<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Otitis media and explain in detail? [/INST] Otitis media is a group of inflammatory diseases of the middle ear. One of the two main types is acute otitis media (AOM), an infection of rapid onset that usually presents with ear pain. In young children this may result in pulling at the ear, increased crying, and poor sleep. Decreased eating and a fever may also be present. The other main type is otitis media with effusion (OME), typically not associated with symptoms, although  occasionally a feeling of fullness is described; it is defined as the presence of non-infectious fluid in the middle ear which may persist for weeks or months often after an episode of acute otitis media. Chronic suppurative otitis media (CSOM) is middle ear inflammation that results in a perforated tympanic membrane with discharge from the ear for more than six weeks. It may be a complication of acute otitis media. Pain is rarely present. All three types of otitis media may be associated with hearing loss. If children with hearing loss due to OME do not learn sign language, it may affect their ability to learn.The cause of AOM is related to childhood anatomy and immune function. Either bacteria or viruses may be involved. Risk factors include exposure to smoke, use of pacifiers, and attending daycare. It occurs more commonly among indigenous peoples and those who have cleft lip and palate or Down syndrome. OME frequently occurs following AOM and may be related to viral upper respiratory infections, irritants such as smoke, or allergies. Looking at the eardrum is important for making the correct diagnosis. Signs of AOM include bulging or a lack of movement of the tympanic membrane from a puff of air. New discharge not related to otitis externa also indicates the diagnosis.A number of measures decrease the risk of otitis media including pneumococcal and influenza vaccination, breastfeeding, and avoiding tobacco smoke. The use of pain medications for AOM is important. This may include paracetamol (acetaminophen), ibuprofen, benzocaine ear drops, or opioids. In AOM, antibiotics may speed recovery but may result in side effects. Antibiotics are often recommended in those with severe disease or under two years old. In those with less severe disease they may only be recommended in those who do not improve after two or three days. The initial antibiotic of choice is typically amoxicillin. In those with frequent infections tympanostomy tubes may decrease recurrence. In children with otitis media with effusion antibiotics may increase resolution of symptoms, but may cause diarrhoea, vomiting and skin rash.Worldwide AOM affects about 11% of people a year (about 325 to 710 million cases). Half the cases involve children less than five years of age and it is more common among males. Of those affected about 4.8% or 31 million develop chronic suppurative otitis media. The total number of people with CSOM is estimated at 65–330 million people. Before the age of ten OME affects about 80% of children at some point. Otitis media resulted in 3,200 deaths in 2015 – down from 4,900 deaths in 1990.

Signs and symptoms
The primary symptom of acute otitis media is ear pain; other possible symptoms include fever, reduced hearing during periods of illness, tenderness on touch of the skin above the ear, purulent discharge from the ears, irritability, ear blocking sensation and diarrhea (in infants). Since an episode of otitis media is usually precipitated by an upper respiratory tract infection (URTI), there are often accompanying symptoms like a cough and nasal discharge.  One might also experience a feeling of fullness in the ear.
Discharge from the ear can be caused by acute otitis media with perforation of the eardrum, chronic suppurative otitis media, tympanostomy tube otorrhea, or acute otitis externa. Trauma, such as a basilar skull fracture, can also lead to cerebrospinal fluid otorrhea (discharge of CSF from the ear) due to cerebral spinal drainage from the brain and its covering (meninges).

Causes
The common cause of all forms of otitis media is dysfunction of the Eustachian tube. This is usually due to inflammation of the mucous membranes in the nasopharynx, which can be caused by a viral upper respiratory tract infection (URTI), strep throat, or possibly by allergies.By reflux or aspiration of unwanted secretions from the nasopharynx into the normally sterile middle-ear space, the fluid may then become infected — usually with bacteria. The virus that caused the initial upper respiratory infection can itself be identified as the pathogen causing the infection.

Diagnosis
As its typical symptoms overlap with other conditions, such as acute external otitis, symptoms alone are not sufficient to predict whether acute otitis media is present; it has to be complemented by visualization of the tympanic membrane. Examiners may use a pneumatic otoscope with a rubber bulb attached to assess the mobility of the tympanic membrane. Other methods to diagnose otitis media is with a tympanometry, reflectometry or hearing test.
In more severe cases, such as those with associated hearing loss or high fever, audiometry, tympanogram, temporal bone CT and MRI can be used to assess for associated complications, such as mastoid effusion, subperiosteal abscess formation, bony destruction, venous thrombosis or meningitis.Acute otitis media in children with moderate to severe bulging of the tympanic membrane or new onset of otorrhea (drainage) is not due to external otitis. Also, the diagnosis may be made in children who have mild bulging of the ear drum and recent onset of ear pain (less than 48 hours) or intense erythema (redness) of the ear drum.
To confirm the diagnosis, middle-ear effusion and inflammation of the eardrum have to be identified; signs of these are fullness, bulging, cloudiness and redness of the eardrum. It is important to attempt to differentiate between acute otitis media and otitis media with effusion (OME), as antibiotics are not recommended for OME. It has been suggested that bulging of the tympanic membrane is the best sign to differentiate AOM from OME, with a bulging of the membrane suggesting AOM rather than OME.Viral otitis may result in blisters on the external side of the tympanic membrane, which is called bullous myringitis (myringa being Latin for "eardrum").However, sometimes even examination of the eardrum may not be able to confirm the diagnosis, especially if the canal is small. If wax in the ear canal obscures a clear view of the eardrum it should be removed using a blunt cerumen curette or a wire loop. Also, an upset young childs crying can cause the eardrum to look inflamed due to distension of the small blood vessels on it, mimicking the redness associated with otitis media.

Acute otitis media
The most common bacteria isolated from the middle ear in AOM are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus.

Otitis media with effusion
Otitis media with effusion (OME), also known as serous otitis media (SOM) or secretory otitis media (SOM), and colloquially referred to as glue ear, is fluid accumulation that can occur in the middle ear and mastoid air cells due to negative pressure produced by dysfunction of the Eustachian tube. This can be associated with a viral upper respiratory infection (URI) or bacterial infection such as otitis media. An effusion can cause conductive hearing loss if it interferes with the transmission of vibrations of middle ear bones to the vestibulocochlear nerve complex that are created by sound waves.Early-onset OME is associated with feeding of infants while lying down, early entry into group child care, parental smoking, lack, or too short a period of breastfeeding and greater amounts of time spent in group child care, particularly those with a large number of children. These risk factors increase the incidence and duration of OME during the first two years of life.

Chronic suppurative otitis media
Chronic suppurative otitis media (CSOM) is a chronic inflammation of the middle ear and mastoid cavity that is characterised by discharge from the middle ear through a perforated tympanic membrane for at least 6 weeks. CSOM occurs following an upper respiratory tract infection that has led to acute otitis media. This progresses to a prolonged inflammatory response causing mucosal (middle ear) oedema, ulceration and perforation.  The middle ear attempts to resolve this ulceration by production of granulation tissue and polyp formation.  This can lead to increased discharge and failure to arrest the inflammation, and to development of CSOM, which is also often associated with cholesteatoma. There may be enough pus that it drains to the outside of the ear (otorrhea), or the pus may be minimal enough to be seen only on examination with an otoscope or binocular microscope. Hearing impairment often accompanies this disease. People are at increased risk of developing CSOM when they have poor eustachian tube function, a history of multiple episodes of acute otitis media, live in crowded conditions, and attend paediatric day care facilities.  Those with craniofacial malformations such as cleft lip and palate, Down syndrome, and microcephaly are at higher risk.Worldwide approximately 11% of the human population is affected by AOM every year, or 709 million cases. About 4.4% of the population develop CSOM.According to the World Health Organization, CSOM is a primary cause of hearing loss in children. Adults with recurrent episodes of CSOM have a higher risk of developing permanent conductive and sensorineural hearing loss.
In Britain, 0.9% of children and 0.5% of adults have CSOM, with no difference between the sexes. The incidence of CSOM across the world varies dramatically where high income countries have a relatively low prevalence while in low income countries the prevalence may be up to three times as great. Each year 21,000 people worldwide die due to complications of CSOM.

Adhesive otitis media
Adhesive otitis media occurs when a thin retracted ear drum becomes sucked into the middle-ear space and stuck (i.e., adherent) to the ossicles and other bones of the middle ear.

Prevention
AOM is far less common in breastfed infants than in formula-fed infants, and the greatest protection is associated with exclusive breastfeeding (no formula use) for the first six months of life. A longer duration of breastfeeding is correlated with a longer protective effect.Pneumococcal conjugate vaccines (PCV) in early infancy decrease the risk of acute otitis media in healthy infants. PCV is recommended for all children, and, if implemented broadly, PCV would have a significant public health benefit. Influenza vaccination in children appears to reduce rates of AOM by 4% and the use of antibiotics by 11% over 6 months. However, the vaccine resulted in increased adverse-effects such as fever and runny nose. The small reduction in AOM may not justify the side effects and inconvenience of influenza vaccination every year for this purpose alone. PCV does not appear to decrease the risk of otitis media when given to high-risk infants or for older children who have previously experienced otitis media.Risk factors such as season, allergy predisposition and presence of older siblings are known to be determinants of recurrent otitis media and persistent middle-ear effusions (MEE). History of recurrence, environmental exposure to tobacco smoke, use of daycare, and lack of breastfeeding have all been associated with increased risk of development, recurrence, and persistent MEE. Pacifier use has been associated with more frequent episodes of AOM.Long-term antibiotics, while they decrease rates of infection during treatment, have an unknown effect on long-term outcomes such as hearing loss. This method of prevention has been associated with emergence of antibiotic-resistant otitic bacteria. They are thus not recommended.There is moderate evidence that the sugar substitute xylitol may reduce infection rates in those who go to daycare.Evidence does not support zinc supplementation as an effort to reduce otitis rates except maybe in those with severe malnutrition such as marasmus.Probiotics do not show evidence of preventing acute otitis media in children.

Management
Oral and topical pain killers are effective to treat the pain caused by otitis media. Oral agents include ibuprofen, paracetamol (acetaminophen), and opiates. Evidence for the combination over single agents is lacking. Topical agents shown to be effective include antipyrine and benzocaine ear drops. Decongestants and antihistamines, either nasal or oral, are not recommended due to the lack of benefit and concerns regarding side effects. Half of cases of ear pain in children resolve without treatment in three days and 90% resolve in seven or eight days. The use of steroids is not supported by the evidence for acute otitis media.

Antibiotics
It is important to weigh the benefits and harms before using antibiotics for acute otitis media. As over 82% of acute episodes settle without treatment, about 20 children must be treated to prevent one case of ear pain, 33 children to prevent one perforation, and 11 children to prevent one opposite-side ear infection. For every 14 children treated with antibiotics, one child has an episode of either vomiting, diarrhea or a rash. If pain is present, pain medications may be used. For people requiring surgery to treat otitis media with effusion, preventative antibiotics may not help reduce the risk of post-surgical complications.For bilateral acute otitis media in infants younger than 24 months of age, there is evidence that the benefits of antibiotics outweigh the harms. A 2015 Cochrane review concluded that watchful waiting is the preferred approach for children over six months with non severe acute otitis media.
Most children older than 6 months of age who have acute otitis media do not benefit from treatment with antibiotics. If antibiotics are used, a narrow-spectrum antibiotic like amoxicillin is generally recommended, as broad-spectrum antibiotics may be associated with more adverse events. If there is resistance or use of amoxicillin in the last 30 days then amoxicillin-clavulanate or another penicillin derivative plus beta lactamase inhibitor is recommended. Taking amoxicillin once a day may be as effective as twice or three times a day. While less than 7 days of antibiotics have fewer side effects, more than seven days appear to be more effective. If there is no improvement after 2–3 days of treatment a change in therapy may be considered. Azithromycin appears to have less side effects than either high dose amoxicillin or amoxicillin/clavulanate.

Tympanostomy tube
Tympanostomy tubes (also called "grommets") are recommended with three or more episodes of acute otitis media in 6 months or four or more in a year, with at least one episode or more attacks in the preceding 6 months. There is tentative evidence that children with recurrent acute otitis media (AOM) who receive tubes have a modest improvement in the number of further AOM episodes (around one fewer episode at six months and less of an improvement at 12 months following the tubes being inserted). Evidence does not support an effect on long-term hearing or language development. A common complication of having a tympanostomy tube is otorrhea, which is a discharge from the ear. The risk of persistent tympanic membrane perforation after children have grommets inserted may be low. It is still uncertain whether or not grommets are more effective than a course of antibiotics.Oral antibiotics should not be used to treat uncomplicated acute tympanostomy tube otorrhea. They are not sufficient for the bacteria that cause this condition and have side effects including increased risk of opportunistic infection. In contrast, topical antibiotic eardrops are useful.

Otitis media with effusion
The decision to treat is usually made after a combination of physical exam and laboratory diagnosis, with additional testing including audiometry, tympanogram, temporal bone CT and MRI. Decongestants, glucocorticoids, and topical antibiotics are generally not effective as treatment for non-infectious, or serous, causes of mastoid effusion. Moreover, it is recommended against using antihistamines and decongestants in children with OME. In less severe cases or those without significant hearing impairment, the effusion can resolve spontaneously or with more conservative measures such as autoinflation. In more severe cases, tympanostomy tubes can be inserted, possibly with adjuvant adenoidectomy as it shows a significant benefit as far as the resolution of middle ear effusion in children with OME is concerned.

Chronic suppurative otitis media
Topical antibiotics are of uncertain benefit as of 2020. Some evidence suggests that topical antibiotics may be useful either alone or with antibiotics by mouth. Antiseptics are of unclear effect. Topical antibiotics (quinolones) are probably better at resolving ear discharge than antiseptics.

Alternative medicine
Complementary and alternative medicine is not recommended for otitis media with effusion because there is no evidence of benefit. Homeopathic treatments have not been proven to be effective for acute otitis media in a study with children.  An osteopathic manipulation technique called the Galbreath technique was evaluated in one randomized controlled clinical trial; one reviewer concluded that it was promising, but a 2010 evidence report found the evidence inconclusive.

Outcomes
Complications of acute otitis media consists of perforation of the ear drum, infection of the mastoid space behind the ear (mastoiditis), and more rarely intracranial complications can occur, such as bacterial meningitis, brain abscess, or dural sinus thrombosis. It is estimated that each year 21,000 people die due to complications of otitis media.

Membrane rupture
In severe or untreated cases, the tympanic membrane may perforate, allowing the pus in the middle-ear space to drain into the ear canal. If there is enough, this drainage may be obvious. Even though the perforation of the tympanic membrane suggests a highly painful and traumatic process, it is almost always associated with a dramatic relief of pressure and pain. In a simple case of acute otitis media in an otherwise healthy person, the bodys defenses are likely to resolve the infection and the ear drum nearly always heals.
An option for severe acute otitis media in which analgesics are not controlling ear pain is to perform a tympanocentesis, i.e., needle aspiration through the tympanic membrane to relieve the ear pain and to identify the causative organism(s).

Hearing loss
Children with recurrent episodes of acute otitis media and those with otitis media with effusion or chronic suppurative otitis media have higher risks of developing conductive and sensorineural hearing loss. Globally approximately 141 million people have mild hearing loss due to otitis media (2.1% of the population). This is more common in males (2.3%) than females (1.8%).This hearing loss is mainly due to fluid in the middle ear or rupture of the tympanic membrane. Prolonged duration of otitis media is associated with ossicular complications and, together with persistent tympanic membrane perforation, contributes to the severity of the disease and hearing loss. When a cholesteatoma or granulation tissue is present in the middle ear, the degree of hearing loss and ossicular destruction is even greater.Periods of conductive hearing loss from otitis media may have a detrimental effect on speech development in children. Some studies have linked otitis media to learning problems, attention disorders, and problems with social adaptation. Furthermore, it has been demonstrated that individuals with otitis media have more depression/anxiety-related disorders compared to individuals with normal hearing </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Inguinal hernia and explain in detail? [/INST] An inguinal hernia is a hernia (protrusion) of abdominal-cavity contents through the inguinal canal. Symptoms, which may include pain or discomfort especially with or following coughing, exercise, or bowel movements, are absent in about a third of patients. Symptoms often get worse throughout the day and improve when lying down. A bulging area may occur that becomes larger when bearing down. Inguinal hernias occur more often on the right than left side. The main concern is strangulation, where the blood supply to part of the intestine is blocked. This usually produces severe pain and tenderness of the area.Risk factors for the development of a hernia include: smoking, chronic obstructive pulmonary disease, obesity, pregnancy, peritoneal dialysis, collagen vascular disease, and previous open appendectomy, among others. Predisposition to hernias is genetic and they occur more often in certain families. Deleterious mutations causing predisposition to hernias seem to have dominant inheritance (especially for men). It is unclear if inguinal hernias are associated with heavy lifting. Hernias can often be diagnosed based on signs and symptoms. Occasionally medical imaging is used to confirm the diagnosis or rule out other possible causes.Groin hernias that do not cause symptoms in males do not need to be repaired. Repair, however, is generally recommended in females due to the higher rate of femoral hernias which have more complications. If strangulation occurs immediate surgery is required. Repair may be done by open surgery or by laparoscopic surgery. Open surgery has the benefit of possibly being done under local anesthesia rather than general anesthesia. Laparoscopic surgery generally has less pain following the procedure.In 2015 inguinal, femoral and abdominal hernias affected about 18.5 million people. About 27% of males and 3% of females develop a groin hernia at some time in their life. Groin hernias occur most often before the age of one and after the age of fifty. Globally, inguinal, femoral and abdominal hernias resulted in 60,000 deaths in 2015 and 55,000 in 1990.

Signs and symptoms
Hernias usually present as bulges in the groin area that can become more prominent when coughing, straining, or standing up. The bulge commonly disappears on lying down. Mild discomfort can develop over time. The inability to "reduce", or place the bulge back into the abdomen usually means the hernia is incarcerated which requires emergency surgery.
As the hernia progresses, contents of the abdominal cavity, such as the intestines, can descend into the hernia and run the risk of being pinched within the hernia, causing an intestinal obstruction. Significant pain at the hernia site is suggestive of a more severe course, such as incarceration (the hernia cannot be reduced back into the abdomen) and subsequent ischemia and strangulation (when the hernia becomes deprived of blood supply). If the blood supply of the portion of the intestine caught in the hernia is compromised, the hernia is deemed "strangulated" and gut ischemia and gangrene can result, with potentially fatal consequences. The timing of complications is not predictable.

Pathophysiology
In males, indirect hernias follow the same route as the descending testes, which migrate from the abdomen into the scrotum during the development of the urinary and reproductive organs. The larger size of their inguinal canal, which transmitted the testicle and accommodates the structures of the spermatic cord, might be one reason why men are 25 times more likely to have an inguinal hernia than women. Although several mechanisms such as strength of the posterior wall of the inguinal canal and shutter mechanisms compensating for raised intra-abdominal pressure prevent hernia formation in normal individuals, the exact importance of each factor is still under debate. The physiological school of thought thinks that the risk of hernia is due to a physiological difference between patients who develop a hernia and those who do not, namely the presence of aponeurotic extensions from the transversus abdominis aponeurotic arch.Inguinal hernias mostly contain the omentum or a part of the small intestines, however, some unusual contents may be an appendicitis, diverticulitis, colon cancer, urinary bladder, ovaries, and rarely malignant lesions.

Diagnosis
There are two types of inguinal hernia, direct and indirect, which are defined by their relationship to the inferior epigastric vessels. Direct inguinal hernias occur medial to the inferior epigastric vessels when abdominal contents herniate through a weak spot in the fascia of the posterior wall of the inguinal canal, which is formed by the transversalis fascia. Indirect inguinal hernias occur when abdominal contents protrude through the deep inguinal ring, lateral to the inferior epigastric vessels; this may be caused by failure of embryonic closure of the processus vaginalis.
In the case of the female, the opening of the superficial inguinal ring is smaller than that of the male. As a result, the possibility for hernias through the inguinal canal in males is much greater because they have a larger opening and therefore a much weaker wall through which the intestines may protrude.

Inguinal hernias, in turn, belong to groin hernias, which also includes femoral hernias. A femoral hernia is not via the inguinal canal, but via the femoral canal, which normally allows passage of the common femoral artery and vein from the pelvis to the leg.
In Amyands hernia, the content of the hernial sac is the vermiform appendix.

In Littres hernia, the content of the hernial sac contains a Meckels diverticulum.
Clinical classification of hernia is also important according to which hernia is classified into

Reducible hernia: is one which can be pushed back into the abdomen by putting manual pressure to it.
Irreducible/Incarcerated hernia: is one which cannot be pushed back into the abdomen by applying manual pressure.Irreducible hernias are further classified into

Obstructed hernia: is one in which the lumen of the herniated part of intestine is obstructed.
Strangulated hernia: is one in which the blood supply of the hernia contents is cut off, thus, leading to ischemia. The lumen of the intestine may be patent or not.

Direct inguinal hernia
The direct inguinal hernia enters through a weak point in the fascia of the abdominal wall, and its sac is noted to be medial to the inferior epigastric vessels.  Direct inguinal hernias may occur in males or females, but males are ten times more likely to get a direct inguinal hernia.A direct inguinal hernia protrudes through a weakened area in the transversalis fascia near the medial inguinal fossa within an anatomic region known as the inguinal or Hesselbachs triangle, an area defined by the edge of the rectus abdominis muscle, the inguinal ligament and the inferior epigastric artery. These hernias are capable of exiting via the superficial inguinal ring and are unable to extend into the scrotum.

When a patient develops a simultaneous direct and indirect hernia on the same side, it is called a pantaloon hernia or saddlebag hernia because it resembles a pair of pants with the epigastric vessels in the crotch, and the defects can be repaired separately or together. Another term for pantaloon hernia is Rombergs hernia.
Since the abdominal walls weaken with age, direct hernias tend to occur in the middle-aged and elderly. This is in contrast to indirect hernias which can occur at any age including the young, since their etiology includes a congenital component where the inguinal canal is left more patent (compared to individuals less susceptible to indirect hernias). Additional risk factors include chronic constipation, being overweight or obese, chronic cough, family history and prior episodes of direct inguinal hernias.

Indirect inguinal hernia
An indirect inguinal hernia results from the failure of embryonic closure of the deep inguinal ring after the testicle has passed through it. It is the most common cause of groin hernia. A double indirect inguinal hernia has two sacs.
In the male fetus, the peritoneum gives a coat to the testicle as it passes through this ring, forming a temporary connection called the processus vaginalis. In normal development, the processus is obliterated once the testicle is completely descended.  The permanent coat of peritoneum that remains around the testicle is called the tunica vaginalis.  The testicle remains connected to its blood vessels and the vas deferens, which make up the spermatic cord and descend through the inguinal canal to the scrotum.
The deep inguinal ring, which is the beginning of the inguinal canal, remains as an opening in the fascia transversalis, which forms the fascial inner wall of the spermatic cord.  When the opening is larger than necessary for passage of the spermatic cord, the stage is set for an indirect inguinal hernia.  The protrusion of peritoneum through the internal inguinal ring can be considered an incomplete obliteration of the processus.
In an indirect inguinal hernia, the protrusion passes through the deep inguinal ring and is located lateral to the inferior epigastric artery. Hence, the conjoint tendon is not weakened.
There are three main types

Bubonocele: in this case the hernia is limited in inguinal canal.
Funicular: here the processus vaginalis is closed at its lower end just above the epididymis. The content of the hernial sac can be felt separately from the testis which lies below the hernia.
Complete (or scrotal): here the processus vaginalis is patent throughout. The hernial sac is continuous with the tunica vaginalis of the testis. The hernia descends down to the bottom of the scrotum and it is difficult to differentiate the testis from hernia.In the female, groin hernias are only 4% as common as in males.  Indirect inguinal hernia is still the most common groin hernia for females.  If a woman has an indirect inguinal hernia, her internal inguinal ring is patent, which is abnormal for females.  The protrusion of peritoneum is not called "processus vaginalis" in women, as this structure is related to the migration of the testicle to the scrotum.  It is simply a hernia sac.  The eventual destination of the hernia contents for a woman is the labium majus on the same side, and hernias can enlarge one labium dramatically if they are allowed to progress.

Medical imaging
A physician may diagnose an inguinal hernia, as well as the type, from medical history and physical examination. For confirmation or in uncertain cases, medical ultrasonography is the first choice of imaging, because it can both detect the hernia and evaluate its changes with for example pressure, standing and Valsalva maneuver.When assessed by ultrasound or cross sectional imaging with CT or MRI, the major differential in diagnosing indirect inguinal hernias is differentiation from spermatic cord lipomas, as both can contain only fat and extend along the inguinal canal into the scrotum.On axial CT, lipomas originate inferior or lateral to the cord, and are located inside the cremaster muscle, while inguinal hernias lie anteromedial to the cord and are not intramuscular. Large lipomas may appear nearly indistinguishable as the fat engulfs anatomic boundaries, but they do not change position with coughing or straining.

Differential diagnosis
Differential diagnosis of the symptoms of inguinal hernia mainly includes the following potential conditions:
Femoral hernia
Epididymitis
Testicular torsion
Lipomas
Inguinal adenopathy (Lymph node Swelling)
Groin abscess
Saphenous vein dilation, called Saphena varix
Vascular aneurysm or pseudoaneurysm
Hydrocele
Varicocele
Cryptorchidism (Undescended testes)

Management
Conservative
There is currently no medical recommendation about how to manage an inguinal hernia condition in adults, due to the fact that, until recently, elective surgery used to be recommended. The hernia truss (or hernia belt) is intended to contain a reducible inguinal hernia within the abdomen. It is not considered to provide a cure, and if the pads are hard and intrude into the hernia aperture they may cause scarring and enlargement of the aperture. In addition, most trusses with older designs are not able effectively to contain the hernia at all times, because their pads do not remain permanently in contact with the hernia. The more modern variety of truss is made with non-intrusive flat pads and comes with a guarantee to hold the hernia securely during all activities. They have been described by users as providing greater confidence and comfort when carrying out physically demanding tasks. However, their use is controversial, as data to determine whether they help prevent hernia complications are lacking. A truss also increases the probability of complications, which include strangulation of the hernia, atrophy of the spermatic cord, and atrophy of the fascial margins. This allows the defect to enlarge and makes subsequent repair more difficult. Their popularity is nonetheless likely to increase, as many individuals with small, painless hernias are now delaying hernia surgery due to the risk of post-herniorrhaphy pain syndrome. Elasticated pants used by athletes may also provide useful support for the smaller hernia.

Surgical
Surgical correction of inguinal hernias is called a hernia repair. It is not recommended in minimally symptomatic hernias, for which watchful waiting is advised, due to the risk of post herniorraphy pain syndrome. Surgery is commonly performed as outpatient surgery. There are various surgical strategies which may be considered in the planning of inguinal hernia repair. These include the consideration of mesh use (e.g </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pharyngitis and explain in detail? [/INST] Pharyngitis is inflammation of the back of the throat, known as the pharynx. It typically results in a sore throat and fever. Other symptoms may include a runny nose, cough, headache, difficulty swallowing, swollen lymph nodes, and a hoarse voice. Symptoms usually last 3–5 days. Complications can include sinusitis and acute otitis media. Pharyngitis is a type of upper respiratory tract infection.Most cases are caused by a viral infection. Strep throat, a bacterial infection, is the cause in about 25% of children and 10% of adults. Uncommon causes include other bacteria such as gonorrhea, fungus, irritants such as smoke, allergies, and gastroesophageal reflux disease. Specific testing is not recommended in people who have clear symptoms of a viral infection, such as a cold. Otherwise, a rapid antigen detection test (RADT) or throat swab is recommended. Other conditions that can produce similar symptoms include epiglottitis, thyroiditis, retropharyngeal abscess, and occasionally heart disease.NSAIDs, such as ibuprofen, can be used to help with the pain. Numbing medication, such as topical lidocaine, may also help. Strep throat is typically treated with antibiotics, such as either penicillin or amoxicillin. It is unclear whether steroids are useful in acute pharyngitis, other than possibly in severe cases, but a recent (2020) review found that when used in combination with antibiotics they moderately improved pain and the likelihood of resolution.About 7.5% of people have a sore throat in any 3-month period. Two or three episodes in a year are not uncommon. This resulted in 15 million physician visits in the United States in 2007. Pharyngitis is the most common cause of a sore throat. The word comes from the Greek word pharynx meaning "throat" and the suffix -itis meaning "inflammation".

Classification
Pharyngitis is a type of inflammation caused by an upper respiratory tract infection. It may be classified as acute or chronic. Acute pharyngitis may be catarrhal, purulent, or ulcerative, depending on the causative agent and the immune capacity of the affected individual. Chronic pharyngitis may be catarrhal, hypertrophic, or atrophic.Tonsillitis is a subtype of pharyngitis. If the inflammation includes both the tonsils and other parts of the throat, it may be called pharyngotonsillitis or tonsillopharyngitis. Another subclassification is nasopharyngitis (the common cold).Clergymans sore throat or clergymans throat is an archaic term formerly used for chronic pharyngitis associated with overuse of the voice as in public speaking. It was sometimes called dysphonia clericorum or chronic folliculitis sore throat.

Cause
Most cases are due to an infectious organism acquired from close contact with an infected individual.

Viral
These comprise about 40–80% of all infectious cases and can be a feature of many different types of viral infections.
Adenovirus is the most common of the viral causes. Typically, the degree of neck lymph node enlargement is modest and the throat often does not appear red, although it is painful.
The family Orthomyxoviridae which cause influenza are present with rapid onset high temperature, headache, and generalized ache. A sore throat may be associated.
Infectious mononucleosis ("glandular fever") is caused by the Epstein–Barr virus. This may cause significant lymph-node swelling and an exudative tonsillitis with marked redness and swelling of the throat. The heterophile test can be used if this is suspected.
Herpes simplex virus can cause multiple mouth ulcers.
Measles
Common cold: rhinovirus, coronavirus, respiratory syncytial virus, and parainfluenza virus can cause infection of the throat, ear, and lungs causing standard cold-like symptoms and often pain.

Bacterial
A number of different bacteria can infect the human throat. The most common is group A streptococcus (Streptococcus pyogenes), but others include Streptococcus pneumoniae, Haemophilus influenzae, Bordetella pertussis, Bacillus anthracis, Corynebacterium diphtheriae, Neisseria gonorrhoeae, Chlamydophila pneumoniae, Mycoplasma pneumoniae, and Fusobacterium necrophorum.
Streptococcal pharyngitis
Streptococcal pharyngitis or strep throat is caused by a group A beta-hemolytic streptococcus (GAS). It is the most common bacterial cause of cases of pharyngitis (15–30%). Common symptoms include fever, sore throat, and large lymph nodes. It is a contagious infection, spread by close contact with an infected individual. A definitive diagnosis is made based on the results of a throat culture. Antibiotics are useful to both prevent complications (such as rheumatic fever) and speed recovery.
Fusobacterium necrophorumFusobacterium necrophorum is a normal inhabitant of the oropharyngeal flora and can occasionally create a peritonsillar abscess. In one out of 400 untreated cases, Lemierres syndrome occurs.
DiphtheriaDiphtheria is a potentially life-threatening upper respiratory infection caused by Corynebacterium diphtheriae, which has been largely eradicated in developed nations since the introduction of childhood vaccination programs, but is still reported in the Third World and increasingly in some areas in Eastern Europe. Antibiotics are effective in the early stages, but recovery is generally slow.
OthersA few other causes are rare, but possibly fatal, and include parapharyngeal space infections: peritonsillar abscess ("quinsy abscess"), submandibular space infection (Ludwigs angina), and epiglottitis.

Fungal
Some cases of pharyngitis are caused by fungal infection, such as Candida albicans, causing oral thrush.

Noninfectious
Pharyngitis may also be caused by mechanical, chemical, or thermal irritation, for example cold air or acid reflux. Some medications may produce pharyngitis, such as pramipexole and antipsychotics.

Diagnosis
Differentiating a viral and a bacterial cause of a sore throat based on symptoms alone is difficult. Thus, a throat swab often is done to rule out a bacterial cause.The modified Centor criteria may be used to determine the management of people with pharyngitis </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Acanthosis nigricans and explain in detail? [/INST] Acanthosis nigricans is a medical sign characterised by brown-to-black, poorly defined, velvety hyperpigmentation of the skin. It is usually found in body folds, such as the posterior and lateral folds of the neck, the armpits, groin, navel, forehead and other areas.It is associated with endocrine dysfunction, especially insulin resistance and hyperinsulinaemia, as seen in diabetes mellitus. This activates the insulin-like growth factor receptors, which leads to proliferation of keratinocytes, fibroblasts and other cells in the skin. Activation of other growth factor receptors such as fibroblast growth factor receptors or epidermal growth factor receptor can also be responsible.

Signs and symptoms
Acanthosis nigricans may present with thickened, velvety, relatively darker areas of skin on the neck, armpit and in skin folds.

Causes
It typically occurs in individuals younger than age 40, may be genetically inherited and is associated with obesity or endocrinopathies, such as hypothyroidism, acromegaly, polycystic ovary syndrome, insulin-resistant diabetes or Cushings disease.

Type I – familial
Familial acanthosis: 86  may arise as a result of an autosomal dominant trait, presenting at birth or developing during childhood.: 506 : 676

Type II – endocrine
Endocrine syndromes associated with acanthosis nigricans: 506–7  can develop in many conditions, particularly:: 978  : 86
starts with insulin resistance, such as diabetes mellitus and metabolic syndrome
excess circulating androgens, particularly Cushings disease, acromegaly, polycystic ovary syndrome
Addisons disease and hypothyroidism
Rare diseases, including pinealoma, leprechaunism, lipoatrophic diabetes, pineal hyperplasia syndrome, pituitary basophilism, ovarian hyperthecosis, stromal luteoma, ovarian dermoid cysts, Prader-Willi syndrome, and Alström syndrome.Acanthosis nigricans associated with endocrine dysfunction is more insidious in its onset, is less widespread, and the patients are often concurrently obese.: 676

Type III – obesity and pseudoacanthosis nigricans
In young persons, acanthosis nigricans is a visible marker which strongly suggests insulin resistance. Higher than normal insulin levels in the blood stream cause the growth of darkened skin over certain areas of the body. No skin treatment will get rid of AN. Acanthosis nigricans may lighten up and possibly go away by treating the root cause, insulin resistance, but it can take months or years to do so. Insulin resistance syndromes may be divided into type A (HAIR-AN) and type B syndromes.: 978 The majority of cases of acanthosis nigricans are associated with obesity and otherwise idiopathic. This is likely because of insulin resistance and more likely to occur in darker-skinned persons.: 968  This can also be referred to as pseudoacanthosis nigricans.: 86  In some cases, AN attributable to obesity and insulin resistance will occur on ones face. Most typically it will be present as a horizontal band on the forehead, but may also appear as perioral hyperpigmentation, periorbital hyperpigmentation, or generalized facial skin darkening.

Type IV – drug-related
Acanthosis nigricans has been linked to the use of nicotinic acid, glucocorticoid use, combined oral contraceptive pills, and growth hormone therapy.: 86

Type V – malignancy
Malignant acanthosis nigricans: 86  refers to acanthosis nigricans occurring as a paraneoplastic syndrome associated with a cancer. Malignant acanthosis nigricans is most commonly associated with gastrointestinal adenocarcinomas, as well as genitourinary cancers such as those of the prostate, breast, and ovary. Other cancers, such as those of the lung, stomach, and lymphoma, are occasionally associated with acanthosis nigricans.: 86 This form of acanthosis nigricans is more likely to involve mucous membranes (25–50% of cases) Malignant acanthosis nigricans that may either precede (18%), accompany (60%), or follow (22%) the onset of an internal cancer.: 506  Malignancy-associated acanthosis nigricans is usually rapid in onset and may be accompanied by skin tags, multiple seborrheic keratoses, or tripe palms.: 676

Acral acanthotic anomaly
Acral acanthotic anomaly refers to a variant of acanthosis nigricans limited to the elbows, knees, knuckles, and dorsal surfaces of the feet, in the absence of any other findings, in otherwise healthy individuals. While the etiology remains unknown, its presence does not suggest a likelihood of malignancy.

Pathophysiology
Acanthosis nigricans is caused by increased activation of growth factor receptor proteins, usually due to endocrine dysfunction. This is most commonly insulin-mediated activation of IGF receptors on keratinocytes, as a result of hyperinsulinaemia or insulin resistance, as seen in diabetes mellitus.Factors involved in the development of acanthosis nigricans include:

Increased circulating insulin. This activates keratinocyte IGF receptors, particularly IGF-1. At high concentrations, insulin may also displace IGF-1 from insulin-like growth factor-binding protein (IGFBP). Increased circulating IGF may lead to keratinocyte and dermal fibroblast proliferation.
In hereditary forms of acanthosis nigricans, fibroblast growth factor receptor (FGFR) defects
Increased transforming growth factor (TGF), which appears to be the mechanism for malignancy-associated acanthosis nigricans. TGF acts on epidermal tissue via the epidermal growth factor receptor (EGFR).: 86 In conjunction with increased end levels of IGF, it is likely that perspiration and friction may be necessary predeterminants for lesions, since the level of insulin is usually not enough to activate IGF receptors across the body.

Diagnosis
Acanthosis nigricans is typically diagnosed clinically. A skin biopsy may be needed in unusual cases. If no clear cause is obvious, it may be necessary to search for one. Blood tests, an endoscopy, or X-rays may be required to eliminate the possibility of diabetes or cancer as the cause.: 87 On biopsy, hyperkeratosis, epidermal folding, leukocyte infiltration, and melanocyte proliferation may be seen.: 979 : 87

Differential diagnosis
Acanthosis nigricans should be distinguished from the casal collar appearing in pellagra.

Classification
Acanthosis nigricans is conventionally divided into benign and malignant forms, although may be divided into syndromes according to cause:: 506
Benign This may include obesity-related, hereditary, and endocrine forms of acanthosis nigricans.
Malignant </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Acute prostatitis and explain in detail? [/INST] Acute prostatitis is a serious bacterial infection of the prostate gland. This infection is a medical emergency. It should be distinguished from other forms of prostatitis such as chronic bacterial prostatitis and chronic pelvic pain syndrome (CPPS).

Signs and symptoms
Men with acute prostatitis often have chills, fever, pain in the lower back, perineum, or genital area, urinary frequency and urgency often at night, burning or painful urination, body aches, and a demonstrable infection of the urinary tract, as evidenced by white blood cells and bacteria in the urine. Acute prostatitis may be a complication of prostate biopsy. Often, the prostate gland is very tender to palpation through the rectum.

Diagnosis
Acute prostatitis is relatively easy to diagnose due to its symptoms that suggest infection. The organism may be found in blood or urine, and sometimes in both. Common bacteria are Escherichia coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Enterococcus, Serratia, and Staphylococcus aureus. This can be a medical emergency in some patients and hospitalization with intravenous antibiotics may be required. A complete blood count reveals increased white blood cells. Sepsis from prostatitis is very rare, but may occur in immunocompromised patients; high fever and malaise generally prompt blood cultures, which are often positive in sepsis. A prostate massage should never be done in a patient with suspected acute prostatitis, since it may induce sepsis. Since bacteria causing the prostatitis is easily recoverable from the urine, prostate massage is not required to make the diagnosis. Rectal palpation usually reveals an enlarged, exquisitely tender, swollen prostate gland, which is firm, warm, and, occasionally, irregular to the touch. C-reactive protein is elevated in most cases.Prostate biopsies are not indicated as the (clinical) features (described above) are diagnostic </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Alport syndrome and explain in detail? [/INST] Alport syndrome is a genetic disorder affecting around 1 in 5,000-10,000 children, characterized by glomerulonephritis, end-stage kidney disease, and hearing loss. Alport syndrome can also affect the eyes, though the changes do not usually affect vision, except when changes to the lens occur in later life. Blood in urine is universal. Proteinuria is a feature as kidney disease progresses.The disorder was first identified in a British family by the physician Cecil A. Alport in 1927. Alport syndrome once also had the label hereditary nephritis, but this is misleading as there are many other causes of hereditary kidney disease and nephritis.
Alport syndrome is caused by an inherited defect in type IV collagen—a structural material that is needed for the normal function of different parts of the body. Since type IV collagen is found in the ears, eyes, and kidneys, this explains why Alport syndrome affects different seemingly unrelated parts of the body (ears, eyes, kidneys, etc.).
Depending on where the mutation is located in the genome, Alport syndrome can present itself in many forms. This includes X-linked Alport syndrome (XLAS), autosomal recessive Alport syndrome (ARAS), and autosomal dominant Alport syndrome (ADAS).

Signs and symptoms
These descriptions refer to classic Alport syndrome, which usually causes significant disease from young adult or late childhood life.  Some individuals, usually with milder mutations or carrier status, develop disease later, or show only some of the features of classic disease.

Chronic kidney disease
Blood in urine is a usual feature of Alport syndrome from early infancy, identifiable on urine dipsticks. In young children, episodes of visible (macroscopic) haematuria may occur. Protein begins to appear in urine as the disease progresses.  This is now regarded as an indication for treatment with ACE inhibitors. Progressive loss of kidney function (reflected clinically by increases in serum creatinine or decreases in estimated glomerular filtration rate) can occur and may require treatment with renal replacement: dialysis or a kidney transplant.

Hearing loss
Alport syndrome can also cause hearing loss although some patients are not affected.  Hearing in Alport syndrome patients is normal at birth. Hearing loss in affected patients develops progressively, usually at the stage when kidney function is normal, but there is substantial proteinuria.  However, in some patients, hearing loss is only noted after kidney function has been lost. Characteristically the early changes are reduced ability to hear high-frequency sounds, sensorineural deafness.  This becomes more severe and affects lower frequencies too. Hearing loss is not usually complete in Alport syndrome; good communication is almost always possible with the use of hearing aids.

Eye changes
Various eye abnormalities are often seen including lenticonus, keratoconus, cataracts and corneal erosion as well as retinal flecks in the macula and mid-periphery. These rarely threaten vision. Lenticonus (cone-shaped lens) can be treated by replacement of the lens, as for cataracts. Mild keratoconus can be managed with hard, scleral, piggy-back or other specialty medical contact lenses; progressive cases may be halted with corneal collagen cross linking; and severe cases may require a corneal transplant. Macular abnormalities such as incomplete foveal hypoplasia or staircase foveopathy are common in Alport syndrome.It may also be associated with retinitis pigmentosa.

Leiomyomatosis
Diffuse leiomyomatosis of the oesophagus and tracheobronchial tree has been reported in some families with Alport syndrome. Symptoms usually appear in late childhood and include dysphagia, postprandial vomiting, substernal or epigastric pain, recurrent bronchitis, dyspnea, cough, and stridor. Leiomyomatosis is confirmed by computed tomography (CT) scanning or magnetic resonance imaging (MRI).

Other abnormalities
Aortic dissection has been described very rarely in patients with early-onset disease.  Leiomyomas, tumours of smooth muscle affecting the oesophagus and female genital tract, may occur in a rare overlap syndrome involving the adjacent COL4A5 and COL4A6 genes.

Pathophysiology
Alport Syndrome is a relatively common genetic disorder affecting around 1 in 5,000-10,000 children,

Genetics
Alport syndrome is caused by mutations in COL4A3, COL4A4, and COL4A5, three of six human genes involved in basement membrane (type IV) collagen biosynthesis. Mutations in any of these genes prevent the proper production or assembly of the specialised type IV collagen 345 network which is an important structural component of basement membranes in the kidney, inner ear, and eye. It is also found in other locations, including the alveoli of the lungs.  Basement membranes are thin, sheet-like structures that separate and support cells in many tissues. Type IV collagen 112 type is found in both vertebrates and invertebrates and is the major isoform in most human basement membranes.  When mutations prevent the formation of 345 type IV collagen network in the glomerulus, the 112 network, which is formed in fetal development but usually replaced by 345, persists into adult life.

Inheritance patterns
Alport syndrome can have different inheritance patterns depending on which specific mutation is present.

In most people with Alport syndrome (about 85%), the condition is inherited in an X-linked pattern, due to mutations in the COL4A5 gene. A condition is considered X-linked if the gene involved in the disorder is located on the X chromosome. In males, who have only one X chromosome, one altered copy of the COL4A5 gene is sufficient to cause severe Alport syndrome, explaining why most affected males eventually develop kidney failure. In females, who have two X chromosomes, a mutation in one copy of the COL4A5 gene usually results in blood in the urine, but most affected females do not develop kidney failure.
Alport syndrome can also be inherited in an autosomal recessive pattern if both copies of the COL4A3 or COL4A4 gene, located on chromosome 2, have been mutated. Most often, the parents of a child with an autosomal recessive disorder are not affected but are carriers of one copy of the altered gene.
Past descriptions of an autosomal dominant form are now usually categorized as other conditions. Notably, conditions associated with giant platelets and associated with mutations of MYH9 are no longer considered to be Alport variants.  However apparent autosomal dominant transmission of disease associated with mutations in COL4A3 and COL4A4 does occur.Clinical utility gene card for: Alport syndrome.

Diagnosis
The diagnosis can usually be made on a combination of clinical, family history, and biopsy criteria.

Biopsy of kidneys or skin
To be helpful, kidney biopsies need to be taken before the disease is too advanced.  Changes on conventional (light) microscopy are not characteristic, and the possibility of other diagnoses, particularly focal segmental glomerulosclerosis (FSGS), may be raised.  Electron microscopy shows a characteristic sequence of changes from thinning of the glomerular basement membrane (GBM), developing into areas of thinning and thickening, and finally into a complex appearance with apparent splitting, often described as a basketweave appearance.  Early or very localised changes on this spectrum are not diagnostic, but the later changes are considered diagnostic.Immunohistochemistry or immunofluorescence studies to identify the COL3-4-5 proteins in GBM can be helpful </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bronchiolitis and explain in detail? [/INST] Bronchiolitis is inflammation of the small airways in the lungs. Acute bronchiolitis is due to a viral infection usually affecting children younger than two years of age. Symptoms may include fever, cough, runny nose, wheezing, and breathing problems. More severe cases may be associated with nasal flaring, grunting, or the skin between the ribs pulling in with breathing. If the child has not been able to feed properly, signs of dehydration may be present.Chronic bronchiolitis is the general term used for small airways disease in adults, notably in chronic obstructive pulmonary disease.Acute bronchiolitis is usually the result of infection by respiratory syncytial virus (72% of cases) or human rhinovirus (26% of cases). Diagnosis is generally based on symptoms. Tests such as a chest X-ray or viral testing are not routinely needed.There is no specific treatment. Symptomatic treatment at home is generally sufficient. Occasionally, hospital admission for oxygen, support with feeding, or intravenous fluids is required. Tentative evidence supports nebulized hypertonic saline. Evidence for antibiotics, antivirals, bronchodilators, or nebulized epinephrine is either unclear or not supportive.About 10% to 30% of children under the age of two years are affected by bronchiolitis at some point in time. It commonly occurs in the winter in the Northern Hemisphere. It is the leading cause of hospitalizations in those less than one year of age in the United States. The risk of death among those who are admitted to hospital is about 1%. Outbreaks of the condition were first described in the 1940s.

Signs and symptoms
Bronchiolitis typically presents in children under two years old and is characterized by a constellation of respiratory symptoms that consists of fever, rhinorrhea, cough, wheeze, tachypnea and increased work of breathing such as nasal flaring or grunting that develops over one to three days. Crackles or wheeze are typical findings on listening to the chest with a stethoscope. The child may also experience apnea, or brief pauses in breathing. After the acute illness, it is common for the airways to remain sensitive for several weeks, leading to recurrent cough and wheeze.
Some signs of severe disease include:
increased work of breathing (such as use of accessory muscles of respiration, rib & sternal retraction, tracheal tug)
severe chest wall recession (Hoovers sign)
presence of nasal flaring and/or grunting
increased respiratory rate above normal
hypoxia (low oxygen levels)
cyanosis (bluish skin)
lethargy and decreased activity
poor feeding (less than half of usual fluid intake in preceding 24 hours)
history of stopping breathing

Causes
The term usually refers to acute viral bronchiolitis, a common disease in infancy. This is most commonly caused by respiratory syncytial virus (RSV, also known as human pneumovirus). Other agents that cause this illness include human metapneumovirus, influenza, parainfluenza, coronavirus, adenovirus, rhinovirus and mycoplasma.

Risk factors
Children are at an increased risk for progression to severe respiratory disease if they have any of the following additional factors:
Preterm infant (gestational age less than 37 weeks)
Younger age at onset of illness (less than 3 months of age)
Congenital heart disease
Immunodeficiency
Chronic lung disease
Neurological disorders
Tobacco smoke exposure

Diagnosis
The diagnosis is typically made by clinical examination. Chest X-ray is sometimes useful to exclude bacterial pneumonia, but not indicated in routine cases. Chest x-ray may also be useful in people with impending respiratory failure. Additional testing such as blood cultures, complete blood count, and electrolyte analyses are not recommended for routine use although may be useful in children with multiple comorbidities or signs of sepsis or pneumonia.Testing for the specific viral cause can be done but has little effect on management and thus is not routinely recommended. RSV testing by direct immunofluorescence testing on nasopharyngeal aspirate had a sensitivity of 61% and specificity of 89%. Identification of those who are RSV-positive can help for disease surveillance, grouping ("cohorting") people together in hospital wards to prevent cross infection, predicting whether the disease course has peaked yet, and reducing the need for other diagnostic procedures (by providing confidence that a cause has been identified). Identification of the virus may help reduce the use of antibiotics.Infants with bronchiolitis between the age of two and three months have a second infection by bacteria (usually a urinary tract infection) less than 6% of the time. When further evaluated with a urinalysis, infants with bronchiolitis had a concomitant UTI 0.8% of the time. Preliminary studies have suggested that elevated procalcitonin levels may assist clinicians in determining the presence of bacterial co-infection, which could prevent unnecessary antibiotic use and costs.

Differential diagnosis
There are many childhood illnesses that can present with respiratory symptoms, particularly persistent cough and wheezing. Bronchiolitis may be differentiated from some of these by the characteristic pattern of preceding febrile upper respiratory tract symptoms lasting for 1 to 3 days followed by the persistent cough, tachypnea, and wheezing. However, some infants may present without fever (30% of cases) or may present with apnea without other signs or with poor weight gain prior to onset of symptoms. In such cases, additional laboratory testing and radiographic imaging may be useful. The following are some other diagnoses to consider in an infant presenting with signs of bronchiolitis:
Asthma and reactive airway disease
Bacterial pneumonia
Congenital heart disease
Heart failure
Whooping cough
Allergic reaction
Cystic fibrosis
Chronic pulmonary disease
Foreign body aspiration
Vascular ring

Prevention
Prevention of bronchiolitis relies strongly on measures to reduce the spread of the viruses that cause respiratory infections (that is, handwashing, and avoiding exposure to those symptomatic with respiratory infections). Guidelines are mixed on the use of gloves, aprons, or personal protective equipment. In addition to good hygiene, an improved immune system is a great tool for prevention.One way to improve the immune system is to feed the infant with breast milk, especially during the first month of life. Respiratory infections were shown to be significantly less common among breastfed infants and fully breastfed RSV-positive hospitalized infants had shorter hospital stays than non or partially breastfed infants. Guidelines recommend exclusive breastfeeding for infants for the first 6 months of life.Palivizumab, a monoclonal antibody against RSV, can be administered to prevent bronchiolitis to infants less than one year of age that were born very prematurely or that have underlying heart disease or chronic lung disease of prematurity. Passive immunization therapy requires monthly injections during winter. Otherwise healthy premature infants that were born after a gestational age of 29 weeks should not be administered palivizumab as the harms outweigh the benefits. Passive protection through the administration of other novel monoclonal antibodies is also under evaluation.Immunizations for RSV are being developed but none are available currently outside of clinical trials.Tobacco smoke exposure has been shown to increase both the rates of lower respiratory disease in infants, as well as the risk and severity of bronchiolitis. Tobacco smoke lingers in the environment for prolonged periods and on clothing even when smoking outside the home. Guidelines recommend that parents be fully educated on the risks of tobacco smoke exposure on children with bronchiolitis.

Management
Treatment of bronchiolitis is usually focused on the hydration and symptoms instead of the infection itself since the infection will run its course and complications are typically from the symptoms themselves. Without active treatment, half of cases will go away in 13 days and 90% in three weeks. Children with severe symptoms, especially poor feeding or dehydration, may be considered for hospital admission. Oxygen saturation under 90%-92% as measured with pulse oximetry is also frequently used as an indicator of need for hospitalization. High-risk infants, apnea, cyanosis, malnutrition, and diagnostic uncertainty are additional indications for hospitalization.Most guidelines recommend sufficient fluids and nutritional support for affected children. Measures for which the recommendations were mixed include nebulized hypertonic saline, nebulized epinephrine, and nasal suctioning. Treatments which the evidence does not support include salbutamol, steroids, antibiotics, antivirals, heliox, continuous positive airway pressure (CPAP), chest physiotherapy, and cool mist or steam inhalation.

Diet
Maintaining hydration is an important part of management of bronchiolitis. Infants with mild pulmonary symptoms may require only observation if feeding is unaffected. However, oral intake may be affected by nasal secretions and increased work of breathing. Poor feeding or dehydration, defined as less than 50% of usual intake, is often cited as an indication for hospital admission. Guidelines recommend the use of nasogastric or intravenous fluids in children with bronchiolitis who cannot maintain usual oral intake. The risk of health care caused hyponatremia and fluid retention are minimal with the use of isotonic fluids such as normal saline, breast milk, or formula.

Oxygen
Inadequate oxygen supply to the tissue is one of the main concerns during severe bronchiolitis and oxygen saturation is often closely associated with both the need for hospitalization and continued length of hospital stay in children with bronchiolitis. However, oxygen saturation is a poor predictor of respiratory distress. Accuracy of pulse oximetry is limited in the 76% to 90% range and there is weak correlation between oxygen saturation and respiratory distress as brief hypoxemia is common in healthy infants. Additionally, pulse oximetry is associated with frequent false alarms and parental stress and fatigue. Clinicians may choose not to given additional oxygen to children with bronchiolitis if their oxygen saturation is above 90%. Additionally, clinicians may choose not to use continuous pulse oximetry in these people.When choosing to use oxygen therapy for a child with bronchiolitis, there is evidence that home oxygen may reduce hospitalization rate and length of stay although readmission rates and follow-up visits are increased. Also, the use of humidified, heated, high-flow nasal cannula may be a safe initial therapy to decrease work of breathing and need for intubation. However, evidence is lacking regarding the use of high-flow nasal cannula compared to standard oxygen therapy or continuous positive airway pressure. These practices may still be used in severe cases prior to intubation.Blood gas testing is not recommended for people hospitalized with the disease and is not useful in the routine management of bronchiolitis. People with severe worsening respiratory distress or impending respiratory failure may be considered for capillary blood gas testing.

Hypertonic saline
Guidelines recommend against the use of nebulized hypertonic saline in the emergency department for children with bronchiolitis but it may be given to children who are hospitalized.Nebulized hypertonic saline (3%) has limited evidence of benefit and previous studies lack consistency and standardization. A 2017 review found tentative evidence that it reduces the risk of hospitalization, duration of hospital stay, and improved the severity of symptoms. The majority of evidence suggests that hypertonic saline is safe and effective at improving respiratory symptoms of mild to moderate bronchiolitis after 24 hours of use. However, it does not appear effective in reducing the rate of hospitalization when used in the emergency room or other outpatient settings in which length of therapy is brief. Side effects were mild and resolved spontaneously.

Bronchodilators
Guidelines recommend against the use of bronchodilators in children with bronchiolitis as evidence does not support a change in outcomes with such use. Additionally, there are adverse effects to the use of bronchodilators in children such as tachycardia and tremors, as well as adding increased financial expenses.Several studies have shown that bronchodilation with β-adrenergic agents such as salbutamol may improve symptoms briefly but do not affect the overall course of the illness or reduce the need for hospitalization. However, there are conflicting recommendations about the use of a trial of a bronchodilator, especially in those with history of previous wheezing, due to the difficulty with assessing an objective improvement in symptoms. Bronchiolitis-associated wheezing is likely not effectively alleviated by bronchodilators anyway as it is caused by airway obstruction and plugging of the small airway diameters by luminal debris, not bronchospasm as in asthma-associated wheezing that bronchodilators usually treat well.Anticholinergic inhalers, such as ipratropium bromide, have a modest short-term effect at best and are not recommended for treatment.

Epinephrine
The current state of evidence suggests that nebulized epinephrine is not indicated for children with bronchiolitis except as a trial of rescue therapy for severe cases.Epinephrine is an α and β adrenergic agonist that has been used to treat other upper respiratory tract illnesses, such as croup, as a nebulized solution. A Cochrane meta-analysis in 2011 found no benefit to the use of epinephrine in the inpatient setting and suggested that there may be utility in the outpatient setting in reducing the rate of hospitalization. However, current guidelines do not support the outpatient use of epinephrine given the lack of substantial sustained benefit.A 2017 review found inhaled epinephrine with corticosteroids did not change the need for hospitalization or the time spent in hospital. Other studies suggest a synergistic effect of epinephrine with corticosteroids but have not consistently demonstrated benefits in clinical trials. Guidelines recommend against its use currently.

Unclear evidence
Currently other medications do not yet have evidence to support their use, although they have been studied for use in bronchiolitis. Experimental trials with novel antiviral medications in adults are promising but it remains unclear if the same benefit will be present.
Surfactant had favorable effects for severely critical infants on duration of mechanical ventilation and ICU stay however studies were few and small.
Chest physiotherapy, such as vibration or percussion, to promote airway clearance may slightly reduce duration of oxygen therapy but there is a lack of evidence that demonstrates any other benefits. People with difficulty clearing secretions due to underlying disorders such as spinal muscle atrophy or severe tracheomalacia may be considered for chest physiotherapy.
Suctioning of the nares may provide temporarily relief of nasal congestion but deep suctioning of the nasopharynx has been shown prolong length of hospital stay in infants. Upper airway suctioning may be considered in people with respiratory distress, feeding difficulties, or infants presenting with apnea.
Heliox, a mixture of oxygen and the inert gas helium, may be beneficial in infants with severe acute RSV bronchiolitis who require CPAP but overall evidence is lacking.
DNAse has not been found to be effective but might play a role in severe bronchiolitis complicated by atelectasis.
There are no systematic reviews or controlled trials on the effectiveness of nasal decongestants, such as xylometazoline, for the treatment of bronchiolitits.
Overall evidence is insufficient to support the use of alternative medicine. There is tentative evidence for Chinese herbal medicine, vitamin D, N-acetylcysteine, and magnesium but this is insufficient to recommend their use.

Non-effective treatments
Ribavirin is an antiviral drug which does not appear to be effective for bronchiolitis.
Antibiotics are often given in case of a bacterial infection complicating bronchiolitis, but have no effect on the underlying viral infection and their benefit is not clear. The risks of bronchiolitis with a concomitant serious bacterial infection among hospitalized febrile infants is minimal and work-up and antibiotics are not justified. Azithromycin adjuvant therapy may reduce the duration of wheezing and coughing in children with bronchiolitis but has not effect on length of hospital stay or duration of oxygen therapy.
Corticosteroids, although useful in other respiratory disease such as asthma and croup, have no proven benefit in bronchiolitis treatment and are not advised. Additionally, corticosteroid therapy in children with bronchiolitis may prolong viral shedding and transmissibility. The overall safety of corticosteroids is questionable.
Leukotriene inhibitors, such as montelukast, have not been found to be beneficial and may increase adverse effects.
Immunoglobulins are of unclear benefit.

Epidemiology
Bronchiolitis typically affects infants and children younger than two years, principally during the autumn and winter. It is the leading cause of hospital admission for respiratory disease among infants in the United States and accounts for one out of every 13 primary care visits. Bronchiolitis accounts for 3% of emergency department visits for children under 2 years old </s>


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

Signs and symptoms
The common carotid artery is the large artery whose pulse can be felt on both sides of the neck under the jaw. On the right side it starts from the brachiocephalic artery (a branch of the aorta), and on the left side the artery comes directly off the aortic arch. At the throat it forks into the internal carotid artery and the external carotid artery. The internal carotid artery supplies the brain, and the external carotid artery supplies the face. This fork is a common site for atherosclerosis, an inflammatory build-up of atheromatous plaque inside the common carotid artery, or the internal carotid arteries that causes them to narrow.The plaque can be stable and asymptomatic, or it can be a source of embolization. Emboli break off from the plaque and travel through the circulation to blood vessels in the brain. As the vessels get smaller, an embolus can lodge in the vessel wall and restrict the blood flow to parts of the brain. This ischemia can either be temporary, yielding a transient ischemic attack (TIA), or permanent resulting in a thromboembolic stroke.Transient ischemic attacks are a warning sign and may be followed by severe permanent strokes, particularly within the first two days. TIAs by definition last less than 24 hours and frequently take the form of weakness or loss of sensation of a limb or the trunk on one side of the body or the loss of sight (amaurosis fugax) in one eye. Less common symptoms are artery sounds (bruits), or ringing in the ears (tinnitus).In asymptomatic individuals with a carotid stenosis, the risk of developing a stroke is increased above those without a stenosis. The risk of stroke is possibly related to the degree of stenosis on imaging. Some studies have found an increased risk with increasing degrees of stenosis while other studies have not been able to find such a relationship.

Pathophysiology
Atherosclerosis causes plaque to form within the carotid artery walls, usually at the fork where the common carotid artery divides into the internal and external carotid artery. The plaque build-up can narrow or constrict the artery lumen, a condition called stenosis. Rupture of the plaque can release atherosclerotic debris or blood clots into the artery. A piece of this material can break off and travel (embolize) up through the internal carotid artery into the brain, where it blocks circulation, and can cause death of the brain tissue, a condition referred to as ischemic stroke.Sometimes the stenosis causes temporary symptoms first, known as TIAs, where temporary ischemia occurs in the brain, or retina without causing an infarction. Symptomatic stenosis has a high risk of stroke within the next 2 days. National Institute for Health and Clinical Excellence (NICE) guidelines recommend that people with moderate to severe (50–99% blockage) stenosis, and symptoms, should have "urgent" endarterectomy within 2 weeks.When the plaque does not cause symptoms, people are still at higher risk of stroke than the general population, but not as high as people with symptomatic stenosis. The incidence of stroke, including fatal stroke, is 1–2% per year. The surgical mortality of endarterectomy ranges from 1–2% to as much as 10%. Two large randomized clinical trials have demonstrated that carotid surgery done with a 30-day stroke and death risk of 3% or less will benefit asymptomatic people with ≥60% stenosis who are expected to live at least 5 years after surgery. Surgeons are divided over whether asymptomatic people should be treated with medication alone or should have surgery.The common carotid artery is the large vertical artery in red. The blood supply to the carotid artery starts at the arch of the aorta (bottom). The carotid artery divides into the internal carotid artery and the external carotid artery. The internal carotid artery supplies the brain. Plaque often builds up at that division and causes a narrowing (stenosis). Pieces of plaque can break off and block the small arteries above in the brain, which causes a stroke. Plaque can also build up at the origin of the carotid artery at the aorta.

Diagnosis
Carotid artery stenosis is usually diagnosed by color flow duplex ultrasound scan of the carotid arteries in the neck </s>