetrician Samuel Buford Word.

Signs and symptoms
Most Bartholins cysts do not cause any symptoms, although some may cause pain during walking, sitting, or sexual intercourse (dyspareunia). They are usually between 1 and 4 cm, and are located just medial to the labia minora.  Most Bartholins cysts only affect the left or the right side (unilateral). While small cysts are usually not painful, larger cysts can cause significant pain.

Pathophysiology
A Bartholins gland cyst develops when the duct that drains the gland becomes blocked. Blockage may be caused by an infection or a mucus plug. The secretions from the Bartholins gland are retained, forming a cyst.

Diagnosis
Other conditions that may present similarly include hidradenoma papilliferum, lipomas, epidermoid cysts and Skenes duct cysts, among others conditions. In women who are more than 40 years, a biopsy may be recommended to rule out cancer.

Treatment
If the Bartholins cysts is not painful or uncomfortable, treatment may not be necessary. Small, asymptomatic cysts can be observed over time to assess their development. In cases that require intervention, a catheter may be placed to drain the cyst, or the cyst may be surgically opened to create a permanent pouch (marsupialization). Intervention has a success rate of 85%, regardless of the method used, to alleviate swelling and discomfort.Catheterization is a minor procedure that can be performed locally as an outpatient procedure. A small tube with a balloon on the end (known as a Word catheter) may be inserted into the cyst. The balloon is then inflated to keep it in place. The catheter stays in place for 2 to 4 weeks, draining the fluid and causing a normal gland opening to form, after which the catheter is removed. The catheters do not generally impede normal activity, but sexual intercourse is generally abstained from while the catheter is in place.Cysts may also be opened permanently, a procedure called marsupialization, which involves opening the gland through an incision to ensure that the secretion channel remains open. If a cyst is infected, it may break open and start to heal on its own after 3 to 4 days. Nonprescription pain medication such as ibuprofen relieves pain, and a sitz bath may increase comfort and reduce pain </s>