<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 Diastasis recti and can you explain it in depth? [/INST] Diastasis recti,  or rectus abdominis diastasis, is defined as a gap of about 2.7 cm or greater between the two sides of the rectus abdominis muscle. The distance between the right and left rectus abdominis muscles is created by the stretching of the linea alba, a connective collagen sheath created by the aponeurosis insertions of the transverse abdominis, internal oblique, and external oblique. This condition has no associated morbidity or mortality.Diastasis of the rectus abdominis muscle most frequently occurs in newborns and pregnant women; however, it may occur in any adult woman or man. In the newborn, the rectus abdominis is not fully developed and may not be sealed together at midline. Diastasis recti is more common in premature newborns. In pregnant or postpartum women, the condition is caused by the stretching of the rectus abdominis by the growing uterus. It is more common in multiparous women (women who have had multiple pregnancies) owing to repeated episodes of stretching. When the defect occurs during pregnancy, the uterus can sometimes be seen bulging through the abdominal wall beneath the skin. Non-pregnant women are more susceptible to develop diastasis recti when over the age of 35 or with high birth weight of child, multiple birth pregnancy, or multiple pregnancies. Additional causes can be attributed to excessive abdominal exercises after the first trimester of pregnancy.Strength training of all the core muscles, including the abdominis recti muscle, may or may not reduce the size of the gap in pregnant or postpartum women. Crunches may increase the diastasis recti separation. All corrective exercises should be in the form of pulling in the abdominal muscles rather than pushing them outwards. In extreme cases diastasis recti is corrected with a cosmetic surgery procedure known as an abdominoplasty by creating a plication, or folding, of the linea alba and suturing it together, which results in a tighter abdominal wall.

Presentation
A diastasis recti may appear as a ridge running down the midline of the abdomen, anywhere from the xiphoid process to the umbilicus. It becomes more prominent with straining and may disappear when the abdominal muscles are relaxed. The medial borders of the right and left halves of the muscle may be palpated during contraction of the rectus abdominis. The condition can be diagnosed by physical exam, and must be differentiated from an epigastric hernia or incisional hernia, if the patient has had abdominal surgery.  Hernias may be ruled out using ultrasound.In infants, they typically result from a minor defect of the linea alba between the rectus abdominis muscles. This allows tissue from inside the abdomen to herniate anteriorly. On infants, this may manifest as an apparent bubble under the skin of the belly between the umbilicus and xiphisternum (bottom of the breastbone).Examination is performed with the subject lying on the back, knees bent at 90° with feet flat, head slightly lifted placing chin on chest. With muscles tense, the examiner then places fingers in the ridge that is presented. Measurement of the width of separation is determined by the number of fingertips that can fit within the space between the left and right rectus abdominis muscles. Separation consisting of a width of 2 fingertips (approximately 1 1/2 centimeters) or more is the determining factor for diagnosing diastasis recti.

Diagnosis
Diastasis recti can be diagnosed by physical examination, which may include measuring the distance between the rectus abdominis muscles at rest and during contraction at several levels along the linea alba.
Abdominal ultrasonography provides objective evidence for the diagnosis, and also confirms that the bulge is not a hernia.
An abdominal CT scan is an acceptable alternative to an ultrasound.

Treatment
During pregnancy - No treatment is necessary for women while they are still pregnant.
After delivery - Typically the separation of the abdominal muscles will lessen in the mother within the first 8 weeks after childbirth; however, the connective tissue remains stretched for many. The weakening of the musculature may also cause lower back pain, weakened pelvic alignment, and altered posture.
In children - Complications include development of an umbilical or ventral hernia, which is rare and can be corrected with surgery. If an infant with the condition develops vomiting, or redness or pain in the abdominal area, medical attention should be sought.

Strength training
A systematic review of the evidence found that exercise may or may not reduce the size of the gap in pregnant or postpartum women. The authors looked at 8 studies totaling 336 women and concluded: "Due to the low number and quality of included articles, there is insufficient evidence to recommend that exercise may help to prevent or reduce DRAM," or diastasis of the rectus abdominis muscles, also stating that "non-specific exercise may or may not help to prevent or reduce DRAM during the ante- and postnatal periods."However, a study conducted by the Columbia University Program in Physical Therapy stated: "Ninety percent of non‐exercising pregnant women exhibited DRA while only 12.5% of exercising women had the condition. The mean DRA located 4.5 cm above the umbilicus was 9.6 mm (± 6.6) for the exercise group and 38.9 mm (± 17.8) for the non‐exercise group. The mean DRA located at the umbilicus was 11.4 mm (± 3.82) for the exercise group and 59.5 mm (± 23.6) for the non‐exercise group. The mean DRA located 4.5 cm below the umbilicus was 8.2 mm (± 7.4) for the exercise group and 60.4 (± 29.0) for the non‐exercise group."Nevertheless, the following exercises are often recommended to help build abdominal strength, which may or may not help reduce the size of diastasis recti:
Core contraction – In a seated position, place both hands on abdominal muscles. Take small controlled breaths. Slowly contract the abdominal muscles, pulling them straight back towards the spine. Hold the contraction for 30 seconds, while maintaining the controlled breathing. Complete 10 repetitions.
Seated squeeze - Again in a seated position, place one hand above the belly button, and the other below the belly button. With controlled breaths, with a mid-way starting point, pull the abdominals back toward the spine, hold for 2 seconds and return to the mid-way point. Complete 100 repetitions.
Head lift – In a lying down position, knees bent at 90° angle, feet flat, slowly lift the head, chin toward your chest, (concentrate on isolation of the abdominals to prevent hip-flexors from being engaged), slowly contract abdominals toward floor, hold for two seconds, lower head to starting position for 2 seconds. Complete 10 repetitions.
Upright push-up – A stand-up push-up against the wall, with feet together arms-length away from wall, place hands flat against the wall, contract abdominal muscles toward spine, lean body towards wall, with elbows bent downward close to body, pull abdominal muscles in further, with controlled breathing. Release muscles as you push back to starting position. Complete 20 repetitions.
Squat against the wall – Also known as a seated squat, stand with back against the wall, feet out in front of body, slowly lower body to a seated position so knees are bent at a 90° angle, contracting abs toward spine as you raise body back to standing position. Optionally, this exercise can also be done using an exercise ball placed against the wall and the lower back. Complete 20 repetitions.
Squat with squeeze – A variation to the "squat against the wall" is to place a small resistance ball between the knees, and squeeze the ball while lowering the body to the seated position </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 Optic neuropathy and can you explain it in depth? [/INST] Optic neuropathy is damage to the optic nerve from any cause. The optic nerve is a bundle of millions of fibers in the retina that sends visual signals to the brain. [1].
Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy. The main symptom is loss of vision, with colors appearing subtly washed out in the affected eye. A pale disc is characteristic of long-standing optic neuropathy. In many cases, only one eye is affected and patients may not be aware of the loss of color vision until the doctor asks them to cover the healthy eye.

Optic neuropathy is often called optic atrophy, to describe the loss of some or most of the fibers of the optic nerve.

Ischemic optic neuropathy
In ischemic optic neuropathies, there is insufficient blood flow (ischemia) to the optic nerve.  The anterior optic nerve is supplied by the short posterior ciliary artery and choroidal circulation, while the retrobulbar optic nerve is supplied intraorbitally by a pial plexus, which arises from the ophthalmic artery, internal carotid artery, anterior cerebral artery, and anterior communicating arteries. Ischemic optic neuropathies are classified based on the location of the damage and the cause of reduced blood flow, if known.
Anterior ischemic optic neuropathy (AION) includes diseases that affect the optic nerve head and cause swelling of the optic disc.  These diseases often cause sudden rapid visual loss in one eye.  Inflammatory diseases of the blood vessels, like giant-cell arteritis, polyarteritis nodosa, Churg–Strauss syndrome, granulomatosis with polyangiitis, and rheumatoid arthritis can cause arteritic AIONs (AAION).  The vast majority of AIONs are nonarteritic AIONs (NAION).  The most common acute optic neuropathy in patients over 50 years of age, NAION has an annual incidence of 2.3-10.2/100,000. NAION presents as a painless loss of vision, often when awakening, that occurs over hours to days.  Most patients lose the lower half of their visual field (an inferior altitudinal loss), though superior altitudinal loss is also common.  The pathophysiology of NAION is unknown, but it is related to poor circulation in the optic nerve head.  NAION is often associated with diabetes mellitus, elevated intraocular pressure (acute glaucoma, eye surgery), high cholesterol, hypercoagulable states, a drop in blood pressure (bleeding, cardiac arrest, peri-operative esp. cardiac and spine procedures), and sleep apnea.  Rarely, amiodarone, interferon-alpha, and erectile dysfunction drugs have been associated with this disease.
Posterior ischemic optic neuropathy is a syndrome of sudden visual loss with optic neuropathy without initial disc swelling with subsequent development of optic atrophy.  This can occur in patients who are predisposed to AAION and NAION as described above as well as those who had cardiac and spine surgery or serious episodes of hypotension.
Radiation optic neuropathy (RON) is also thought to be due to ischemia of the optic nerve that occurs 3 months to 8 or more years after radiation therapy to the brain and orbit.  It occurs most often around 1.5 years after treatment and results in irreversible and severe vision loss, which may also be associated with damage to the retina (radiation retinopathy). This is thought to be due to damage to dividing glial and vascular endothelial cells. RON can present with transient visual loss followed by acute painless visual loss in one or both eyes several weeks later.  The risk of RON is significantly increased with radiation doses over 50 Gy.

Optic neuritis
Optic neuritis is inflammation of the optic nerve, which is associated with swelling and destruction of the myelin sheath covering the optic nerve.  Young adults, usually females, are most commonly affected. Symptoms of optic neuritis in the affected eye include pain on eye movement, sudden loss of vision, and decrease in color vision (especially reds).  Optic neuritis, when combined with the presence of multiple demyelinating white matter brain lesions on MRI, is suspicious for multiple sclerosis.
Several causes and clinical courses are possible for the optic neuritis. It can be classified in:

Single isolated optic neuritis (SION)
relapsing isolated optic neuritis (RION)
chronic relapsing inflammatory optic neuropathy (CRION)
the neuromyelitis optica (NMO) spectrum disorder
multiple sclerosis associated optic neuritis (MSON)
unclassified optic neuritis (UCON) forms.Medical examination of the optic nerve with an ophthalmoscope may reveal a swollen optic nerve, but the nerve may also appear normal.  Presence of an afferent pupillary defect, decreased color vision, and visual field loss (often central) are suggestive of optic neuritis.  Recovery of visual function is expected within 10 weeks.  However, attacks may lead to permanent axonal loss and thinning of the retinal nerve fiber layer.

Compressive optic neuropathy
Tumors, infections, and inflammatory processes can cause lesions within the orbit and, less commonly, the optic canal.  These lesions may compress the optic nerve, resulting optic disc swelling and progressive visual loss.  Implicated orbital disorders include optic gliomas, meningiomas, hemangiomas, lymphangiomas, dermoid cysts, carcinoma, lymphoma, multiple myeloma, inflammatory orbital pseudotumor, and thyroid ophthalmopathy.  Patients often have bulging out of the eye (proptosis) with mild color deficits and almost normal vision with disc swelling.

Infiltrative optic neuropathy
The optic nerve can be infiltrated by a variety of processes, including tumors, inflammation, and infections.  Tumors that can infiltrate the optic nerve can be primary (optic gliomas, capillary hemangiomas, and cavernous hemangiomas) or secondary (metastatic carcinoma, nasopharyngeal carcinoma, lymphoma, and leukemia).  The most common inflammatory disorder that infiltrates the optic nerve is sarcoidosis.  Opportunistic fungi, viruses, and bacteria may also infiltrate the optic nerve.  The optic nerve may be elevated if the infiltration occurs in the proximal portion of the nerve.  The appearance of the nerve on examination depends on the portion of the nerve that is affected.

Traumatic optic neuropathy
The optic nerve can be damaged when exposed to direct or indirect injury.  Direct optic nerve injuries are caused by trauma to the head or orbit that crosses normal tissue planes and disrupts the anatomy and function of the optic nerve; e.g., a bullet or forceps that physically injures the optic nerve.  Indirect injuries, like blunt trauma to the forehead during a motor vehicle accident, transmit force to the optic nerve without transgressing tissue planes.  This type of force causes the optic nerve to absorb excess energy at the time of impact.  The most common site of injury of the optic nerve is the intracanalicular portion of the nerve.  Deceleration injuries from motor vehicle or bicycle accidents account for 17 to 63 percent of cases.  Falls are also a common cause, and optic neuropathy most commonly occurs when there is a loss of consciousness associated with multi-system trauma and serious brain injury.  In less than three percent of patients, an orbital hemorrhage after an injection behind the eye (retrobulbar block) can cause injury to the optic nerve, but this is readily manageable if it does not involve direct optic nerve injury and is caught early.  The role of high-dose steroids and orbital decompression in treating these patients is controversial and, if administered, must be done very soon after injury with minimal effects.  In patients with an orbital fracture, vomiting or nose blowing can force air into the orbit and possibly compromise the integrity of the optic nerve.

Mitochondrial optic neuropathies
Mitochondria play a central role in maintaining the life cycle of retinal ganglion cells because of their high energy dependence.  Mitochondria are made within the central somata of the retinal ganglion cell, transported down axons, and distributed where they are needed.  Genetic mutations in mitochondrial DNA, vitamin depletion, alcohol and tobacco abuse, and use of certain drugs can cause derangements in efficient transport of mitochondria, which can cause a primary or secondary optic neuropathy.

Nutritional optic neuropathies
A nutritional optic neuropathy may be present in a patient with obvious evidence of under-nutrition (weight loss and wasting). Months of depletion are usually necessary to deplete body stores of most nutrients. Undernourished patients often have many vitamin and nutrient deficiencies and have low serum protein levels. However, the optic neuropathy associated with pernicious anemia and vitamin B12 deficiency can even be seen in well-nourished individuals. Gastric bypass surgery may also cause a vitamin B12 deficiency from poor absorption.
Patients who have nutritional optic neuropathy may notice that colors are not as vivid or bright as before and that the color red is washed out. This normally occurs in both eyes at the same time and is not associated with any eye pain. They might initially notice a blur or fog, followed by a drop in vision. While vision loss may be rapid, progression to blindness is unusual. These patients tend to have blind spots in the center of their vision with preserved peripheral vision. In most cases, the pupils continue to respond normally to light.

Toxic optic neuropathies
The most recognized cause of toxic optic neuropathy is methanol poisoning.  This can be a life-threatening event that normally accidentally occurs when the person mistook or substituted, methanol for ethyl alcohol. The patient initially has nausea and vomiting, followed by respiratory distress, headache, and visual loss 18–48 hours after consumption.  Without treatment, patients can go blind, and their pupils will dilate and stop reacting to light.

Ethylene glycol, a component of automobile antifreeze, is a poison that is toxic to the whole body including the optic nerve. Consumption can be fatal, or recovery can occur with permanent neurologic and ophthalmologic deficits. While the visual loss is not very common, increased intracranial pressure can cause bilateral optic disc swelling from cerebral edema. A clue to the cause of intoxication is the presence of oxalate crystals in the urine. Like methanol intoxication, treatment is ethanol consumption.
Ethambutol, a drug commonly used to treat tuberculosis, is notorious for causing toxic optic neuropathy.  Patients with vision loss from ethambutol toxicity lose vision in both eyes equally. This initially presents with problems with colors (dyschromatopsia) and can leave central visual deficits. If vision loss occurs while using ethambutol, it would be best to discontinue this medication under a doctors supervision. Vision can improve slowly after discontinuing ethambutol but rarely returns to baseline.
Amiodarone is an antiarrhythmic medication commonly used for abnormal heart rhythms (atrial or ventricular tachyarrhythmias). Most patients on this medication get corneal epithelial deposits, but this medication has also been controversially associated with NAION. Patients on amiodarone with new visual symptoms should be evaluated by an ophthalmologist.
Tobacco exposure, most commonly through pipe and cigar smoking, can cause optic neuropathy. Middle-aged or elderly men are often affected and present with painless, slowly progressive, color distortion and visual loss in both eyes. The mechanism is unclear, but this has been reported to be more common in individuals who are already suffering from malnutrition.

Hereditary optic neuropathies
The inherited optic neuropathies typically manifest asa  symmetric bilateral central visual loss. Optic nerve damage in most inherited optic neuropathies is permanent and progressive.

Lebers hereditary optic neuropathy (LHON) is the most frequently occurring mitochondrial disease, and this inherited form of acute or subacute vision loss predominantly affects young males </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 Peritonitis and can you explain it in depth? [/INST] Peritonitis is inflammation of the localized or generalized peritoneum, the lining of the inner wall of the abdomen and cover of the abdominal organs. Symptoms may include severe pain, swelling of the abdomen, fever, or weight loss. One part or the entire abdomen may be tender. Complications may include shock and acute respiratory distress syndrome.Causes include perforation of the intestinal tract, pancreatitis, pelvic inflammatory disease, stomach ulcer, cirrhosis, or a ruptured appendix. Risk factors include ascites (the abnormal build-up of fluid in the abdomen) and peritoneal dialysis. Diagnosis is generally based on examination, blood tests, and medical imaging.Treatment often includes antibiotics, intravenous fluids, pain medication, and surgery. Other measures may include a nasogastric tube or blood transfusion. Without treatment death may occur within a few days. About 20% of people with cirrhosis who are hospitalized have peritonitis.

Signs and symptoms
Abdominal pain
The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness, abdominal guarding, rigidity, which are exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing ones hips, or eliciting the Blumberg sign (meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place). Rigidity is highly specific for diagnosing peritonitis (specificity: 76–100%). The presence of these signs in a person is sometimes referred to as peritonism. The localization of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing visceral innervation of the visceral peritoneal layer), and may become localized later (with involvement of the somatic innervation of the parietal peritoneal layer). Peritonitis is an example of an acute abdomen.

Other symptoms
Diffuse abdominal rigidity (abdominal guarding) is often present, especially in generalized peritonitis
Fever
Sinus tachycardia
Development of ileus paralyticus (i.e., intestinal paralysis), which also causes nausea, vomiting and bloating
Reduced or no passage of abdominal gas and bowel sound

Complications
Sequestration of fluid and electrolytes, as revealed by decreased central venous pressure, may cause electrolyte disturbances, as well as significant hypovolemia, possibly leading to shock and acute kidney failure.
A peritoneal abscess may form (e.g., above or below the liver, or in the lesser omentum)
Sepsis may develop, so blood cultures should be obtained.
Complicated peritonitis typically involves multiple organs.

Causes
Infection
Perforation of part of the gastrointestinal tract is the most common cause of peritonitis. Examples include perforation of the distal esophagus (Boerhaave syndrome), of the stomach (peptic ulcer, gastric carcinoma), of the duodenum (peptic ulcer), of the remaining intestine (e.g., appendicitis, diverticulitis, Meckel diverticulum, inflammatory bowel disease (IBD), intestinal infarction, intestinal strangulation, colorectal carcinoma, meconium peritonitis), or of the gallbladder (cholecystitis). Other possible reasons for perforation include abdominal trauma, ingestion of a sharp foreign body (such as a fish bone, toothpick or glass shard), perforation by an endoscope or catheter, and anastomotic leakage. The latter occurrence is particularly difficult to diagnose early, as abdominal pain and ileus paralyticus are considered normal in people who have just undergone abdominal surgery. In most cases of perforation of a hollow viscus, mixed bacteria are isolated; the most common agents include Gram-negative bacilli (e.g., Escherichia coli) and anaerobic bacteria (e.g., Bacteroides fragilis). Fecal peritonitis results from the presence of faeces in the peritoneal cavity.  It can result from abdominal trauma and occurs if the large bowel is perforated during surgery.
Disruption of the peritoneum, even in the absence of perforation of a hollow viscus, may also cause infection simply by letting micro-organisms into the peritoneal cavity. Examples include trauma, surgical wound, continuous ambulatory peritoneal dialysis, and intra-peritoneal chemotherapy. Again, in most cases, mixed bacteria are isolated; the most common agents include cutaneous species such as Staphylococcus aureus, and coagulase-negative staphylococci, but many others are possible, including fungi such as Candida.
Spontaneous bacterial peritonitis (SBP) is a peculiar form of peritonitis occurring in the absence of an obvious source of contamination. It occurs in people with ascites, including children.
Intra-peritoneal dialysis predisposes to peritoneal infection (sometimes named "primary peritonitis" in this context).
Systemic infections (such as tuberculosis) may rarely have a peritoneal localisation.
Pelvic inflammatory disease

Non-infection
Leakage of sterile body fluids into the peritoneum, such as blood (e.g., endometriosis, blunt abdominal trauma), gastric juice (e.g., peptic ulcer, gastric carcinoma), bile (e.g., liver biopsy), urine (pelvic trauma), menstruum (e.g., salpingitis), pancreatic juice (pancreatitis), or even the contents of a ruptured dermoid cyst. It is important to note that, while these body fluids are sterile at first, they frequently become infected once they leak out of their organ, leading to infectious peritonitis within 24 to 48 hours.
Sterile abdominal surgery, under normal circumstances, causes localised or minimal generalised peritonitis, which may leave behind a foreign body reaction or fibrotic adhesions. However, peritonitis may also be caused by the rare case of a sterile foreign body inadvertently left in the abdomen after surgery (e.g., gauze, sponge).
Much rarer non-infectious causes may include familial Mediterranean fever, TNF receptor associated periodic syndrome, porphyria, and systemic lupus erythematosus.

Risk factors
Previous history of peritonitis
History of alcoholism
Liver disease
Fluid accumulation in the abdomen
Weakened immune system
Pelvic inflammatory disease

Diagnosis
A diagnosis of peritonitis is based primarily on the clinical manifestations described above. Rigidity (involuntary contraction of the abdominal muscles) is the most specific exam finding for diagnosing peritonitis. If focal peritonitis is detected, further work-up should be done. If diffuse peritonitis is detected, then urgent surgical consultation should be obtained, and may warrant surgery without further investigations. Leukocytosis, hypokalemia, hypernatremia, and acidosis may be present, but they are not specific findings. Abdominal X-rays may reveal dilated, edematous intestines, although such X-rays are mainly useful to look for pneumoperitoneum, an indicator of gastrointestinal perforation. The role of whole-abdomen ultrasound examination is under study and is likely to expand in the future. Computed tomography (CT or CAT scanning) may be useful in differentiating causes of abdominal pain. If reasonable doubt still persists, an exploratory peritoneal lavage or laparoscopy may be performed. In people with ascites, a diagnosis of peritonitis is made via paracentesis (abdominal tap): More than 250 polymorphonuclear cells per μL is considered diagnostic. In addition, Gram stain is almost always negative, whereas culture of the peritoneal fluid can determine the microorganism responsible and determine their sensitivity to antimicrobial agents.

Pathology
In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2–4 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in people who are dehydrated, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera </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 Ainhum and can you explain it in depth? [/INST] Ainhum (from Portuguese, pronounced /aj.ˈɲũ/), also known as dactylolysis spontanea, is a painful constriction of the base of the fifth toe frequently followed by bilateral spontaneous autoamputation a few years later.

Signs and symptoms
The groove begins on the lower and internal side of the base of the fifth toe, usually according to the plantar-digital fold. The groove becomes gradually deeper and more circular. The rate of spread is variable, and the disease may progress to a full circle in a few months, or still be incomplete after years. In about 75 percent of cases both feet are affected, though not usually to the same degree. There is no case reported where it begins in any other toe than the fifth, while there is occasionally a groove on the fourth or third toe. The distal part of the toe swells and appears like a small potato. The swelling is due to lymphatic edema distal to the constriction. After a time crusts can appear in the groove which can be infected with staphylococcus.
While the groove becomes deeper, compression of tendons, vessels and nerves occurs. Bone is absorbed by pressure, without any evidence of infection. After a certain time all structures distal the stricture are reduced to an avascular cord. The toe’s connection to the foot becomes increasingly slender, and if it is not amputated, it spontaneously drops off without any bleeding. Normally it takes about five years for an autoamputation to occur.
Cole describes four stages of ainhum:

Pain is present in about 78% of cases. Slight pain is present in the earliest stage of ainhum, caused by pressure on the underlying nerves. Fracture of the phalanx or chronic sepsis is accompanied with severe pain.

Cause
The true cause of ainhum remains unclear. It is not due to infection by parasites, fungi, bacteria or virus, and it is not related to injury. Walking barefoot in childhood had been linked to this disease, but ainhum also occurs in patients who have never gone barefoot. Race seems to be one of the most predisposing factors and it may have a genetic component, since it has been reported to occur within families. Dent et al. discussed a genetically caused abnormality of the blood supply to the foot. It has been related to inadequate posterior tibial artery circulation and absence of plantar arch.

Diagnosis
Histolopathology
Histology shows a change in the prickle cell layer, and this is responsible for the laying down of condensed keratin causing the groove. The junctional tissue is reduced to a slender fibrous thread, almost avascular, and all the tissues beyond the constricting band is repressed by a fibro-fatty mass covered by hyperkeratotic integument.

Imaging
Soft tissue constriction on the medial aspect of the fifth toe is the most frequently presented radiological sign in the early stages. Distal swelling of the toe is considered to be a feature of the disease. In grade III lesions osteolysis is seen in the region of the proximal interphalangeal joint with a characteristic tapering effect. Dispersal of the head of the proximal phalanx is frequently seen. Finally, after autoamputation, the base of the proximal phalanx remains. Radiological examination allows early diagnosis and staging of ainhum. Early diagnosis is crucial to prevent amputation.
Doppler shows decreased blood flow in posterior tibial artery.

Differential diagnosis
Ainhum is an acquired and progressive condition, and thus differs from congenital annular constrictions. Ainhum has been much confused with similar constrictions caused by other diseases such as leprosy, diabetic gangrene, syringomyelia, scleroderma or Vohwinkel syndrome. In this case, it is called pseudo-ainhum, treatable with minor surgery or intralesional corticosteroids, as with ainhum. It has even been seen in psoriasis or it is acquired by the wrapping toes, penis or nipple with hairs, threads or fibers. Oral retinoids, such as tretinoin, and antifibrotic agents like tranilast have been tested for pseudo-ainhum. Impending amputation in Vohwinkel syndrome can sometimes be aborted by therapy with oral etretinate. It is rarely seen in the United States but often discussed in the international medical literature.

Prevention
Wearing shoes to protect barefoot trauma has shown decrease in incidence in ainhum. Congenital pseudoainhum cannot be prevented and can lead to serious birth defects.

Treatment
Incisions across the groove turned out to be ineffective. Excision of the groove followed by z-plasty could relieve pain and prevent autoamputation in Grade I and Grade II lesions. Grade III lesions are treated with disarticulating the metatarsophalangeal joint. This also relieves pain, and all patients have a useful and stable foot. Intralesional injection of corticosteroids is also helpful.

Epidemiology
Ainhum predominantly affects black people, living in West Africa, South America and India. In Nigeria it is a common disease with an incidence of 1.7 per thousand. In tropical and subtropical climates, its incidence has been reported as between 0.015 percent and 2.0 percent of the population </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 Paget–Schroetter disease and can you explain it in depth? [/INST] Paget–Schroetter disease (also known as venous thoracic outlet syndrome) is a form of upper extremity deep vein thrombosis (DVT), a medical condition in which blood clots form in the deep veins of the arms. These DVTs typically occur in the axillary and/or subclavian veins.

Signs and symptoms
The condition is relatively rare </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 Flashing 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 Alcohol abuse and can you explain it in depth? [/INST] Alcohol abuse encompasses a spectrum of unhealthy alcohol drinking behaviors, ranging from binge drinking to alcohol dependence, in extreme cases resulting in health problems for individuals and large scale social problems such as alcohol-related crimes.
Alcohol abuse was a psychiatric diagnosis in the DSM-IV, and has been merged with alcohol dependence into alcohol use disorder in the DSM-5.Globally, excessive alcohol consumption is the seventh leading risk factor for both death and the burden of disease and injury. In short, except for tobacco, alcohol accounts for a higher burden of disease than any other drug. Alcohol use is a major cause of preventable liver disease worldwide, and alcoholic liver disease is the main alcohol-related chronic medical illness. Millions of people of all ages, from adolescents to the elderly, engage in unhealthy drinking. Alcohol use disorder can affect people from all walks of life. There are many factors that play a role in causing someone to have an alcohol use disorder: genetics, psychiatric conditions, trauma, environmental issues, and even parental drinking habits.

Definitions
Risky drinking (also called hazardous drinking) is defined by drinking above the recommended limits:

greater than 14 standard drinks units per week or greater than 4 standard drinks on a single occasion in men
greater than 7 standard drinks units per week or greater than 3 standard drinks on a single occasion in women
any drinking in pregnant women or persons < 21 years oldBinge drinking is a pattern of alcohol consumption that brings blood alcohol concentration ≥ 0.08%, usually corresponding to

≥ 5 standard drinks on a single occasion in men
≥ 4 standard drinks on a single occasion in womenIn the DSM-IV, alcohol abuse and alcohol dependence were defined as distinct disorders from 1994 to 2013. The DSM-5 combined those two disorders into alcohol use disorder with sub-classifications of severity. The DSM-IV definition is no longer used. There is no "alcoholism" diagnosis in medical care.
Alcohol misuse is a term used by United States Preventive Services Task Force to describe a spectrum of drinking behaviors that encompass risky drinking, alcohol abuse, and alcohol dependence (similar meaning to alcohol use disorder but not a term used in DSM).

Signs and symptoms
Individuals with an alcohol use disorder will often complain of difficulty with interpersonal relationships, problems at work or school, and legal problems. Additionally, people may complain of irritability and insomnia. Alcohol abuse is also an important cause of chronic fatigue.
Signs of alcohol abuse are related to alcohols effects on organ systems. However, while these findings are often present, they are not necessary to make a diagnosis of alcohol abuse. Signs of alcohol abuse show its drastic effects on the central nervous system, including inebriation and poor judgment; chronic anxiety, irritability, and insomnia. Alcohols effects on the liver include elevated liver function tests (classically AST is at least twice as high as ALT). Prolonged use leads to cirrhosis and liver failure. With cirrhosis, patients develop an inability to process hormones and toxins. The skin of a patient with alcoholic cirrhosis can feature spider angiomas, palmar erythema and — in acute liver failure — jaundice and ascites. The derangements of the endocrine system lead to the enlargement of the male breasts. The inability to process toxins leads to liver disease, such as hepatic encephalopathy.Alcohol abuse can result in brain damage which causes impairments in executive functioning such as impairments to working memory and visuospatial function, and can cause an abnormal personality as well as affective disorders to develop. Binge drinking is associated with individuals reporting fair to poor health compared to non-binge drinking individuals and which may progressively worsen over time. Alcohol also causes impairment in a persons critical thinking. A persons ability to reason in stressful situations is compromised, and they seem very inattentive to what is going on around them. Social skills are significantly impaired in people who have alcoholism due to the neurotoxic effects of alcohol on the brain, especially the prefrontal cortex area of the brain. The prefrontal cortex is responsible for cognitive functions such as working memory, impulse control and decision making.  This region of the brain is vulnerable to chronic alcohol-induced oxidative DNA damage.  The social skills that are impaired by alcohol abuse include impairments in perceiving facial emotions, difficulty with perceiving vocal emotions and theory of mind deficits; the ability to understand humour is also impaired in alcohol abusers. Adolescent binge drinkers are most sensitive to damaging neurocognitive functions especially executive functions and memory. People who abuse alcohol are less likely to survive critical illness with a higher risk for having sepsis and were more likely to die during hospitalization.A smaller volume of consumed alcohol has a greater impact on the older adult than it does on a younger individual. As a result, the American Geriatrics Society recommends for an older adult with no known risk factors less than one drink a day or fewer than two drinks per occasion regardless of gender.

Violence
Alcohol abuse is significantly associated with suicide and violence. Alcohol is the most significant health concern in Native American communities because of very high rates of alcohol dependence and abuse; up to 80 percent of suicides and 60 percent of violent acts are a result of alcohol abuse in Native American communities.In the United States alcohol-related violence is related to more severe injuries and chronic cases.

Pregnancy
Alcohol abuse among pregnant women causes their baby to develop fetal alcohol syndrome. Fetal alcohol syndrome is the pattern of physical abnormalities and the impairment of mental development which is seen with increasing frequency among children with alcoholic mothers. Alcohol exposure in a developing fetus can result in slowed development of the fetal brain, resulting in severe retardation or death. Surviving infants may have severe abnormalities such as abnormal eyes, fissures, lips and incomplete cerebella. Some infants may develop lung disease. It is even possible that the baby throughout pregnancy will develop heart defects such as ventricular septal defect or atrial septal defect. Experts suggest that pregnant women take no more than one unit of alcohol per day. However, other organizations advise complete abstinence from alcohol while pregnant.

Adolescence
Adolescence and the onset of puberty have both a physiological and social impact on a developing person. About half of grade 12 students have been drunk, and a third binge drink. About 3% drink every day. One of these social impacts is the increase in risk-taking behaviors, such as the emergence of alcohol use. Children aged 16 and under who consume alcohol heavily display symptoms of conduct disorder. Its symptoms include troublesome behaviour in school, constantly lying, learning disabilities and social impairments.Alcohol abuse during adolescence greatly increases the risk of developing an alcohol use disorder in adulthood due to changes to neurocircuitry that alcohol abuse causes in the vulnerable adolescent brain. Younger ages of initial consumption among males in recent studies has shown to be associated with increased rates of alcohol abuse within the general population.Societal inequalities (among other factors) have influenced an adolescents decision to consume alcohol. One study suggests that girls were scrutinized for "drinking like men", whereas magazines that target the male population sent underlying messages to boys and or men that drinking alcohol was "masculine". (Bogren, 2010)

Causes
The cause of alcohol abuse is complex. Alcohol abuse is related to economic and biological origins and is associated with adverse health consequences. Peer pressure influences individuals to abuse alcohol; however, most of the influence of peers is due to inaccurate perceptions of the risks of alcohol abuse. According to Gelder, Mayou and Geddes (2005)  easy accessibility of alcohol is one of the reasons people engage in alcohol abuse as this substance is easily obtained in shops. Another influencing factor among adolescents and college students are the perceptions of social norms for drinking; people will often drink more to keep up with their peers, as they believe their peers drink more than they actually do. They might also expect to drink more given the context (e.g. sporting event, house party, etc.). This perception of norms results in higher alcohol consumption than is normal.
Alcohol abuse is also associated with acculturation, because social and cultural factors such as an ethnic groups norms and attitudes can influence alcohol abuse.

Mental illness
A person misusing alcohol may be doing so because they find alcohols effects provide relief from a psychological problem, such as anxiety or depression. Often both the alcohol misuse and psychological problems need to be treated at the same time.The numbing effects of alcohol and narcotics can become a coping strategy for traumatized people who are unable to dissociate themselves from the trauma. However, the altered or intoxicated state of the abuser prevents the full consciousness necessary for healing.

Puberty
Gender differences may affect drinking patterns and the risk for developing alcohol use disorders. Sensation-seeking behaviors have been previously shown to be associated with advanced pubertal maturation, as well as the company of deviant peers. Early pubertal maturation, as indicated by advanced morphological and hormonal development, has been linked to increased alcohol usage in both male and female individuals. Additionally, when controlling for age, this association between advanced development and alcohol use still held true.

Mechanisms
Excessive alcohol use causes neuroinflammation and leads to myelin disruptions and white matter loss. The developing adolescent brain is at increased risk of brain damage and other long-lasting alterations to the brain. Adolescents with an alcohol use disorder damage the hippocampal, prefrontal cortex, and temporal lobes.  Chronic alcohol exposure can result in increased DNA damage in the brain, as well as reduced  DNA repair and increased neuronal cell death.  Alcohol metabolism generates genotoxic acetaldehyde and reactive oxygen species.Until recently, the underlying mechanisms mediating the link between pubertal maturation and increased alcohol use in adolescence was poorly understood. Now research has suggested that sex steroid hormone levels may play a role in this interaction. When controlling for age, it was demonstrated that elevated estradiol and testosterone levels in male teenagers undergoing pubertal development was linked to increased alcohol consumption. It has been suggested that sex hormones promote alcohol consumption behaviors in teens by stimulating areas in the male adolescent brain associated with reward processing. The same associations with hormone levels were not demonstrated in females undergoing pubertal development. It is hypothesized that sex steroid hormones, such as testosterone and estradiol, are stimulating areas in the male brain that function to promote sensation-seeking and status-seeking behaviors and result in increased alcohol usage.Additionally, the enzyme TTTan aromatase, which functions in the male brain to convert testosterone to estradiols, has been linked to addictive and reward-seeking behaviors. Therefore, the increased activity of the enzyme may be influencing male adolescent alcohol-usage behaviors during pubertal development. The underlying mechanisms for female alcohol consumption and abuse is still under examination, but is believed to be largely influenced by morphological, rather than hormonal, changes during puberty as well as the presence of deviant peer groups.The brain goes through dynamic changes during adolescence as a result of advancing pubertal maturation, and alcohol can damage long- and short-term growth processes in teenagers. The rapid effect of drugs releases the neurotransmitter dopamine which acts as reinforcement for the behavior.Alcohol is the most recreationally used drug internationally, throughout history it has played a variety of roles, from medicine to a mood enhancer. Alcoholism and alcohol abuse however have undergone rigorous examination as a disease which has pervasive physiological and biosocial implications. The genesis and maintenance of the disease involves the mind, body, society and culture. A common anthropological approach to understanding alcoholism is one which relates to a social factor, and this is cross-cultural studies. The description and analysis of the degree of possibilities in drinking and its results among various populations indeed constitutes one of anthropologys major contributions to the field of alcohol studies. Understanding interactions between factors and evaluating ideas regarding how alcohol usage correlates to other cultural elements requires a number of cross-cultural comparisons. Anthropologists have analyzed a large global sample of cultures examining the association between particular traits for each which relate to the cultural components of alcoholism, these include significant measures which emphasize the social system, reliance and anxiety and strength as physical and social measures. These are the primary drivers of consuming alcohol affecting individuals on a psychosocial level.Individualistic cultures such as the United States or Australia are amongst some of the highest consumers of alcohol in the whole world, however this rate of consumption does not necessarily coincide with the rate of abuse as countries like Russia which are highly collectivist see the highest rates of Alcoholism. Research suggests that people who score highly on individualism, a trait commonly fostered by the culture, report a lower rate of alcohol abuse and alcohol related disorders so much so that the association was negative, however a higher average consumption of alcohol per week. It is implied that individuals will drink more in a given setting, or on average because they are less receptive towards negative social attitudes surrounding excessive consumption. This however acts on another component, by where individualism protects from maladaptive consumption by lowering the need to drink socially. The final axis by which individualism protects from abusive consumption is that it promotes higher degrees of individualization and achievement values which promote personally suited rewards, this allow the individual to be more cognizant of potential alcohol abuse, and therefore protect from damaging mentalities in those who already identify as drinkers.Alcohol abuse also has a variety of biosocial implications, such as the physiologically effects of a detox, how the detox period interacts with ones social life and how these interactions can make beating alcoholism a complex, difficult process. Alcohol abuse can lead to a number of physical issues and may even create a mental health condition, leading to a double classification for the alcoholic. The stress, the social perceptions of these issues may reinforce abusive drinking habits. Alcoholism is the most severe form of alcohol dependence and abuse, it is often in fact a complicated hereditary disease. While it can run it families this is only a correlation and does not prove that the inherited factors play a role. Genetic influences on its genesis are suggested by numerous different sources of evidence. Alcoholism among adopted people has a stronger correlation with their biological parents than with their adopted parents, according to adoption research. Alcohol especially has a large effect on young and developing brains and chances of further abuse, the culture surrounding the acceptable age of drinking therefore can be a biosocial factor. This however isnt always preventable, alcohol when consumed during pregnancy is profoundly damaging. The umbilical cord allows the mothers blood alcohol to reach the infant. Consumption of alcohol during pregnancy can result in miscarriage, and a number of physical and cognitive that can last a lifetime to the child. Therefore the biological implications of alcohol abuse are also further reaching than just the physical issues experienced by the consumer.

Diagnosis
DSM-IV
Alcohol abuse was defined in the DSM-IV as a maladaptive pattern of drinking. For its diagnosis, at least one of the following criteria had to be fulfilled in the last 12 months:

Recurrent use of alcohol resulting in a failure to fulfill major role obligations at work, school, or home
Recurrent alcohol use in situations in which it is physically hazardous
Recurrent alcohol-related legal problems
Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol

DSM-5
The alcohol abuse diagnosis is no longer used in the DSM-5 (released in 2013), it is now part of the alcohol use disorder diagnosis. Of the four alcohol abuse criteria, all except the one referring to alcohol-related legal problems are included in the alcohol use disorder criteria.

Screening
The Alcohol Use Disorders Identification Test (AUDIT) is considered the most accurate alcohol screening tool for identifying potential alcohol misuse, including dependence. It was developed by the World Health Organisation, designed initially for use in primary healthcare settings with supporting guidance.

Prevention
Preventing or reducing the harm has been called for via increased taxation of alcohol, stricter regulation of alcohol advertising, and the provision of brief Interventions. Brief Interventions for alcohol abuse reduce the incidence of unsafe sex, sexual violence, unplanned pregnancy, and, likely, STD transmission. Information and education on social norms and the harms associated with alcohol abuse delivered via the internet or face-to-face has not been found to result in any meaningful benefit in changing harmful drinking behaviours in young people.According to European law, individuals who are suffering from alcohol abuse or other related problems cannot be given a drivers license, or if in possession of a license cannot get it renewed. This is a way to prevent individuals driving under the influence of alcohol, but does not prevent alcohol abuse per se.An individuals need for alcohol can depend on their familys alcohol use history. For instance, if it is discovered that their family history with alcohol has a strong pattern, there might be a need for education to be set in place to reduce the likelihood of reoccurrence (Powers, 2007). However, studies have established that those with alcohol abuse tend to have family members who try to provide help. On many of these occasions, the family members would try to help the individual to change or to help improve the individuals lifestyle.

Treatment
Youth treatment and intervention should focus on eliminating or reducing the effects of adverse childhood experiences, like childhood maltreatment, since these are common risk factors contributing to the early development of alcohol abuse.  Approaches like contingency management and motivational interviewing have shown to be effective means of treating substance abuse in impulsive adolescents by focusing on positive rewards and redirecting them towards healthier goals. Educating youth about what is considered heavy drinking along with helping them focus on their own drinking behaviors has been shown to effectively change their perceptions of drinking and could potentially help them to avoid alcohol abuse.
Completely stopping the use of alcohol, or "abstinence", is the ideal goal of treatment. The motivation required to achieve abstinence is dynamic; family, friends and health practitioners play a role in affecting this motivation.Some people who abuse alcohol may be able to reduce the amount they drink, also called "drinking in moderation". If this method does not work, the person may need to try abstinence. Abstinence has been regularly achieved by many alcoholics in Alcoholics Anonymous.Mindfulness-based intervention programs (that encourage people to be aware of their own experiences in the present moment and of emotions that arise from thoughts) can reduce the consumption of alcohol.A major barrier to seeking treatment for those struggling with alcohol abuse is the stigma associated with alcohol abuse itself.  Those who struggle with alcohol abuse are less likely to utilize substance (or alcohol) abuse treatment services when they perceived higher stigma with alcohol abuse.  The stigmatization of individuals who abuse alcohol has been linked to increased levels of depression, increased levels of anxiety, decreased levels of self-esteem, and poor sleeping habits. While negative thoughts and views around the subject of alcohol abuse can keep those struggling with this issue from seeking the treatment they need, there have been several things that have been found to reduce this stigma. Social support can be an effective tool for counteracting the harmful effects of stigma and shame on those struggling with alcohol abuse. Social support can help push those struggling with alcohol abuse to overcome the negative connotation associated with their struggle and finally seek the treatment that they need.

Prognosis
Alcohol abuse during adolescence, especially early adolescence (i.e. before age 15), may lead to long-term changes in the brain which leaves them at increased risk of alcoholism in later years; genetic factors also influence age of onset of alcohol abuse and risk of alcoholism. For example, about 40 percent of those who begin drinking alcohol before age 15 develop alcohol dependence in later life, whereas only 10 percent of those who did not begin drinking until 20 years or older developed an alcohol problem in later life. It is not entirely clear whether this association is causal, and some researchers have been known to disagree with this view.Alcohol use disorders often cause a wide range of cognitive impairments that result in significant impairment of the affected individual. If alcohol-induced neurotoxicity has occurred a period of abstinence for on average a year is required for the cognitive deficits of alcohol abuse to reverse.College/university students who are heavy binge drinkers (three or more times in the past two weeks) are 19 times more likely to be diagnosed with alcohol dependence, and 13 times more likely to be diagnosed with alcohol abuse compared to non-heavy episodic drinkers, though the direction of causality remains unclear. Occasional binge drinkers (one or two times in the past two weeks), were found to be four times more likely to be diagnosed with alcohol abuse or dependence compared to non-heavy episodic drinkers.

Epidemiology
Alcohol abuse is said to be most common in people aged between 15 and 24 years, according to Moreira 2009. However, this particular study of 7275 college students in England collected no comparative data from other age groups or countries.
Causes of alcohol abuse are complex and are likely the combination of many factors, from coping with stress to childhood development. The US Department of Health & Human Services identifies several factors influencing adolescent alcohol use, such as risk-taking, expectancies, sensitivity and tolerance, personality and psychiatric comorbidity, hereditary factors, and environmental aspects.Studies show that child maltreatment such as neglect, physical, and/or sexual abuse, as well as having parents with alcohol abuse problems, increases the likelihood of that child developing alcohol use disorders later in life. According to Shin, Edwards, Heeren, & Amodeo (2009), underage drinking is more prevalent among teens that experienced multiple types of childhood maltreatment regardless of parental alcohol abuse, putting them at a greater risk for alcohol use disorders. Genetic and environmental factors play a role in the development of alcohol use disorders, depending on age. The influence of genetic risk factors in developing alcohol use disorders increase with age ranging from 28% in adolescence and 58% in adults.

Societal and economic costs
Alcohol abuse is associated with many accidents, fights, and offences, including criminal. Alcohol is responsible in the world for 1.8 million deaths and results in disability in approximately 58.3 million people. Approximately 40 percent of the 58.3 million people disabled through alcohol abuse are disabled due to alcohol-related neuropsychiatric disorders. Alcohol abuse is highly associated with adolescent suicide. Adolescents who abuse alcohol are 17 times more likely to commit suicide than adolescents who dont drink. Additionally, alcohol abuse increases the risk of individuals either experiencing or perpetrating sexual violence. Alcohol availability and consumption  rates and alcohol rates are positively associated with violent crimes, through specifics differ between particular countries and cultures.

By country
According to studies of present and former alcoholic drinkers in Canada, 20% of them are aware that their drinking has negatively impacted their lives in various vital areas including finances, work and relationships.Problems caused by alcohol abuse in Ireland cost about 3.7 billion euro in 2007.In South Africa, where HIV infection is epidemic, alcohol abusers exposed themselves to double the risk of this infection.The introduction of alcopops, sweet and pleasantly flavoured alcoholic drinks, was responsible for half of the increase in alcohol abuse in 15- and 16-year-olds, according to one survey in Sweden. In the case of girls, the alcopops, which disguise the taste of alcohol, were responsible for two thirds of the increase. The introduction of alcopops to Sweden was a result of Sweden joining the European Union and adopting the entire European Union law.Alcohol misuse costs the United Kingdoms National Health Service £3 billion per year. The cost to employers is 6.4 billion pounds sterling per year </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 White dot syndromes and can you explain it in depth? [/INST] White dot syndromes are inflammatory diseases characterized by the presence of white dots on the fundus, the interior surface of the eye.  The majority of individuals affected with white dot syndromes are younger than fifty years of age. Some symptoms include blurred vision and visual field loss. There are many theories for the etiology of white dot syndromes including infectious, viral, genetics and autoimmune.
Classically recognized white dot syndromes include:
Acute posterior multifocal placoid pigment epitheliopathy
Birdshot chorioretinopathy
Multiple evanescent white dot syndrome
Acute zonal occult outer retinopathy
Multifocal choroiditis and panuveitis
Punctate inner choroiditis
Serpiginous choroiditis

Specific white dot syndromes
Specific characteristics regarding the white dots and predicted etiology are presented of selected diseases.

Acute posterior multifocal placoid pigment epitheliopathy
Acute posterior multifocal placoid pigment epitheliopathy primarily occurs in adults (with a mean age of 27).  Symptoms include blurred vision in both eyes, but the onset may occur at a different time in each eye. There are yellow-white placoid lesions in the posterior pole at the level of the retinal pigment epithelium. Some suggest a genetic predisposition to the disease, while others postulate an abnormal immune response to a virus.

Birdshot choroidopathy
Multiple evanescent white dot syndrome
Multiple evanescent white dot syndrome occurs mostly in females. Symptoms include a sudden loss of central vision, but patients eventually regain normal vision. The white dots are small and located in the posterior pole at the level of the retinal pigment epithelium. The white dots may disappear after the first few weeks of the disease. The cause is generally unknown, but a viral illness has been reported prior to multiple evanescent white dot syndrom in one-third of cases. Since the disease occurs primarily in females, hormonal status might be a contributing factor.

Acute zonal occult outer retinopathy
Some discrepancy exists as to whether acute zonal occult outer retinopathy is considered a white dot syndrome. However, it may definitely be related to other diseases included in the white dot syndrome group. Acute zonal occult outer retinopathy occurs in young to middle age adults and may eventually progress to retinal cell death.  Symptoms include acute visual field loss and photopsias. Suspected causes include autoimmune, viral, and fungal.

Multifocal choroiditis and panuveitis
Multifocal choroiditis occurs mainly in myopic females. The fundus presents with yellow or gray lesions (white dots) at the level of the choroid and retinal pigment epithelium. The size of the white dots are between 50 and 500 micrometres and localized in the macula. The disease is characterized by vitritis and anterior chamber inflammation. Decreased vision due to vitreous inflammation may occur. Unlike multiple evanescent white dot syndrome, multifocal choroiditis is a chronic disorder and macular scarring contributes to severe visual loss. Theories regarding the cause include an exogenous pathogen sensitizing an individual to antigens within photoreceptors, retinal pigment epithelium, or choroid.

Punctate inner choroiditis
Punctate inner choroiditis is an inflammatory choroiditis which occurs mainly in young females. Symptoms include blurred vision and scotomas.  Gray-white or yellow lesions are mainly present in the posterior pole and are between 100 and 300 micrometres in size. Punctate inner choroiditis is one of the so-called White dot syndromes which come under the heading posterior uveitis. The appearance of punctate (punched out) areas is at the level of the inner choroid. These lesions are typically located centrally at the back of the eye, or the posterior pole.

Serpiginous choroiditis
Serpiginous choroiditis, also known as geographic or helicoid choroidopathy, is an uncommon chronic progressive inflammatory condition affecting adult men and women equally in the second to seventh decades of life.

Nature of white dots
The white dots of the white dot syndromes are lesions that vary in their location in the fundus and in most cases tend to disappear. White dots appear early in the disease stages of punctate inner choroiditis and multiple evanescent white dot syndrome. In this case, the white dot is localized in the posterior pole, small (between 25 and 100 μm), and do not clump together. In contrast, white dots appear later in the disease stages of birdshot choroidopathy, serpiginous choroiditis, and acute posterior multifocal placoid pigment epitheliopathy. The white dots in these diseases may be present throughout the entire fundus, larger (50 to 500 μm), and tend to clump together. Among all these syndromes, there exists some retinal vessel inflammation. The differences in the dots are usually in the size, position, and depth of the lesion within the choroid.The way in which the dots form in some of the white dot syndromes has been reported. The dot appears as a small granuloma which is composed of lymphocytes and macrophages. The lesion may occur within the choroid, between Bruchs membrane and retinal pigment epithelium, or between the retinal pigment epithelium and photoreceptors.  Despite the differences in location, the white dots all are of similar composition. The center of the lesion consists of macrophages and epithelioid cells. CD4+ T cells are on the periphery of the granuloma. Benezra has theorized that a large amount of CD8+ T suppressor cells are observed in the later stages of the disease in order to down regulate the inflammatory immune reaction.The formation of a granuloma occurs when activated antigen presenting cells, specifically dendritic cells, "bind to T cells and induce…the release of pro-inflammatory cytokines and chemokines." This response attracts additional antigen presenting cells and will eventually become a granuloma. Choroidal dendritic cells span several levels within the choroid and also associate with the retinal pigment epithelium.  Usually, the dendritic cells disappear after removing the antigen. If removal did not occur, the formation of a granuloma would result. The white color of the dots when illuminated may be due to the granulomas composed only of "white cells".  Each granuloma will disappear leaving no trace of its presence but in some cases it may leave a punched out scar.  It is important to note that the formation of white dots may occur more frequently but is undetected. In normal cases, inflammation of the retina or choroid does not occur.  Muller and retinal pigment epithelium cells normally release immunosuppressive factors, but certain combinations of cytokines may stimulate retinal pigment epithelium cells to release factors encouraging inflammation.Generally, mild intraocular inflammation results in a small, discrete, evanescent lesions. Larger dots, having less discrete borders, are the result of high intensity intraocular inflammation. In essence, an immune response with the normal amount and appropriate cytokine release will result in small white dots and a misregulated response eventually will produce scarring of the retinal tissue. Treatment is required in the latter case to combat loss of vision. The white dots usually disappear naturally. Corticosteroids have been shown to speed up this process.  The differences in the immune response of each patient may contribute to the differences seen between the white dot syndromes.

Distinct diseases
Due to the number of common features among the multiple syndromes, many suggest that the white dot syndromes are not distinct and represent a spectrum of one disease. Gass described the AZOOR complex which consists of multiple evanescent white dot syndrome, nultifocal choroiditis, punctate inner choroiditis, acute idiopathic blind spot enlargement, acute macular neuroretinopathy, acute annular outer retinopathy, and acute zonal occult outer retinopathy. He suggested these diseases represent one disease due to common factors such as a high occurrence in females, unexplained visual field loss, and reduced electroretinographic amplitudes. Reddy et al. conducted a study on the blind spots in multifocal choroiditis, punctate inner choroiditis, multiple evanescent white dot syndrome, and diffuse subretinal fibrosis syndrome. Clinical and electroretinographic evidence suggested the diseases are distinct. However, numerous differences do occur in fundus appearance, the clinical course of the diseases, and electrophysiology.

Suspected etiology
One cause of the White Dot Syndromes as suggested by Gass involves viral or infectious agents </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 Paroxysmal nonkinesigenic dyskinesia 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 Trichilemmal cyst and can you explain it in depth? [/INST] A trichilemmal cyst  is a common cyst that forms from a hair follicle, most often on the scalp, and is smooth, mobile, and filled with keratin, a protein component found in hair, nails, skin, and horns. Trichilemmal cysts are clinically and histologically distinct from trichilemmal horns, hard tissue that is much rarer and not limited to the scalp. Rarely, these cysts may grow more extensively and form rapidly multiplying trichilemmal tumors, also called proliferating trichilemmal cysts, which are benign, but may grow aggressively at the cyst site. Very rarely, trichilemmal cysts can become cancerous.

Classification
Trichilemmal cysts may be classified as sebaceous cysts, although technically speaking are not sebaceous. "True" sebaceous cysts,  which originate from sebaceous glands and which contain sebum, are relatively rare and are known as steatocystoma simplex or, if multiple, as steatocystoma multiplex. Medical professionals have suggested that the term "sebaceous cyst" be avoided since it can be misleading.: 31  In practice, however, the term is still often used for epidermoid and pilar cysts.

Pathogenesis
Trichilemmal cysts are derived from the outer root sheath of the hair follicle. Their origin is currently unknown, but they may be produced by budding from the external root sheath as a genetically determined structural aberration. They arise preferentially in areas of high hair follicle concentrations, so 90% of cases occur on the scalp. They are solitary in 30% and multiple in 70% of cases.Histologically, they are lined by stratified squamous epithelium that lacks a granular cell layer and are filled with compact "wet" keratin.  Areas consistent with proliferation can be found in some cysts. In rare cases, this leads to formation of a tumor, known as a proliferating trichilemmal cyst. The tumor is clinically benign, although it may display nuclear atypia, dyskeratotic cells, and mitotic figures. These features can be misleading, and a diagnosis of squamous cell carcinoma may be mistakenly rendered.

Treatment
Surgical excision is required to treat a trichilemmal cyst. The method of treatment varies depending on the physicians training </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 Solar urticaria and can you explain it in depth? [/INST] Solar urticaria (SU) is a rare condition in which exposure to ultraviolet or UV radiation, or sometimes even visible light, induces a case of urticaria or hives that can appear in both covered and uncovered areas of the skin. It is classified as a type of physical urticaria. The classification of disease types is somewhat controversial. One classification system distinguished various types of SU based on the wavelength of the radiation that causes the breakout; another classification system is based on the type of allergen that initiates a breakout.The agent in the human body responsible for the reaction to radiation, known as the photoallergen, has not yet been identified. The disease itself can be difficult  to diagnose  properly because it is so similar to other dermatological disorders, such as polymorphic light eruption or PMLE. The most helpful test is a diagnostic phototest, a specialized test which confirms the presence of an abnormal sunburn reaction. Once recognized, treatment of the disease commonly involves the administration of antihistamines, and desensitization treatments such as phototherapy. In more extreme cases, the use of immunosuppressive drugs and even plasmapheresis may be considered.The initial discovery of the disease is credited to P. Merklen in 1904, but it did not have a name until the suggestion of "solar urticaria" was given by Duke in 1923. However, their research contributed to the study of this uncommon disease. More than  one hundred cases have been reported in the past century.

Signs and symptoms
Generally, the areas affected are exposed skin not usually protected by clothing; however it can also occur in areas covered by clothing. Areas constantly subjected to the suns rays may only be slightly affected if at all. People with extreme cases will also have reactions to artificial light sources that emit a UV wavelength. Parts of the body only thinly covered can also potentially be subjected to an outbreak.
Life with SU can be difficult. Patients are subject to constant itching and pain, as within minutes of the initial exposure to UV radiation a rash will appear. The urticarial reaction begins in the form of pruritus, later progressing to erythema and edema in the exposed areas of the skin. If vast areas of the body are affected, the loss of fluid into the skin could lead to light-headedness, headache, nausea, and vomiting. Extremely rarely, patients have been reported to experience an increase in heart rate that can cause a stroke or heart attack due to the body cavity swelling. Other rare side effects can be   bronchospasm and glucose instability issues. Also, if a large area of the body is suddenly exposed the person may be subject to an anaphylactic reaction. Once free of exposure, the rash will usually fade away within several hours; rare and extreme cases can take a day or two to normalize depending on severity of the reaction.

Causes
Solar urticaria is an immunoglobulin E-mediated hypersensitivity that can be introduced through primary or secondary factors, or induced by exogenous photosensitization. Primary SU is believed to be a type I hypersensitivity (a mild to severe reaction to an antigen including anaphylaxis) in which an antigen, or substance provoking an immune response, is "induced by UV or visible radiation." Secondary SU can occur when a person comes into contact with chemicals such as tar, pitch, and dyes. People who use drugs such as benoxaprofen or patients with erythropoietic protoporphyria may also contract this secondary form. These items that cause this photosensitivity are exogenous photosensitizers because they are outside of the body and cause it to have a greater sensitivity to light.Also, there have been a few unorthodox (unusual) causes of solar urticaria. For those susceptible to visible light, white T-shirts may increase the chances of experiencing an outbreak. In one case, doctors found that the white T-shirt absorbed UVA radiation from the sun and transformed it into visible light which caused the reaction. Another patient was being treated with the antibiotic tetracycline for a separate dermatological disorder and broke out in hives when exposed to the sun, the first case to implicate tetracycline as a solar urticaria inducing agent.It is not yet known what specific agent in the body brings about the allergic reaction to the radiation. When patients with SU were injected with an irradiated autologous serum, many developed urticaria within the area of injection. When people who did not have SU were injected, they did not demonstrate similar symptoms. This indicates that the reaction is only a characteristic of the patients with solar urticaria and that it is not phototoxic. It is possible that this photoallergen is located on the binding sites of IgE that are found on the surface of mast cells. The photoallergen is believed to begin its configuration through the absorption of radiation by a chromophore. The molecule, because of the radiation, is transformed resulting in the formation of a new photoallergen.

Diagnosis
Solar urticaria can be difficult to diagnose, but its presence can be confirmed by the process of phototesting. There are several forms of these tests including photopatch tests, phototests, photoprovocation tests, and laboratory tests. All of these are necessary to determine the exact condition of the patient. Photopatch tests are patch tests conducted when it is believed that a patient is experiencing certain symptoms due to an allergy that will only occur when in contact with sunlight. After the procedure, the patient is given a low dosage of UVA radiation.
Another test known as a phototest is the most useful in identifying solar urticaria. In this test, one centimeter segments of skin are subject to varying amounts of UVA and UVB radiation in order to determine the specific dosage of the certain form of radiation that causes the urticaria to form. When testing for its less intense form (fixed solar urticaria), phototesting should be conducted only in the areas where the hives have appeared to avoid the possibility of getting false-negative results.A third form of testing is the photoprovocation test which is used to identify disorders instigated by sun burns. The process of this test involves exposing one area of a patients arm to certain dosage of UVB radiation and one area on the other arm to a certain dosage of UVA radiation. The amount of radiation that the patient is exposed to is equal to that "received in an hour of midday summer sun." If the procedure produces a rash, then the patient will undergo a biopsy. Finally, there are laboratory tests which generally involve procedures such as blood, urine, and fecal biochemical tests. In some situations, a skin biopsy may be performed.

Classification
Solar urticaria, due to its particular features, is considered to be a type of physical urticaria or light sensitivity. Physical urticaria arises from physical  factors in the environment,  which in the  case of solar urticaria is   UV radiation or light. SU may be classified based on the wavelength of the radiative energy that causes the allergic reaction; known as Harbers classification, six types have been identified in this system. Type I solar urticaria is caused by UVB (ultraviolet B) radiation, with wavelengths ranging from 290 to 320 nm. Type II is induced by UVA (ultraviolet A) radiation with wavelengths that can range from 320 to 400 nm. The wavelength range of type III and IV spans from 400 to 500 nm, while type V can be caused by UVB radiation to visible light (280–600 nm). Type VI has only been known to occur at 400 nm.Another classification distinguishes two types. The first is a hypersensitivity caused by a reaction to photoallergens located only in people with SU; while the second is caused by photoallergens that can be found in both people with SU and people without it.A subgroup of solar urticaria, fixed solar urticaria, has also been identified. It is a rare, less intense form of the disease with wheals (swollen areas of the skin) that affect certain, fixed areas of the body. Fixed solar urticaria is induced by a broad spectrum of radiative energy with wavelengths ranging from 300 to 700 nm.

Differential diagnosis
Polymorphous light eruption (PMLE) is the easiest disease to mistake for solar urticaria because the locations of the lesions are similar (the V of the neck and the arms). However, patients with SU are more likely to develop lesions on the face. Also, a reaction with PMLE will take a greater amount of time to appear than with solar urticaria. Lupus erythematosus has been mistaken for SU; however, lesions from lupus erythematosus will take a longer amount of time to go away. Furthermore, when being tested for the two diseases, patients with SU have a reaction immediately while patients with lupus erythematosus will have a delayed reaction. Patients who have experienced solar urticarial symptoms from a young age could mistakenly be thought to have erythropoietic protoporphyria. However, the main symptom for this disease is pain and patients with have been found to have abnormal levels of protoporphyrin in their blood while these levels are normal in SU patients. Finally, cholinergic urticaria, or urticaria induced by heat, can occasionally appear to be solar urticaria because the heat from the sun will cause a person with the disease to have a reaction.

Management
Antihistamines
Histamines are proteins associated with many allergic reactions. When the UV radiation or light comes in contact with a person with solar urticaria, histamine is released from mast cells. When this occurs, the permeability of vessels near the area of histamine release is increased. This allows blood fluid to enter the vessels and cause inflammation. Antihistamines suppress the activity of the histamine.Diphenhydramine, a first-generation H1 receptor antagonist or medicine that combats the H1 receptor that is associated with many allergic reactions, has been found to be the most potent antihistamine for this particular disease. Patients prescribed 50 milligrams four times per day have been able to sustain normal exposure to the sun without developing a reaction.
Patients with less potent forms of solar urticaria such as fixed solar urticaria can be treated with the medication fexofenadine, which may also be used prophylactically to prevent recurrence.

Desensitization
This form of treatment is meant to reduce the intensity or altogether eliminate the allergic reactions people have by gradually increasing exposure to the form of radiation that brings about the reaction. In the case of solar urticaria, phototherapy and photochemotherapy are the two major desensitization treatments.Phototherapy can be used for prevention. Exposure to a certain form of light or UV radiation  enables the patient to build up a tolerance and outbreaks can be reduced. This type of treatment is generally conducted in the spring. However, the benefits of this  therapy only last for two to three days.Photochemotherapy, or PUVA, is considered superior to phototherapy because it produces a longer-lasting tolerance of the radiation that initiates the outbreak. When treatment first begins, the main goal is to build up the patients tolerance to UVA radiation enough so that they can be outdoors without having an episode of solar urticaria. Therefore, treatments are regulated at three per week while constantly increasing the exposure to UVA radiation. Once the patient has reached an adequate level of desensitization, treatments are reduced to once or twice per week.

Immunoglobulin E (IgE) Therapy
Some patients and researchers have successfully treated solar urticaria with Omalizumab (trade name Xolair) which is commonly used to treat Idiopathic Urticaria. Omalizumab is a recombinant humanized monoclonal antibody against IgE. It acts by binding free IgE at the same site that IgE would bind to its high-affinity receptor (FcεRI) on mast cells, thereby reducing free IgE in the serum

Immunosuppression
Doctors will sometimes prescribe immunosuppressive drugs such as prednisolone and ciclosporin if the patient has an intense form of solar urticaria. However, the side effects of these medicines can be severe which is why they are reserved for the most extreme of cases.

Plasmapheresis
In more extreme cases, plasmapheresis can be considered. This technique is used to remove the blood plasma or fluid in the red blood cells and then return the cells to the body. It "removes a circulating factor from the blood that may be involved in causing the urticaria," but is still being tested and is not always effective. When the treatment is a success, the patients photosensitivity is decreased to the degree that they can undergo PUVA which can result in the relief of the urticarial outbreaks for an extended period of time. The major setback to this treatment is that the side effects can be severe and may include anaphylactoid reactions.

Epidemiology
In the United States, only about 4% of patients with photosensitive disorders are reported to have been diagnosed with solar urticaria. Internationally, the number is slightly larger at 5.3%. Solar urticaria may occur in all races but studies monitoring 135 African Americans and 110 Caucasians with photodermatoses found that 2.2% of the African Americans had SU and 8% of the Caucasians had the disease showing that Caucasians have a better chance of getting the disease </s>


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<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 Familial amyloid polyneuropathy and can you explain it in depth? [/INST] Familial amyloid polyneuropathy, also called transthyretin-related hereditary amyloidosis, transthyretin amyloidosis abbreviated also as ATTR (hereditary form), or Corino de Andrades disease, is an autosomal dominant neurodegenerative disease. It is a form of amyloidosis, and was first identified and described by Portuguese neurologist Mário Corino da Costa Andrade, in 1952. FAP is distinct from senile systemic amyloidosis (SSA), which is not inherited, and which was determined to be the primary cause of death for 70% of supercentenarians who have been autopsied. FAP can be ameliorated by liver transplantation.

Presentation
Usually manifesting itself between 20 and 40 years of age, it is characterized by pain, paresthesia, muscular weakness and autonomic dysfunction. In its terminal state, the kidneys and the heart are affected. FAP is characterized by the systemic deposition of amyloidogenic variants of the transthyretin protein, especially in the peripheral nervous system, causing a progressive sensory and motor polyneuropathy.

Cause
FAP is caused by a mutation of the TTR gene, located on human chromosome 18q12.1-11.2. A replacement of valine by methionine at position 30 (TTR V30M) is the mutation most commonly found in FAP. The transthyretin protein is a tetramer. The tetramer has to dissociate into misfolded monomers to aggregate into a variety of structures including amyloid fibrils. Because most patients are heterozygotes, they deposit both mutant and wild type TTR subnits.FAP is inherited in an autosomal dominant manner. This means that the defective gene responsible for the disorder is located on an autosome (chromosome 18 is an autosome), and only one copy of the defective gene is sufficient to cause the disorder, when inherited from a parent who has the disorder.

Diagnosis
Clinical suspicion for FAP is raised on the basis of a family history of neuropathy and physical exam showing signs of neuropathy. Diagnosis can be made using genetic testing to identify mutations in the TTR gene, but may include other corroborative investigation. Nerve conduction testing typically shows an axonal polyneuropathy, with sensory involvement greater than motor. Superimposed mononeuropathies may also be evident, such as a median mononeuropathy at the wrist (carpal tunnel syndrome). Electromyography (EMG) may show evidence of chronic denervation and reinnervation. Autonomic testing, including quantitative sweat testing, can reveal involvement of the autonomic nervous system. Occasionally, biopsy of skin, nerve, or muscle may be performed, which can show signs of denervation and amyloid deposition with response to anti-TTR antibodies. Additional testing should be performed to identify involvement of the heart or kidneys.Sudomotor function through electrochemical skin conductance may provide a measure of subclinical autonomic involvement.

Treatments
The medication tafamidis has been approved for the treatment of transthyretin familial amyloid polyneuropathy in Europe. Studies have found that it delays neurological problems when started early. The US Food and Drug Administrations Peripheral and Central Nervous System Drugs Advisory Committee rejected the drug in June 2012, in a 13-4 vote </s>


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