<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 Partial androgen insensitivity syndrome and can you explain it in depth? [/INST] Partial androgen insensitivity syndrome (PAIS) is a condition that results in the partial inability of the cell to respond to androgens.  It is an X linked recessive condition. The partial unresponsiveness of the cell to the presence of androgenic hormones impairs the masculinization of male genitalia in the developing fetus, as well as the development of male secondary sexual characteristics at puberty, but does not significantly impair female genital or sexual development.  As such, the insensitivity to androgens is clinically significant only when it occurs in individuals with a Y chromosome (or more specifically, an SRY gene). Clinical features include ambiguous genitalia at birth and primary amenhorrhoea with clitoromegaly with inguinal masses. Mullerian structures are not present in the individual.
PAIS is one of three types of androgen insensitivity syndrome, which is divided into three categories that are differentiated by the degree of genital masculinization: complete androgen insensitivity syndrome (CAIS) is indicated when the external genitalia is that of a typical female, mild androgen insensitivity syndrome (MAIS) is indicated when the external genitalia is that of a typical male, and partial androgen insensitivity syndrome (PAIS) is indicated when the external genitalia is partially, but not fully masculinized.Androgen insensitivity syndrome is the largest single entity that leads to 46,XY undermasculinization.There are differing opinions on whether treatment is necessary. Treatment may include irreversible and far reaching surgical operations such as gonadectomy, as well as hormone replacement therapy, or vaginoplasty if the patient has desire to engage in penetrative sex.

Signs and symptoms
A supplemental system of phenotypic grading that uses seven classes instead of the traditional three was proposed by pediatric endocrinologist Charmian A. Quigley et al. in 1995.  The first six grades of the scale, grades 1 through 6, are differentiated by the degree of genital masculinization; grade 1 is indicated when the external genitalia is fully masculinized, grade 6 is indicated when the external genitalia is fully feminized, and grades 2 through 5 quantify four degrees of increasingly feminized genitalia that lie in the interim.  Grade 7 is indistinguishable from grade 6 until puberty, and is thereafter differentiated by the presence of secondary terminal hair; grade 6 is indicated when secondary terminal hair is present, whereas grade 7 is indicated when it is absent.  The Quigley scale can be used in conjunction with the traditional three classes of AIS to provide additional information regarding the degree of genital masculinization, and is particularly useful when the diagnosis is PAIS.

Partial androgen insensitivity syndrome is diagnosed when the degree of androgen insensitivity in an individual with a 46,XY karyotype is great enough to partially prevent the masculinization of the genitalia, but is not great enough to completely prevent genital masculinization.  This includes any phenotype resulting from androgen insensitivity where the genitalia is partially, but not completely masculinized.  Genital ambiguities are frequently detected during clinical examination at birth, and consequently, a PAIS diagnosis can be made during infancy as part of a differential diagnostic workup.Pubertal undervirilization is common, including gynecomastia, decreased secondary terminal hair, and / or a high pitched voice.  The phallic structure ranges from a penis with varying degrees of diminished size and hypospadias to a slightly enlarged clitoris.  Wolffian structures (the epididymides, vasa deferentia, and seminal vesicles) are typically partially or fully developed.  The prostate is typically small or impalpable.  Müllerian remnants are rare, but have been reported.The gonads in individuals with PAIS are testes, regardless of phenotype; during the embryonic stage of development, testes form in an androgen-independent process that occurs due to the influence of the SRY gene on the Y chromosome.  Cryptorchidism is common, and carries with it a 50% risk of germ cell malignancy.  If the testes are located intrascrotally, there may still be significant risk of germ cell malignancy; studies have not yet been published to assess this risk.Predominantly male phenotypes vary in the degree of genital undermasculinization to include micropenis, chordee, bifid scrotum, and / or pseudovaginal perineoscrotal hypospadias.  Impotence may be fairly common, depending on phenotypic features; in one study of 15 males with PAIS, 80% of those interviewed indicated that they had some degree of impotence.  Anejaculation appears to occur somewhat independently of impotence; some men are still able to ejaculate despite impotence, and others without erectile difficulties cannot.  Predominantly female phenotypes include a variable degree of labial fusion and clitoromegaly.  Ambiguous phenotypic states include a phallic structure that is intermediate between a clitoris and a penis, and a single perineal orifice that connects to both the urethra and the vagina (i.e. urogenital sinus).  At birth, it may not be possible to immediately differentiate the external genitalia of individuals with PAIS as being either male or female, although the majority of individuals with PAIS are raised male.

Given the wide diversity of phenotypes associated with PAIS, the diagnosis is often further specified by assessing genital masculinization.  Grades 2 through 5 of the Quigley scale quantify four degrees of increasingly feminized genitalia that correspond to PAIS.Grade 2, the mildest form of PAIS, presents with a predominantly male phenotype that presents with minor signs of undermasculinized genitalia, such as isolated hypospadias, which can be severe.  Hypospadias may manifest with a partially formed channel from the urethral opening to the glans.  Until recently, it was thought that isolated micropenis was not a manifestation of PAIS.  However, in 2010, two cases of PAIS manifesting with isolated micropenis were documented.

Grade 3, the most common phenotypic form of PAIS, features a predominantly male phenotype that is more severely undermasculinized, and typically presents with micropenis and pseudovaginal perineoscrotal hypospadias with bifid scrotum.Grade 4 presents with a gender ambiguous phenotype, including a phallic structure that is intermediate between a clitoris and a penis.  The urethra typically opens into a common channel with the vagina (i.e. urogenital sinus).Grade 5, the form of PAIS with the greatest degree of androgen insensitivity, presents with a mostly female phenotype, including separate urethral and vaginal orifices, but also shows signs of slight masculinization including mild clitoromegaly and / or partial labial fusion.Previously, it was erroneously thought that individuals with PAIS were always infertile; at least one case report has been published that describes fertile men that fit the criteria for grade 2 PAIS (micropenis, penile hypospadias, and gynecomastia).

Comorbidity
All forms of androgen insensitivity are associated with infertility, though exceptions have been reported for both the mild and partial forms.PAIS is associated with a 50% risk of germ cell malignancy when the testes are undescended.  If the testes are located intrascrotally, there may still be significant risk of germ cell malignancy; studies have not yet been published to assess this risk.  Some men with PAIS may experience sexual dysfunction including impotence and anejaculation.  A few AR mutations that cause PAIS are also associated with prostate and breast cancers.
Vaginal hypoplasia, a relatively frequent finding in CAIS and some forms of PAIS, is associated with sexual difficulties including vaginal penetration difficulties and dyspareunia.There are indications that individuals with an intersex condition may be more prone to psychological difficulties, due at least in part to parental attitudes and behaviors, and concludes that preventative long-term psychological counseling for parents as well as for affected individuals should be initiated at the time of diagnosis. More recent research based on interviews of people with intersex variations indicate a need for more family protection from intervention and more family support.
Lifespan is not thought to be affected by AIS.

Diagnosis
Unfortunately, the number of differentials to consider for PAIS is particularly large.  Prompt diagnosis is particularly urgent when a child is born with ambiguous genitalia, as some causes are associated with potentially life-threatening adrenal crises.  Determination of testosterone, testosterone precursors and dihydrotestosterone (DHT) at baseline and / or after human chorionic gonadotropin (hCG) stimulation can be used to exclude such defects in androgen biosynthesis.Approximately one half of all 46,XY individuals born with ambiguous genitalia will not receive a definitive diagnosis. Androgen receptor (AR) gene mutations cannot be found in 27%  to 72%  of individuals with PAIS.  As a result, genetic analysis can be used to confirm a diagnosis of PAIS, but it cannot be used to rule out PAIS.  Evidence of abnormal androgen binding in a genital skin fibroblast study has long been the gold standard for the diagnosis of PAIS, even when an AR mutation is not present.  However, some cases of PAIS, including AR-mutant-positive cases, will show normal androgen binding.  A family history consistent with X-linked inheritance is more commonly found in AR-mutant-positive cases than AR-mutant-negative cases.The use of dynamic endocrine tests is particularly helpful in isolating a diagnosis of PAIS.  One such test is the human chorionic gonadotropin (hCG) stimulation test.  If the gonads are testes, there will be an increase in the level of serum testosterone in response to the hCG, regardless of testicular descent.  The magnitude of the testosterone increase can help differentiate between androgen resistance and gonadal dysgenesis, as does evidence of a uterus on ultrasound examination.  Testicular function can also be assessed by measuring serum anti-Müllerian hormone levels, which in turn can further differentiate PAIS from gonadal dysgenesis and bilateral anorchia.Another useful dynamic test involves measuring the response to exogenous steroids; individuals with AIS show a decreased response in serum sex hormone binding globulin (SHBG) after a short term administration of anabolic steroids.  Two studies  indicate that measuring the response in SHBG after the administration of stanozolol could help to differentiate individuals with PAIS from those with other causes of ambiguous genitalia, although the response in individuals with predominantly male phenotypes overlaps somewhat with the response in normal males.

Management
Management of AIS is currently limited to symptomatic management; methods to correct a malfunctioning androgen receptor protein that result from an AR gene mutation are not currently available.  Areas of management include sex assignment, genitoplasty, gonadectomy in relation to tumor risk, hormone replacement therapy, and genetic and psychological counseling. Non-consensual interventions are still often performed, although general awareness on the resulting psychological traumatization is rising.

Sex assignment
The decision of whether to raise an individual with PAIS as a boy or a girl may not be obvious; grades 3 and 4 in particular present with a phenotype that may be difficult to classify as primarily male or female, and some will be incapable of virilization at puberty.  Parents of an affected newborn should seek immediate help at a center with an experienced multidisciplinary team, and should avoid gender assignment beforehand.  Older guidelines from 2006 advised against waiting for the child to decide for themselves.  According to them, key considerations involved in assigning gender include the appearance of the genitalia, the extent to which the child can virilize at puberty, surgical options and the postoperative sexual function of the genitalia, genitoplasty complexity, potential for fertility, and the projected gender identity of the child.  The majority of individuals with PAIS are raised male. More recently, the interests of intersex people themselves are being taken into consideration by the medical community. Some parents have pushed their children with intersex variations to display gender normative roles and behaviours, or to engage in hormonal and surgical interventions to make their bodies appear more aesthetically normative. Research based on interviews of people with intersex variations indicate a need for more family protection from intervention and more family support.
Virilization capacity can be assessed by measuring the response to a trial of exogenous androgens; some studies have measured the growth of the phallus in response to exogenous testosterone or dihydrotestosterone, while others have measured the change in sex hormone binding globulin (SHBG) in response to the artificial androgen stanozolol to assess androgen sensitivity.  Some experts have cautioned that it remains to be proved that a good response to exogenous androgens in neonates is a good predictor of androgen response at puberty.  If a mutation in the AR gene is found, it is important to determine whether the mutation is inherited or de novo (i.e. a somatic mutation); a certain amount of the wild-type androgen receptor will be present in cases of somatic mutation, which can induce virilization at puberty.  A genital skin fibroblast study  and a human chorionic gonadotropin (hCG) stimulation test  may also provide information helpful in the assessment of virilization capacity.
Psychosexual development is influenced by many factors, including the timing, amount, and type of androgen exposure, receptor functionality, and environment, and is thus difficult to predict.  Gender identity begins to develop before 3 years of age, although the earliest age at which it can be reliably assessed has yet to be determined.  Approximately 25% of individuals with PAIS are dissatisfied with their assigned gender, regardless of being raised as male or female.  One study reports that 46,XY individuals born with micropenis and no hypospadias are better off being raised male, despite the success of some being raised female.  Studies involving the more ambiguous phenotypic forms of PAIS are less decisive.  Homosexuality with respect to assigned gender  and atypical gender role behavior  are known to occur more frequently in individual with PAIS, and may occur with or without gender dysphoria; neither should be interpreted as an indication of incorrect gender assignment.  If an affected child does express feelings of gender dysphoria, the opportunity to explore such feelings with a psychologist experienced in treating intersex conditions should be accommodated.  If feelings of gender dysphoria persist, gender reassignment should be initiated, possibly with the aid of a specialist in the field.

Genitoplasty
Genitoplasty, unlike gender assignment, can be irreversible, and there is no guarantee that adult gender identity will develop as assigned despite surgical intervention.  Some aspects of genitoplasty are still being debated; a variety of different opinions have been presented by professionals, self-help groups, and patients over the last few decades.  Points of consideration include what conditions justify genitoplasty, the extent and type of genitoplasty that should be employed, when genitoplasty should be performed, and what the goals of genitoplasty should be.  Gender assignment itself does not predicate the need for immediate genitoplasty; in some cases, surgical intervention can be delayed to allow the affected child to reach an age and maturity sufficient to have a role in such decisions.  Some studies suggest that early surgeries can still produce satisfactory outcomes, while others suggest it to be unlikely.  Even surgeries that are planned as one-stage procedures often require further major surgery.  Scarring and tissue loss that result from repeated surgical procedures are of particular concern, due to the presumed negative impact on sexual function.While it is thought that feminizing genitoplasty typically requires fewer surgeries to achieve an acceptable result and results in fewer urologic difficulties, there is no evidence that feminizing surgery results in a better psychosocial outcome.  In one study, individuals with grade 3 PAIS who were raised male rated their body image and sexual function similarly to those who were raised female, even though they were more likely to have genitalia that were abnormal in size and appearance; more than half of the male participants had a stretched penile length that was below 2.5 standard deviations of the mean, while only 6% of female participants presented with a short vagina in adulthood, and participating physicians gave a lower cosmetic rating to the surgical results of the men than the women.  Both male and female participants cited the appearance of their genitalia as being the greatest contributing factor to their dissatisfaction with their body image.  In two larger studies, the common predictor of gender reassignment was stigmatization related to having an intersex condition.
The outcome of masculinizing genitoplasty is dependent on the amount of erectile tissue and the extent of hypospadias.  Procedures include correction of penile curvature and chordee, reconstruction of the urethra, hypospadias correction, orchidopexy, and Müllerian remnant removal to prevent infection and pseudo-incontinence.  Erectile prosthesis may be inserted in cases of successful neophalloplasty in adulthood, although it has a high morbidity.  Additional surgeries may be required to correct postsurgical complications such as stenosis of the anastomosis between the native urethra and the graft, urethral fistulas, and posterior displacement of the balanic meatus.  Successful masculinizing genitoplasty performed on individuals with grade 3 PAIS often requires multiple surgeries.

If feminizing genitoplasty is performed in infancy, the result will need to be refined at puberty through additional surgery.  Procedures include clitoral reduction / recession, labiaplasty, repair of the common urogenital sinus, vaginoplasty, and vaginal dilation through non-surgical pressure methods.  Clitoral reduction / recession surgery carries with it the risk of necrosis as well as the risk of impairing the sexual function of the genitalia, and thus should not be performed for less severe clitoromegaly.  Clitoral surgery should be focused on function rather than appearance, with care being taken to spare the erectile function and innervation of the clitoris.  If PAIS presents with a common urogenital sinus, the American Academy of Pediatrics currently recommends that surgery to separate the urethra from the vagina be performed at an early age.  As is the case for CAIS, vaginal dilation using pressure dilation methods should be attempted before the surgical creation of a neovagina is considered, and neither should be performed before puberty.  Complications of feminizing genitoplasty can include vaginal stenosis, meatal stenosis, vaginourethral fistula, female hypospadias, urinary tract injuries, and recurrent clitoromegaly.  Successful feminizing genitoplasty performed on individuals with grade 3 PAIS often requires multiple surgeries, although more surgeries are typically required for successful masculinizing genitoplasty in this population.Many surgical procedures have been developed to create a neovagina, as none of them is ideal.  Surgical intervention should be considered only after non-surgical pressure dilation methods have failed to produce a satisfactory result.  Neovaginoplasty can be performed using skin grafts, a segment of bowel, ileum, peritoneum, Interceed, buccal mucosa, amnion, or dura mater.  Success of such methods should be determined by sexual function, and not by vaginal length alone, as has been done in the past.  Ileal or cecal segments may be problematic because of a shorter mesentery, which may produce tension on the neovagina, leading to stenosis.  The sigmoid neovagina is thought to be self-lubricating, without the excess mucus production associated with segments of small bowel.  Vaginoplasty may create scarring at the introitus (the vaginal opening), requiring additional surgery to correct.  Vaginal dilators are required postoperatively to prevent vaginal stenosis from scarring.  Other complications include bladder and bowel injuries.  Yearly exams are required, as neovaginoplasty carries a risk of carcinoma, although carcinoma of the neovagina is uncommon.  Neither neovaginoplasty nor vaginal dilation should be performed before puberty.

Gonadectomy
Gonadectomy at time of diagnosis is the current recommendation for PAIS if presenting with cryptorchidism. The risk of malignancy when testes are located intrascrotally is unknown; the current recommendation is to biopsy the testes at puberty, allowing investigation of at least 30 seminiferous tubules, with diagnosis preferably based on OCT3/4 immunohistochemistry, followed by regular examinations.  Hormone replacement therapy is required after gonadectomy, and should be modulated over time to replicate the hormone levels naturally present in the body during the various stages of puberty.  Artificially induced puberty results in the same, normal development of secondary sexual characteristics, growth spurt, and bone mineral accumulation.  Women with PAIS may have a tendency towards bone mineralization deficiency, although this increase is thought to be less than is typically seen in CAIS, and is similarly managed.

Hormonal replacement therapy
Testosterone has been used to successfully treat undervirilization in some  but not all  men with PAIS, despite having supraphysiological levels of testosterone to start with.  Treatment options include transdermal gels or patches, oral or injectable testosterone undecanoate, other injectable testosterone esters, testosterone pellets, or buccal testosterone systems.  Supraphysiological doses may be required to achieve the desired physiological effect, which may be difficult to achieve using non-injectable testosterone preparations.  Exogenous testosterone supplementation in unaffected men can produce various unwanted side effects, including prostatic hypertrophy, polycythemia, gynecomastia, hair loss, acne, and the suppression of the hypothalamic-pituitary-gonadal axis, resulting in the reduction of gonadotropins (i.e., luteinizing hormone and follicle-stimulating hormone) and spermatogenic defect.  These effects may not manifest at all in men with AIS, or might only manifest at a much higher concentration of testosterone, depending on the degree of androgen insensitivity.  Those undergoing high dose androgen therapy should be monitored for safety and efficacy of treatment, possibly including regular breast and prostate examinations.  Some individuals with PAIS have a sufficiently high sperm count to father children; at least one case report has been published that describes fertile men who fit the criteria for grade 2 PAIS (micropenis, penile hypospadias, and gynecomastia).  Several publications have indicated that testosterone treatment can correct low sperm counts in men with MAIS.  At least one case report has been published that documents the efficacy of treating a low sperm-count with tamoxifen in an individual with PAIS.

Counseling
Depending on phenotypic features, impotence and other sexual problems such as anejaculation or sexual aversion may be fairly common among individuals with PAIS, but do not necessarily indicate low libido.  Support groups for individuals with PAIS may help affected individuals discuss their concerns more comfortably.  Some individuals with PAIS may try to avoid intimate relationships out of fear of rejection; individual therapy may help some to overcome social anxiety, and restore focus to interpersonal relationships instead of solely on sexual function and activity.

Society and culture
Adults with partial androgen insensitivity syndrome include Australian-Maltese advocate Tony Briffa, considered to be the worlds first openly intersex mayor and public office-bearer </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 Perihepatitis 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 Subarachnoid hemorrhage and can you explain it in depth? [/INST] Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space—the area between the arachnoid membrane and the pia mater surrounding the brain. Symptoms may include a severe headache of rapid onset, vomiting, decreased level of consciousness, fever, and sometimes seizures. Neck stiffness or neck pain are also relatively common. In about a quarter of people a small bleed with resolving symptoms occurs within a month of a larger bleed.SAH may occur as a result of a head injury or spontaneously, usually from a ruptured cerebral aneurysm. Risk factors for spontaneous cases include high blood pressure, smoking, family history, alcoholism, and cocaine use. Generally, the diagnosis can be determined by a CT scan of the head if done within six hours of symptom onset. Occasionally, a lumbar puncture is also required. After confirmation further tests are usually performed to determine the underlying cause.Treatment is by prompt neurosurgery or endovascular coiling. Medications such as labetalol may be required to lower the blood pressure until repair can occur. Efforts to treat fevers are also recommended. Nimodipine, a calcium channel blocker, is frequently used to prevent vasospasm. The routine use of medications to prevent further seizures is of unclear benefit. Nearly half of people with a SAH due to an underlying aneurysm die within 30 days and about a third who survive have ongoing problems. Between ten and fifteen percent die before reaching a hospital.Spontaneous SAH occurs in about one per 10,000 people per year. Females are more commonly affected than males. While it becomes more common with age, about 50% of people present under 55 years old. It is a form of stroke and comprises about 5 percent of all strokes. Surgery for aneurysms was introduced in the 1930s. Since the 1990s many aneurysms are treated by a less invasive procedure called endovascular coiling, which is carried out through a large blood vessel.

Signs and symptoms
The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as "like being kicked in the head", or the "worst ever", developing over seconds to minutes). This headache often pulsates towards the occiput (the back of the head). About one-third of people have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid hemorrhage. Vomiting may be present, and 1 in 14 have seizures. Confusion, decreased level of consciousness or coma may be present, as may neck stiffness and other signs of meningism.Neck stiffness usually presents six hours after initial onset of SAH. Isolated dilation of a pupil and loss of the pupillary light reflex may reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull). Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure: subhyaloid hemorrhage (bleeding under the hyaloid membrane, which envelops the vitreous body of the eye) and vitreous hemorrhage may be visible on fundoscopy. This is known as Terson syndrome (occurring in 3–13 percent of cases) and is more common in more severe SAH.Oculomotor nerve abnormalities (affected eye looking downward and outward and inability to lift the eyelid on the same side) or palsy (loss of movement) may indicate bleeding from the posterior communicating artery. Seizures are more common if the hemorrhage is from an aneurysm; it is otherwise difficult to predict the site and origin of the hemorrhage from the symptoms. SAH in a person known to have seizures is often diagnostic of a cerebral arteriovenous malformation.The combination of intracerebral hemorrhage and raised intracranial pressure (if present) leads to a "sympathetic surge", i.e. over-activation of the sympathetic system. This is thought to occur through two mechanisms, a direct effect on the medulla that leads to activation of the descending sympathetic nervous system and a local release of inflammatory mediators that circulate to the peripheral circulation where they activate the sympathetic system. As a consequence of the sympathetic surge there is a sudden increase in blood pressure; mediated by increased contractility of the ventricle and increased vasoconstriction leading to increased systemic vascular resistance. The consequences of this sympathetic surge can be sudden, severe, and are frequently life-threatening. The high plasma concentrations of adrenaline also may cause cardiac arrhythmias (irregularities in the heart rate and rhythm), electrocardiographic changes (in 27 percent of cases) and cardiac arrest (in 3 percent of cases) may occur rapidly after the onset of hemorrhage. A further consequence of this process is neurogenic pulmonary edema where a process of increased pressure within the pulmonary circulation causes leaking of fluid from the pulmonary capillaries into the air spaces, the alveoli, of the lung.Subarachnoid hemorrhage may also occur in people who have had a head injury. Symptoms may include headache, decreased level of consciousness and hemiparesis (weakness of one side of the body). SAH is a frequent occurrence in traumatic brain injury, and carries a poor prognosis if it is associated with deterioration in the level of consciousness.While thunderclap headache is the characteristic symptom of subarachnoid hemorrhage, less than 10% of those with concerning symptoms have SAH on investigations. A number of other causes may need to be considered.

Causes
Most cases of SAH are due to trauma such as a blow to the head. Traumatic SAH usually occurs near the site of a skull fracture or intracerebral contusion. It often happens in the setting of other forms of traumatic brain injury. In these cases prognosis is poorer; however, it is unclear if this is a direct result of the SAH or whether the presence of subarachnoid blood is simply an indicator of a more severe head injury.In 85 percent of spontaneous cases the cause is a cerebral aneurysm—a weakness in the wall of one of the arteries in the brain that becomes enlarged. They tend to be located in the circle of Willis and its branches. While most cases are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture. Aspirin also appears to increase the risk.In 15–20 percent of cases of spontaneous SAH, no aneurysm is detected on the first angiogram. About half of these are attributed to non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain (i.e. mesencephalon). In these, the origin of the blood is uncertain. The remainder are due to other disorders affecting the blood vessels (such as cerebral arteriovenous malformations), disorders of the blood vessels in the spinal cord, and bleeding into various tumors.Cocaine abuse and sickle cell anemia (usually in children) and, rarely, anticoagulant therapy, problems with blood clotting and pituitary apoplexy can also result in SAH. Dissection of the vertebral artery, usually caused by trauma, can lead to subarachnoid hemorrhage if the dissection involves the part of the vessel inside the skull.

Pathophysiology
Cerebral vasospasm is one of the complications caused by subarachnoid hemorrhage. It usually happens from the third day after the aneurysm event, and reaches its peak on 5th to 7th day. There are several mechanisms proposed for this complication. Blood products released from subarachnoid hemorrhage stimulates the tyrosine kinase pathway causing the release of calcium ions from intracellular storage, resulting in smooth muscle contraction of cerebral arteries. Oxyhaemoglobin in cerebrospinal fluid (CSF) causes vasoconstriction by increasing free radicals, endothelin-1, prostaglandin and reducing the level of nitric oxide and prostacyclin. Besides, the disturbances of autonomic nervous system innervating cerebral arteries is also thought to cause vasospasm.

Diagnosis
As only 10 percent of people admitted to the emergency department with a thunderclap headache are having an SAH, other possible causes are usually considered simultaneously, such as meningitis, migraine, and cerebral venous sinus thrombosis. Intracerebral hemorrhage, in which bleeding occurs within the brain itself, is twice as common as SAH and is often misdiagnosed as the latter. It is not unusual for SAH to be initially misdiagnosed as a migraine or tension headache, which can lead to a delay in obtaining a CT scan. In a 2004 study, this occurred in 12 percent of all cases and was more likely in people who had smaller hemorrhages and no impairment in their mental status. The delay in diagnosis led to a worse outcome. In some people, the headache resolves by itself, and no other symptoms are present. This type of headache is referred to as "sentinel headache", because it is presumed to result from a small leak (a "warning leak") from an aneurysm. A sentinel headache still warrants investigations with CT scan and lumbar puncture, as further bleeding may occur in the subsequent three weeks.The initial steps for evaluating a person with a suspected subarachnoid hemorrhage are obtaining a medical history and performing a physical examination. The diagnosis cannot be made on clinical grounds alone and in general medical imaging and possibly a lumbar puncture is required to confirm or exclude bleeding.

Imaging
The modality of choice is computed tomography (CT scan), without contrast, of the brain. This has a high sensitivity and will correctly identify 98.7% of cases within six hours of the onset of symptoms. A CT scan can rule out the diagnosis in someone with a normal neurological exam if done within six hours. Its efficacy declines thereafter, and magnetic resonance imaging (MRI) is more sensitive than CT after several days.

Angiography
After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as determined by the CT scan appearance), the choice is between cerebral angiography (injecting radiocontrast through a catheter to the brain arteries) and CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm (see below).In emergency department patients complaining of acute-onset headache without significant risk factors for SAH, evidence suggests that CT scanning of the head followed by CT angiography can reliably exclude SAH without the need for a lumbar puncture. The risk of missing an aneurysmal bleed as the cause of SAH with this approach is less than 1%.

Lumbar puncture
Lumbar puncture, in which cerebrospinal fluid (CSF) is removed from the subarachnoid space of the spinal canal using a hypodermic needle, shows evidence of bleeding in three percent of people in whom a non-contrast CT was found normal. A lumbar puncture or CT scan with contrast is therefore regarded as mandatory in people with suspected SAH when imaging is delayed to after six hours from the onset of symptoms and is negative. At least three tubes of CSF are collected. If an elevated number of red blood cells is present equally in all bottles, this indicates a subarachnoid hemorrhage. If the number of cells decreases per bottle, it is more likely that it is due to damage to a small blood vessel during the procedure (known as a "traumatic tap"). While there is no official cutoff for red blood cells in the CSF no documented cases have occurred at less than "a few hundred cells" per high-powered field.The CSF sample is also examined for xanthochromia—the yellow appearance of centrifugated fluid. This can be determined by spectrophotometry (measuring the absorption of particular wavelengths of light) or visual examination. It is unclear which method is superior. Xanthochromia remains a reliable ways to detect SAH several days after the onset of headache. An interval of at least 12 hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the hemoglobin from the red blood cells to be metabolized into bilirubin.

ECG
Electrocardiographic changes are relatively common in subarachnoid hemorrhage, occurring in 40–70 percent of cases. They may include QT prolongation, Q waves, cardiac dysrhythmias, and ST elevation that mimics a heart attack.Also one of the characteristic ECG changes that could be found in patients with subarachnoid hemorrhage, is the J waves or Osborn waves, which are positive deflections that occur at the junction between QRS complexes and ST segments, where the S point, also known as the J point, has a myocardial infarction-like elevation. J waves or Osborn waves, which represent an early repolarization and delayed depolarization of the heart ventricles, are thought to be caused by the high catecholamines surge released in patients with subarachnoid hemorrhage or brain damage, the issue that might lead to ventricular fibrillation and cardiac arrest in unmanaged patients.

Classification
There are several grading scales available for SAH. The Glasgow Coma Scale (GCS) is ubiquitously used for assessing consciousness. Its three specialized scores are used to evaluate SAH; in each, a higher number is associated with a worse outcome. These scales have been derived by retrospectively matching characteristics of people with their outcomes.
The first widely used scale for neurological condition following SAH was published by Botterell and Cannell in 1956 and referred to as the Botterell Grading Scale. This was modified by Hunt and Hess in 1968:
The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan.
This scale has been modified by Claassen and coworkers, reflecting the additive risk from SAH size and accompanying intraventricular hemorrhage (0 – none; 1 – minimal SAH w/o IVH; 2 – minimal SAH with IVH; 3 – thick SAH w/o IVH; 4 – thick SAH with IVH);.The World Federation of Neurosurgeons (WFNS) classification uses Glasgow coma score and focal neurological deficit to gauge severity of symptoms.
A comprehensive classification scheme has been suggested by Ogilvy and Carter to predict outcome and gauge therapy. The system consists of five grades and it assigns one point for the presence or absence of each of five factors: age greater than 50; Hunt and Hess grade 4 or 5; Fisher scale 3 or 4; aneurysm size greater than 10 mm; and posterior circulation aneurysm 25 mm or more.

Screening and prevention
Screening for aneurysms is not performed on a population level; because they are relatively rare, it would not be cost-effective. However, if someone has two or more first-degree relatives who have had an aneurysmal subarachnoid hemorrhage, screening may be worthwhile.Autosomal dominant polycystic kidney disease (ADPKD), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8 percent of cases, but most such aneurysms are small and therefore unlikely to rupture. As a result, screening is only recommended in families with ADPKD where one family member has had a ruptured aneurysm.An aneurysm may be detected incidentally on brain imaging; this presents a conundrum, as all treatments for cerebral aneurysms are associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic data both in people having previously had a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those having previously had a SAH were more likely to bleed from other aneurysms. In contrast, those having never bled and had small aneurysms (smaller than 10 mm) were very unlikely to have a SAH and were likely to sustain harm from attempts to repair these aneurysms. On the basis of the ISUIA and other studies, it is now recommended that people are considered for preventive treatment only if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture. Moreover, there is only limited evidence that endovascular treatment of unruptured aneurysms is actually beneficial.

Treatment
Management involves general measures to stabilize the person while also using specific investigations and treatments. These include the prevention of rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications.Stabilizing the person is the first priority. Those with a depressed level of consciousness may need to be intubated and mechanically ventilated. Blood pressure, pulse, respiratory rate, and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an intensive care unit may be preferable, especially since 15 percent may have further bleeding soon after admission. Nutrition is an early priority, mouth or nasogastric tube feeding being preferable over parenteral routes. In general, pain control is restricted to less-sedating agents such as codeine, as sedation may impact on the mental status and thus interfere with the ability to monitor the level of consciousness. Deep vein thrombosis is prevented with compression stockings, intermittent pneumatic compression of the calves, or both. A bladder catheter is usually inserted to monitor fluid balance. Benzodiazepines may be administered to help relieve distress. Antiemetic drugs should be given to awake persons.People with poor clinical grade on admission, acute neurologic deterioration, or progressive enlargement of ventricles on CT scan are, in general, indications for the placement of an external ventricular drain by a neurosurgeon. The external ventricular drain may be inserted at the bedside or in the operating room. In either case, strict aseptic technique must be maintained during insertion. In people with aneurysmal subarachnoid hemorrhage the EVD is used to remove cerebrospinal fluid, blood, and blood byproducts that increase intracranial pressure and may increase the risk for cerebral vasospasm.

Preventing rebleeding
Efforts to keep a persons systolic blood pressure somewhere between 140 and 160 mmHg is generally recommended. Medications to achieve this may include labetalol or nicardipine.People whose CT scan shows a large hematoma, depressed level of consciousness, or focal neurologic signs may benefit from urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are stabilized more extensively and undergo a transfemoral angiogram or CT angiogram later. It is hard to predict who will have a rebleed, yet it may happen at any time and carries a dismal prognosis. After the first 24 hours have passed, rebleeding risk remains around 40 percent over the subsequent four weeks, suggesting that interventions should be aimed at reducing this risk as soon as possible. Some predictors of early rebleeding are high systolic blood pressure, the presence of a hematoma in the brain or ventricles, poor Hunt-Hess grade (III-IV), aneurysms in the posterior circulation, and an aneurysm >10 mm in size.If a cerebral aneurysm is identified on angiography, two measures are available to reduce the risk of further bleeding from the same aneurysm: clipping and coiling. Clipping requires a craniotomy (opening of the skull) to locate the aneurysm, followed by the placement of clips around the neck of the aneurysm. Coiling is performed through the large blood vessels (endovascularly): a catheter is inserted into the femoral artery in the groin and advanced through the aorta to the arteries (both carotid arteries and both vertebral arteries) that supply the brain. When the aneurysm has been located, platinum coils are deployed that cause a blood clot to form in the aneurysm, obliterating it. The decision as to which treatment is undertaken is typically made by a multidisciplinary team consisting of a neurosurgeon, neuroradiologist, and often other health professionals.In general, the decision between clipping and coiling is made on the basis of the location of the aneurysm, its size and the condition of the person. Aneurysms of the middle cerebral artery and its related vessels are hard to reach with angiography and tend to be amenable to clipping. Those of the basilar artery and posterior cerebral artery are hard to reach surgically and are more accessible for endovascular management. These approaches are based on general experience, and the only randomized controlled trial directly comparing the different modalities was performed in relatively well people with small (less than 10 mm) aneurysms of the anterior cerebral artery and anterior communicating artery (together the "anterior circulation"), who constitute about 20 percent of all people with aneurysmal SAH. This trial, the International Subarachnoid Aneurysm Trial (ISAT), showed that in this group the likelihood of death or being dependent on others for activities of daily living was reduced (7.4 percent absolute risk reduction, 23.5 percent relative risk reduction) if endovascular coiling was used as opposed to surgery. The main drawback of coiling is the possibility that the aneurysm will recur; this risk is extremely small in the surgical approach. In ISAT, 8.3 percent needed further treatment in the longer term. Hence, people who have undergone coiling are typically followed up for many years afterwards with angiography or other measures to ensure recurrence of aneurysms is identified early. Other trials have also found a higher rate of recurrence necessitating further treatments.

Vasospasm
Vasospasm, in which the blood vessels constrict and thus restrict blood flow, is a serious complication of SAH. It can cause ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in parts of the brain. It can be fatal if severe. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. About one third of people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those have permanent damage as a result. It is possible to screen for the development of vasospasm with transcranial Doppler every 24–48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm.The pathogenesis of cerebral vasospasm following subarachnoid hemorrhage is attributed to the higher levels of endothelin 1, a potent vasoconstrictor, and the lower levels of endothelial NOS (eNOS), a potent vasodilator. Both of which are produced from a series of events that begin from the inflammatory reaction caused by the products released from erythrocytes degradation. Following subarachnoid hemorrhage, different clotting factors and blood products are released into the surrounding perivascular spaces known as (Virchow-Robin spaces). The released clotting factors like; fibrinopeptides, thromboxane A2 and others lead to microthrombosis around near vessels that leads to extrinsic vasoconstriction of these vessels. Besides that extrinsic vasoconstriction, the erythrocytes degradation products like; bilirubin and oxyhemoglobin lead to neuroinflammation that in turn increases the production of reactive oxygen species (ROS) which increases and decreases the production of endothelin 1 and endothelial NOS, respectively, the issue that yields in intrinsic vasoconstriction of the neighboring blood vessels and results in cerebral ischemia if left untreated.The use of calcium channel blockers, thought to be able to prevent the spasm of blood vessels by preventing calcium from entering smooth muscle cells, has been proposed for prevention. The calcium channel blocker nimodipine when taken by mouth improves outcome if given between the fourth and twenty-first day after the bleeding, even if it does not reduce the amount of vasospasm detected on angiography. It is the only Food and Drug Administration (FDA)-approved drug for treating cerebral vasospasm. In traumatic subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended. Other calcium channel blockers and magnesium sulfate have been studied, but are not presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously.Nimodipine is readily authorized in the form of tablets and solution for infusion for the prevention and treatment of complications due to vasospasm following subarachnoid hemorrhage. Another sustained formulation of nimodipine administered via an external ventricular drain (EVD), called EG-1962, is also available. In contrast to the tablets and solution formulations of Nimodipine which require an administration every 4hrs for a total of 21 days, the sustained formulation, EG-1962, needs to be administered once directly into the ventricles. The CSF concentrations from EG-1962, however, were at least 2 orders of magnitude higher than those with oral nimodipine. These results supported a phase 3 study that demonstrated a favorable safety profile for EG-1962 but yielded inconclusive efficacy results due to notable differences in clinical outcome based on baseline disease severity.Some older studies have suggested that statin therapy might reduce vasospasm, but a subsequent meta-analysis including further trials did not demonstrate benefit on either vasospasm or outcomes. While corticosteroids with mineralocorticoid activity may help prevent vasospasm their use does not appear to change outcomes.
A protocol referred to as "triple H" is often used as a measure to treat vasospasm when it causes symptoms; this is the use of intravenous fluids to achieve a state of hypertension (high blood pressure), hypervolemia (excess fluid in the circulation), and hemodilution (mild dilution of the blood). Evidence for this approach is inconclusive; no randomized controlled trials have been undertaken to demonstrate its effect.If the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of vasospasms and administer vasodilator medication (drugs that relax the blood vessel wall) directly into the artery. Angioplasty (opening the constricted area with a balloon) may also be performed.

Other complications
Hydrocephalus (obstruction of the flow of cerebrospinal fluid) may complicate SAH in both the short and long term. It is detected on CT scanning, on which there is enlargement of the lateral ventricles. If the level of consciousness is decreased, drainage of the excess fluid is performed by therapeutic lumbar puncture, extraventricular drain (a temporary device inserted into one of the ventricles), or occasionally a permanent shunt. Relief of hydrocephalus can lead to an enormous improvement in a persons condition. Fluctuations in blood pressure and electrolyte imbalance, as well as pneumonia and cardiac decompensation occur in about half the hospitalized persons with SAH and may worsen prognosis. Seizures occur during the hospital stay in about a third of cases.People have often been treated with preventative antiepileptic medications. This is controversial and not based on good evidence. In some studies, use of these medications was associated with a worse prognosis; although it is unclear whether this might be because the drugs themselves actually cause harm, or because they are used more often in persons with a poorer prognosis. There is a possibility of a gastric hemorrhage due to stress ulcers.

Prognosis
Short-term outcomes
SAH is often associated with a poor outcome. The death rate (mortality) for SAH is between 40 and 50 percent, but trends for survival are improving. Of those that survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever. Delay in diagnosis of minor SAH (mistaking the sudden headache for migraine) contributes to poor outcome. Factors found on admission that are associated with poorer outcome include poorer neurological grade; systolic hypertension; a previous diagnosis of heart attack or SAH; liver disease; more blood and larger aneurysm on the initial CT scan; location of an aneurysm in the posterior circulation; and higher age. Factors that carry a worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from vasospasm, development of intracerebral hematoma, or intraventricular hemorrhage (bleeding into the ventricles of the brain) and presence of fever on the eighth day of admission.So-called "angiogram-negative subarachnoid hemorrhage", SAH that does not show an aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysm, but it is still associated with a risk of ischemia, rebleeding, and hydrocephalus. Perimesencephalic SAH (bleeding around the mesencephalon in the brain), however, has a very low rate of rebleeding or delayed ischemia, and the prognosis of this subtype is excellent.The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding. It is difficult to isolate the effects of SAH from those of other aspects of traumatic brain injury; it is unknown whether the presence of subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred. People with moderate and severe traumatic brain injury who have SAH when admitted to a hospital have as much as twice the risk of dying as those who do not. They also have a higher risk of severe disability and persistent vegetative state, and traumatic SAH has been correlated with other markers of poor outcome such as post traumatic epilepsy, hydrocephalus, and longer stays in the intensive care unit.  More than 90 percent of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12 have a good outcome.There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of the gene encoding apolipoprotein E that also plays a role in Alzheimers disease) seems to increase risk for delayed ischemia and a worse outcome. The occurrence of hyperglycemia (high blood sugars) after an episode of SAH confers a higher risk of poor outcome.

Long-term outcomes
Neurocognitive symptoms, such as fatigue, mood disturbances, and other related symptoms, are common sequelae. Even in those who have made good neurological recovery, anxiety, depression, posttraumatic stress disorder, and cognitive impairment are common; 46 percent of people who have had a subarachnoid hemorrhage have cognitive impairment that affects their quality of life. Over 60 percent report frequent headaches. Aneurysmal subarachnoid hemorrhage may lead to damage of the hypothalamus and the pituitary gland, two areas of the brain that play a central role in hormonal regulation and production. More than a quarter of people with a previous SAH may develop hypopituitarism (deficiencies in one or more of the hypothalamic–pituitary hormones such as growth hormone, luteinizing hormone, or follicle-stimulating hormone). SAH is also associated with SIADH and cerebral salt wasting, and is the most common cause of the latter.

Epidemiology
According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.Although the group of people at risk for SAH is younger than the population usually affected by stroke, the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage. The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55. Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.Genetics may play a role in a persons disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage. But lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption. Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked. Some protection of uncertain significance is conferred by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. There is likely an inverse relationship between total serum cholesterol and the risk of non-traumatic SAH, though confirmation of this association is hindered by a lack of studies. Approximately 4 percent of aneurysmal bleeds occur after sexual intercourse and 10 percent of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these are small and unlikely to rupture.

History
While the clinical picture of subarachnoid hemorrhage may have been recognized by Hippocrates, the existence of cerebral aneurysms and the fact that they could rupture was not established until the 18th century </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 Dysequilibrium syndrome and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Gingival and periodontal pocket and can you explain it in depth? [/INST] Gingival and periodontal pockets (also informally referred to as gum pockets) are dental terms indicating the presence of an abnormal depth of the gingival sulcus near the point at which the gingival tissue contacts the tooth.

Tooth gingival interface
The interface between a tooth and the surrounding gingival tissue is a dynamic structure.  The gingival tissue forms a crevice surrounding the tooth, similar to a miniature, fluid-filled moat, wherein food debris, endogenous and exogenous cells, and chemicals float. The depth of this crevice, known as a sulcus, is in a constant state of flux due to microbial invasion and subsequent immune response. Located at the depth of the sulcus is the epithelial attachment, consisting of approximately 1 mm of junctional epithelium and another 1 mm of gingival fiber attachment, comprising the 2 mm of biologic width naturally found in the oral cavity.  The sulcus is literally the area of separation between the surrounding epithelium and the surface of the encompassed tooth.

Gingival pocket
A gingival pocket presents when the marginal gingiva experiences an edematous reaction, whether due to localized irritation and subsequent inflammation, systemic issues, or drug induced gingival hyperplasia.  Regardless of the etiology, when gingival hyperplasia occurs, greater than normal (the measurement in a pre-pathological state) periodontal probing measurements can be read, creating the illusion that periodontal pockets have developed.  This phenomenon is also referred to as a false pocket or pseudopocket.  The epithelial attachment does not migrate, it simply remains at the same attachment level found in pre-pathological health.  The only anatomical landmark experiencing migration is the gingival margin in a coronal direction.
In a gingival pocket, no destruction of the connective tissue fibers (gingival fibers) or alveolar bone occurs. This early sign of disease in the mouth is completely reversible when the etiology of the edematous reaction is eliminated and frequently occurs without dental surgical therapy.  However, in certain situations, a gingivectomy is necessary to reduce the gingival pocket depths to a healthy 1–3 mm.

Periodontal pocket
As the original sulcular depth increases and the apical migration of the junctional epithelium has simultaneously occurred, the pocket is now lined by pocket epithelium (PE) instead of junctional epithelium (JE). To have a true periodontal pocket, a probing measurement of 4 mm or more must be clinically evidenced.  In this state, much of the gingival fibers that initially attached the gingival tissue to the tooth have been irreversibly destroyed. The depth of the periodontal pockets must be recorded in the patient record for proper monitoring of periodontal disease. Unlike in clinically healthy situations, parts of the sulcular epithelium can sometimes be seen in periodontally involved gingival tissue if air is blown into the periodontal pocket, exposing the newly denuded roots of the tooth. A periodontal pocket can become an infected space and may result in an abscess formation with a papule on the gingival surface. Incision and drainage of the abscess may be necessary, as well as systemic antibiotics; placement of local antimicrobial delivery systems within the periodontal pocket to reduce localized infections may also be considered.
It is classified as supra bony and infra bony based on its depth in relation to alveolar bone.

Mucogingival defect
If the destruction continues unabated apically and reaches the junction of the attached gingiva and alveolar mucosa, the pocket would thus be in violation of the mucogingival junction and would be termed a mucogingival defect.

Pocket formation
For the periodontal pocket to form, several elements need to be present. It all starts with the dental plaque . The invasion of the bacteria from the plaque eventually triggers inflammatory response. This in turn results in the gradual destruction of the tissues surrounding the teeth, known as the periodontium.  Plaque that has been present long enough to harden and calcify will welcome additional bacteria to the pocket and make it virtually impossible to clean by means of a traditional toothbrush.  Continuous destruction of surrounding tissues due to inflammation will lead to degradation of attachment and bone, eventually causing tooth loss. Certain circumstances can worsen the condition and are known as risk factors </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 Torus and can you explain it in depth? [/INST] In geometry, a torus (plural tori, colloquially donut or doughnut) is a surface of revolution generated by revolving a circle in three-dimensional space about an axis that is coplanar with the circle.
If the axis of revolution does not touch the circle, the surface has a ring shape and is called a torus of revolution. If the axis of revolution is tangent to the circle, the surface is a horn torus. If the axis of revolution passes twice through the circle, the surface is a spindle torus. If the axis of revolution passes through the center of the circle, the surface is a degenerate torus, a double-covered sphere. If the revolved curve is not a circle, the surface is a related shape, a toroid.
Real-world objects that approximate a torus of revolution include swim rings, inner tubes and ringette rings. Eyeglass lenses that combine spherical and cylindrical correction are toric lenses.A torus should not be confused with a solid torus, which is formed by rotating a disk, rather than a circle, around an axis. A solid torus is a torus plus the volume inside the torus. Real-world objects that approximate a solid torus include O-rings, non-inflatable lifebuoys, ring doughnuts, and bagels.
In topology, a ring torus is homeomorphic to the Cartesian product of two circles: S1 × S1, and the latter is taken to be the definition in that context. It is a compact 2-manifold of genus 1. The ring torus is one way to embed this space into Euclidean space, but another way to do this is the Cartesian product of the embedding of S1 in the plane with itself. This produces a geometric object called the Clifford torus, a surface in 4-space.
In the field of topology, a torus is any topological space that is homeomorphic to a torus. The surface of a coffee cup and a doughnut are both topological tori with genus one.
An example of a torus can be constructed by taking a rectangular strip of flexible material, for example, a rubber sheet, and joining the top edge to the bottom edge, and the left edge to the right edge, without any half-twists (compare Möbius strip).

Geometry
A torus can be defined parametrically by:
where

θ, φ are angles which make a full circle, so their values start and end at the same point,
R is the distance from the center of the tube to the center of the torus,
r is the radius of the tube.Angle θ represents rotation around the tube, whereas φ represents rotation around the torus axis of revolution. R is known as the "major radius" and r is known as the "minor radius". The ratio R divided by r is known as the "aspect ratio". The typical doughnut confectionery has an aspect ratio of about 3 to 2.
An implicit equation in Cartesian coordinates for a torus radially symmetric about the z-axis is

or the solution of f(x, y, z) = 0, where

Algebraically eliminating the square root gives a quartic equation,

The three classes of standard tori correspond to the three possible aspect ratios between R and r:

When R > r, the surface will be the familiar ring torus or anchor ring.
R = r corresponds to the horn torus, which in effect is a torus with no "hole".
R < r describes the self-intersecting spindle torus; its inner shell is a lemon and its outer shell is an apple
When R = 0, the torus degenerates to the sphere.When R ≥ r, the interior

of this torus is diffeomorphic (and, hence, homeomorphic) to a product of a Euclidean open disk and a circle. The volume of this solid torus and the surface area of its torus are easily computed using Pappuss centroid theorem, giving:
These formulas are the same as for a cylinder of length 2πR and radius r, obtained from cutting the tube along the plane of a small circle, and unrolling it by straightening out (rectifying) the line running around the center of the tube. The losses in surface area and volume on the inner side of the tube exactly cancel out the gains on the outer side.
Expressing the surface area and the volume by the distance p of an outermost point on the surface of the torus to the center, and the distance q of an innermost point to the center (so that R = p + q/2 and r = p − q/2), yields

As a torus is the product of two circles, a modified version of the spherical coordinate system is sometimes used.
In traditional spherical coordinates there are three measures, R, the distance from the center of the coordinate system, and θ and φ, angles measured from the center point.
As a torus has, effectively, two center points, the centerpoints of the angles are moved; φ measures the same angle as it does in the spherical system, but is known as the "toroidal" direction. The center point of θ is moved to the center of r, and is known as the "poloidal" direction. These terms were first used in a discussion of the Earths magnetic field, where "poloidal" was used to denote "the direction toward the poles".In modern use, toroidal and poloidal are more commonly used to discuss magnetic confinement fusion devices.

Topology
Topologically, a torus is a closed surface defined as the product of two circles: S1 × S1. This can be viewed as lying in C2 and is a subset of the 3-sphere S3 of radius √2. This topological torus is also often called the Clifford torus. In fact, S3 is filled out by a family of nested tori in this manner (with two degenerate circles), a fact which is important in the study of S3 as a fiber bundle over S2 (the Hopf bundle).
The surface described above, given the relative topology from R3, is homeomorphic to a topological torus as long as it does not intersect its own axis. A particular homeomorphism is given by stereographically projecting the topological torus into R3 from the north pole of S3.
The torus can also be described as a quotient of the Cartesian plane under the identifications

        (
        x
        ,
        y
        )
        ∼
        (
        x
        +
        1
        ,
        y
        )
        ∼
        (
        x
        ,
        y
        +
        1
        )
        ,

    {\displaystyle (x,y)\sim (x+1,y)\sim (x,y+1),\,}
  or, equivalently, as the quotient of the unit square by pasting the opposite edges together, described as a fundamental polygon ABA−1B−1.

The fundamental group of the torus is just the direct product of the fundamental group of the circle with itself:

          π

            1

        (

            T

            2

        )
        =

          π

            1

        (

          S

            1

        )
        ×

          π

            1

        (

          S

            1

        )
        ≅

          Z

        ×

          Z

        .

    {\displaystyle \pi _{1}(\mathbf {T} ^{2})=\pi _{1}(S^{1})\times \pi _{1}(S^{1})\cong \mathbf {Z} \times \mathbf {Z} .}
  Intuitively speaking, this means that a closed path that circles the torus "hole" (say, a circle that traces out a particular latitude) and then circles the torus "body" (say, a circle that traces out a particular longitude) can be deformed to a path that circles the body and then the hole. So, strictly latitudinal and strictly longitudinal paths commute. An equivalent statement may be imagined as two shoelaces passing through each other, then unwinding, then rewinding.
If a torus is punctured and turned inside out then another torus results, with lines of latitude and longitude interchanged. This is equivalent to building a torus from a cylinder, by joining the circular ends together, in two ways: around the outside like joining two ends of a garden hose, or through the inside like rolling a sock (with the toe cut off). Additionally, if the cylinder was made by gluing two opposite sides of a rectangle together, choosing the other two sides instead will cause the same reversal of orientation.
The first homology group of the torus is isomorphic to the fundamental group (this follows from Hurewicz theorem since the fundamental group is abelian).

Two-sheeted cover
The 2-torus double-covers the 2-sphere, with four ramification points. Every conformal structure on the 2-torus can be represented as a two-sheeted cover of the 2-sphere. The points on the torus corresponding to the ramification points are the Weierstrass points. In fact, the conformal type of the torus is determined by the cross-ratio of the four points.

n-dimensional torus
The torus has a generalization to higher dimensions, the n-dimensional torus, often called the n-torus or hypertorus for short. (This is the more typical meaning of the term "n-torus", the other referring to n holes or of genus n.) Recalling that the torus is the product space of two circles, the n-dimensional torus is the product of n circles. That is:

            T

            n

        =

                  S

                    1

                ×
                ⋯
                ×

                  S

                    1

              ⏟

            n

        .

    {\displaystyle \mathbf {T} ^{n}=\underbrace {S^{1}\times \cdots \times S^{1}} _{n}.}
  The 1-torus is just the circle: T1 = S1. The torus discussed above is the 2-torus, T2. And similar to the 2-torus, the n-torus, Tn can be described as a quotient of Rn under integral shifts in any coordinate. That is, the n-torus is Rn modulo the action of the integer lattice Zn (with the action being taken as vector addition). Equivalently, the n-torus is obtained from the n-dimensional hypercube by gluing the opposite faces together.
An n-torus in this sense is an example of an n-dimensional compact manifold. It is also an example of a compact abelian Lie group. This follows from the fact that the unit circle is a compact abelian Lie group (when identified with the unit complex numbers with multiplication). Group multiplication on the torus is then defined by coordinate-wise multiplication.
Toroidal groups play an important part in the theory of compact Lie groups. This is due in part to the fact that in any compact Lie group G one can always find a maximal torus; that is, a closed subgroup which is a torus of the largest possible dimension. Such maximal tori T have a controlling role to play in theory of connected G. Toroidal groups are examples of protori, which (like tori) are compact connected abelian groups, which are not required to be manifolds.
Automorphisms of T are easily constructed from automorphisms of the lattice Zn, which are classified by invertible integral matrices of size n with an integral inverse; these are just the integral matrices with determinant ±1. Making them act on Rn in the usual way, one has the typical toral automorphism on the quotient.
The fundamental group of an n-torus is a free abelian group of rank n. The k-th homology group of an n-torus is a free abelian group of rank n choose k. It follows that the Euler characteristic of the n-torus is 0 for all n. The cohomology ring H•(Tn, Z) can be identified with the exterior algebra over the Z-module Zn whose generators are the duals of the n nontrivial cycles.

Configuration space
As the n-torus is the n-fold product of the circle, the n-torus is the configuration space of n ordered, not necessarily distinct points on the circle. Symbolically, Tn = (S1)n. The configuration space of unordered, not necessarily distinct points is accordingly the orbifold Tn/Sn, which is the quotient of the torus by the symmetric group on n letters (by permuting the coordinates).
For n = 2, the quotient is the Möbius strip, the edge corresponding to the orbifold points where the two coordinates coincide. For n = 3 this quotient may be described as a solid torus with cross-section an equilateral triangle, with a twist; equivalently, as a triangular prism whose top and bottom faces are connected with a 1/3 twist (120°): the 3-dimensional interior corresponds to the points on the 3-torus where all 3 coordinates are distinct, the 2-dimensional face corresponds to points with 2 coordinates equal and the 3rd different, while the 1-dimensional edge corresponds to points with all 3 coordinates identical.
These orbifolds have found significant applications to music theory in the work of Dmitri Tymoczko and collaborators (Felipe Posada, Michael Kolinas, et al.), being used to model musical triads.

Flat torus
A flat torus is a torus with the metric inherited from its representation as the quotient, R2/L, where L is a discrete subgroup of R2 isomorphic to Z2. This gives the quotient the structure of a Riemannian manifold. Perhaps the simplest example of this is when L = Z2: R2/Z2, which can also be described as the Cartesian plane under the identifications (x, y) ~ (x + 1, y) ~ (x, y + 1). This particular flat torus (and any uniformly scaled version of it) is known as the "square" flat torus.
This metric of the square flat torus can also be realised by specific embeddings of the familiar 2-torus into Euclidean 4-space or higher dimensions. Its surface has zero Gaussian curvature everywhere. Its surface is flat in the same sense that the surface of a cylinder is flat. In 3 dimensions, one can bend a flat sheet of paper into a cylinder without stretching the paper, but this cylinder cannot be bent into a torus without stretching the paper (unless some regularity and differentiability conditions are given up, see below).
A simple 4-dimensional Euclidean embedding of a rectangular flat torus (more general than the square one) is as follows:

        (
        x
        ,
        y
        ,
        z
        ,
        w
        )
        =
        (
        R
        cos

        u
        ,
        R
        sin

        u
        ,
        P
        cos

        v
        ,
        P
        sin

        v
        )

    {\displaystyle (x,y,z,w)=(R\cos u,R\sin u,P\cos v,P\sin v)}
  where R and P are positive constants determining the aspect ratio. It is diffeomorphic to a regular torus but not isometric. It can not be analytically embedded (smooth of class Ck, 2 ≤ k ≤ ∞) into Euclidean 3-space. Mapping it into 3-space requires one to stretch it, in which case it looks like a regular torus. For example, in the following map:

        (
        x
        ,
        y
        ,
        z
        )
        =
        (
        (
        R
        +
        P
        sin

        v
        )
        cos

        u
        ,
        (
        R
        +
        P
        sin

        v
        )
        sin

        u
        ,
        P
        cos

        v
        )
        .

    {\displaystyle (x,y,z)=((R+P\sin v)\cos u,(R+P\sin v)\sin u,P\cos v).}
  If R and P in the above flat torus parametrization form a unit vector (R, P) = (cos(η), sin(η)) then u, v, and 0 < η < π/2 parameterize the unit 3-sphere as Hopf coordinates. In particular, for certain very specific choices of a square flat torus in the 3-sphere S3, where η = π/4 above, the torus will partition the 3-sphere into two congruent solid tori subsets with the aforesaid flat torus surface as their common boundary. One example is the torus T defined by

        T
        =

          {

            (
            x
            ,
            y
            ,
            z
            ,
            w
            )
            ∈

                S

                3

            ∣

              x

                2

            +

              y

                2

            =

                1
                2

            ,

              z

                2

            +

              w

                2

            =

                1
                2

          }

        .

    {\displaystyle T=\left\{(x,y,z,w)\in \mathbf {S} ^{3}\mid x^{2}+y^{2}={\frac {1}{2}},\ z^{2}+w^{2}={\frac {1}{2}}\right\}.}
  Other tori in S3 having this partitioning property include the square tori of the form Q⋅T, where Q is a rotation of 4-dimensional space R4, or in other words Q is a member of the Lie group SO(4).
It is known that there exists no C2 (twice continuously differentiable) embedding of a flat torus into 3-space. (The idea of the proof is to take a large sphere containing such a flat torus in its interior, and shrink the radius of the sphere until it just touches the torus for the first time. Such a point of contact must be a tangency. But that would imply that part of the torus, since it has zero curvature everywhere, must lie strictly outside the sphere, which is a contradiction.) On the other hand, according to the Nash-Kuiper theorem, which was proven in the 1950s, an isometric C1 embedding exists. This is solely an existence proof and does not provide explicit equations for such an embedding.
In April 2012, an explicit C1 (continuously differentiable) embedding of a flat torus into 3-dimensional Euclidean space R3 was found. It is similar in structure to a fractal as it is constructed by repeatedly corrugating an ordinary torus. Like fractals, it has no defined Gaussian curvature. However, unlike fractals, it does have defined surface normals. It is a flat torus in the sense that as metric spaces, it is isometric to a flat square torus. (These infinitely recursive corrugations are used only for embedding into three dimensions; they are not an intrinsic feature of the flat torus.) This is the first time that any such embedding was defined by explicit equations or depicted by computer graphics.

Genus g surface
In the theory of surfaces there is another object, the "genus" g surface. Instead of the product of n circles, a genus g surface is the connected sum of g two-tori. To form a connected sum of two surfaces, remove from each the interior of a disk and "glue" the surfaces together along the boundary circles. To form the connected sum of more than two surfaces, sum two of them at a time until they are all connected. In this sense, a genus g surface resembles the surface of g doughnuts stuck together side by side, or a 2-sphere with g handles attached.
As examples, a genus zero surface (without boundary) is the two-sphere while a genus one surface (without boundary) is the ordinary torus. The surfaces of higher genus are sometimes called n-holed tori (or, rarely, n-fold tori). The terms double torus and triple torus are also occasionally used.
The classification theorem for surfaces states that every compact connected surface is topologically equivalent to either the sphere or the connect sum of some number of tori, disks, and real projective planes.

Toroidal polyhedra
Polyhedra with the topological type of a torus are called toroidal polyhedra, and have Euler characteristic V − E + F = 0. For any number of holes, the formula generalizes to V − E + F = 2 − 2N, where N is the number of holes.
The term "toroidal polyhedron" is also used for higher-genus polyhedra and for immersions of toroidal polyhedra.

Automorphisms
The homeomorphism group (or the subgroup of diffeomorphisms) of the torus is studied in geometric topology. Its mapping class group ( the connected components of the homeomorphism group) is surjective onto the group GL(n, Z) of invertible integer matrices, which can be realized as linear maps on the universal covering space Rn that preserve the standard lattice Zn (this corresponds to integer coefficients) and thus descend to the quotient.
At the level of homotopy and homology, the mapping class group can be identified as the action on the first homology (or equivalently, first cohomology, or on the fundamental group, as these are all naturally isomorphic; also the first cohomology group generates the cohomology algebra:

          MCG

            Ho

        (

            T

            n

        )
        =
        Aut

        (

          π

            1

        (
        X
        )
        )
        =
        Aut

        (

            Z

            n

        )
        =
        GL

        (
        n
        ,

          Z

        )
        .

    {\displaystyle \operatorname {MCG} _{\operatorname {Ho} }(\mathbf {T} ^{n})=\operatorname {Aut} (\pi _{1}(X))=\operatorname {Aut} (\mathbf {Z} ^{n})=\operatorname {GL} (n,\mathbf {Z} ).}
  Since the torus is an Eilenberg–MacLane space K(G, 1), its homotopy equivalences, up to homotopy, can be identified with automorphisms of the fundamental group); all homotopy equivalences of the torus can be realized by homeomorphisms – every homotopy equivalence is homotopic to a homeomorphism.
Thus the short exact sequence of the mapping class group splits (an identification of the torus as the quotient of Rn gives a splitting, via the linear maps, as above):

        1
        →

          Homeo

            0

        (

            T

            n

        )
        →
        Homeo

        (

            T

            n

        )
        →

          MCG

            TOP

        (

            T

            n

        )
        →
        1.

    {\displaystyle 1\to \operatorname {Homeo} _{0}(\mathbf {T} ^{n})\to \operatorname {Homeo} (\mathbf {T} ^{n})\to \operatorname {MCG} _{\operatorname {TOP} }(\mathbf {T} ^{n})\to 1.}
  The mapping class group of higher genus surfaces is much more complicated, and an area of active research.

Coloring a torus
The toruss chromatic number is seven, meaning every graph that can be embedded on the torus has a chromatic number of at most seven. (Since the complete graph

              K

                7

    {\displaystyle {\mathsf {K_{7}}}}
   can be embedded on the torus, and

        χ
        (

              K

                7

        )
        =
        7

    {\displaystyle \chi ({\mathsf {K_{7}}})=7}
  , the upper bound is tight.) Equivalently, in a torus divided into regions, it is always possible to color the regions using no more than seven colors so that no neighboring regions are the same color. (Contrast with the four color theorem for the plane.)

de Bruijn torus
In combinatorial mathematics, a de Bruijn torus is an array of symbols from an alphabet (often just 0 and 1) that contains every m-by-n matrix exactly once.  It is a torus because the edges are considered wraparound for the purpose of finding matrices. Its name comes from the De Bruijn sequence, which can be considered a special case where n is 1 (one dimension).

Cutting a torus
A solid torus of revolution can be cut by n (> 0) planes into maximally

            (

                  n
                  +
                  2

                  n
                  −
                  1

            )

        +

            (

                  n

                  n
                  −
                  1

            )

        =

              1
              6

        (

          n

            3

        +
        3

          n

            2

        +
        8
        n
        )

    {\displaystyle {\begin{pmatrix}n+2\\n-1\end{pmatrix}}+{\begin{pmatrix}n\\n-1\end{pmatrix}}={\tfrac {1}{6}}(n^{3}+3n^{2}+8n)}
  parts.The first 11 numbers of parts, for 0 ≤ n ≤ 10 (including the case of n = 0, not covered by the above formulas), are as follows:

1, 2, 6, 13, 24, 40, 62, 91, 128, 174, 230, ... (sequence A003600 in the OEIS).

See also
Notes
Nociones de Geometría Analítica y Álgebra Lineal, ISBN 978-970-10-6596-9, Author: Kozak Ana Maria, Pompeya Pastorelli Sonia, Verdanega Pedro Emilio, Editorial: McGraw-Hill, Edition 2007, 744 pages, language: Spanish
Allen Hatcher. Algebraic Topology. Cambridge University Press, 2002. ISBN 0-521-79540-0.
V. V </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 Paronychia and can you explain it in depth? [/INST] Paronychia is an inflammation of the skin around the nail, which can occur suddenly, when it is usually due to the bacterium Staphylococcus aureus, or gradually when it is commonly caused by the fungus Candida albicans. The term is from Greek: παρωνυχία from para around, onyx nail, and the abstract noun suffix -ia.Risk factors include repeatedly washing hands and trauma to the cuticle such as may occur from repeated nail biting or hangnails.
Treatment includes antibiotics and antifungals, and if pus is present, the consideration of incision and drainage.Paronychia is commonly misapplied as a synonym for herpetic whitlow or felon.

Definition and etymology
Paronychia is an inflammation of the skin around the nail, which can occur suddenly (acute), when it is usually due to the bacterium Staphylococcus aureus, or gradually (chronic) when it is commonly caused by Candida albicans.The term is from Greek: παρωνυχία from para, "around", onyx, "nail" and the noun suffix -ia.

Signs and symptoms
The index and middle fingers are most commonly affected and may present with redness, swelling and pain. Pus or discharge may be present.

Causes
Acute paronychia is usually caused by bacteria. It is often treated with antibiotics, either topical (applied to the skin) or oral (taken by mouth), or both. Chronic paronychia is most often caused by a yeast infection of the soft tissues around the nail, but can also be traced to a bacterial infection. If the infection is continuous, the cause is often fungal and needs antifungal cream or paint to be treated.Risk factors include repeatedly washing hands and trauma to the cuticle such as may occur from repeated nail biting. or hangnails. In the context of bartending, it is known as "bar rot".Prosectors paronychia is a primary inoculation of tuberculosis of the skin and nails, named after its association with prosectors, who prepare specimens for dissection. Paronychia around the entire nail is sometimes referred to as "runaround paronychia".Painful paronychia in association with a scaly, erythematous, keratotic rash (papules and plaques) of the ears, nose, fingers, and toes may be indicative of acrokeratosis paraneoplastica, which is associated with squamous-cell carcinoma of the larynx.Paronychia can occur with diabetes, drug-induced immunosuppression, or systemic diseases such as pemphigus.

Diagnosis
Types
Paronychia may be divided as occurring suddenly, acute, or gradually, chronic.

Acute
Acute paronychia is an infection of the folds of tissue surrounding the nail of a finger or, less commonly, a toe, lasting less than six weeks. The infection generally starts in the paronychium at the side of the nail, with local redness, swelling, and pain.: 660  Acute paronychia is usually caused by direct or indirect trauma to the cuticle or nail fold, and may be from relatively minor events, such as dishwashing, an injury from a splinter or thorn, nail biting, biting or picking at a hangnail, finger sucking, an ingrown nail, or manicure procedures.: 339

Chronic
Chronic paronychia is an infection of the folds of tissue surrounding the nail of a finger or, less commonly, a toe, lasting more than six weeks. It is a nail disease prevalent in individuals whose hands or feet are subject to moist local environments, and is often due to contact dermatitis.: 660  In chronic paronychia, the cuticle separates from the nail plate, leaving the region between the proximal nail fold and the nail plate vulnerable to infection.: 343  It can be the result of dish washing, finger sucking, aggressively trimming the cuticles, or frequent contact with chemicals (mild alkalis, acids, etc.).
Alternatively, paronychia may be divided as follows:
Candidal paronychia is an inflammation of the nail fold produced by C. albicans.: 310
Pyogenic paronychia is an inflammation of the folds of skin surrounding the nail caused by bacteria.: 254  Generally, acute paronychia is pyogenic, as it is usually caused by a bacterial infection.

Differential
Differential diagnosis of paronychia includes:

Cellulitis is a superficial infection and presents as erythema and swelling to the affected portion of the body with no area of fluctuance. Treatment is with oral antibiotics.
Whitlow or felon is a subcutaneous infection of the digital pulp space. The area becomes warm, red, tense, and very painful due to the confinement of the infection, creating pressure in the individual compartments created by the septa of the finger pad. These require excision and drainage, usually with a longitudinal incision and blunt dissection to ensure adequate drainage.
Herpetic whitlow is a viral infection of the distal finger caused by HSV. Patients usually develop a burning, pruritic sensation before the infection erupts. A physical exam shows vesicles and vesicopustules, along with pain and erythema. It is important to not confuse this with a felon or a paronychia as incision and drainage of herpetic whitlow could result in a secondary bacterial infection and failure to heal.
Onychomycosis is a fungal infection of the nail that causes whitish-yellowish discoloration. Sometimes, it is difficult to treat and requires oral antibiotics instead of topical.
Nail psoriasis  can affect the fingernails and toenails. It may cause thickening of the nails with areas of pitting, ridges, irregular contour, and even raising of the nail from the nail bed.
Squamous-cell carcinoma is mainly cancer of the skin, but can also affect the nail bed. It is a rare malignant subungual tumor subject to misdiagnosis as chronic paronychia.

Treatment
When no pus is present, warm soaks for acute paronychia are reasonable, though evidence to support its use is lacking.Chronic paronychia is treated by avoiding whatever is causing it, a topical antifungal, and a topical steroid. In those who do not improve following these measures, oral antifungals and steroids may be used or the nail fold may be removed surgically.

Antibiotics
No strong evidence has been found to recommend topical vs. oral antibiotics, and this may be physician-dependent based on experience. Antibiotics used should have S. aureus coverage </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 Acephaly and can you explain it in depth? [/INST]  </s>