<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 Rib fracture and can you explain it in depth? [/INST] A rib fracture is a break in a rib bone. This typically results in chest pain that is worse with inspiration. Bruising may occur at the site of the break. When several ribs are broken in several places a flail chest results. Potential complications include a pneumothorax, pulmonary contusion, and pneumonia.Rib fractures usually occur from a direct blow to the chest such as during a motor vehicle collision or from a crush injury. Coughing or metastatic cancer may also result in a broken rib. The middle ribs are most commonly fractured. Fractures of the first or second ribs are more likely to be associated with complications. Diagnosis can be made based on symptoms and supported by medical imaging.Pain control is an important part of treatment. This may include the use of paracetamol (acetaminophen), NSAIDs, or opioids. A nerve block may be another option. While fractured ribs can be wrapped, this may increase complications. In those with a flail chest, surgery may improve outcomes. They are a common injury following trauma.

Signs and symptoms
This typically results in chest pain that is worse with inspiration. Bruising may occur at the site of the break.

Complications
When several ribs are broken in several places a flail chest results. Potential complications include a pneumothorax, pulmonary contusion, and pneumonia.

Causes
Rib fractures can occur with or without direct trauma during recreational activity. Cardiopulmonary resuscitation (CPR) has also been known to cause thoracic injury, including but not limited to rib and sternum fractures. They can also occur as a consequence of diseases such as cancer or rheumatoid arthritis. While for elderly individuals a fall can cause a rib fracture, in adults automobile accidents are a common event for such an injury.

Diagnosis
Signs of a broken rib may include:
Pain on inhalation
Swelling in chest area
Bruise in chest area
Increasing shortness of breath
Coughing up blood (rib may have damaged lung)Plain X-rays often pick up displaced fractures but often miss undisplaced fractures. CT scanning is generally able to pick up both types of fractures.Because children have more flexible chest walls than adults do, their ribs are more likely to bend than to break; therefore the presence of rib fractures in children is evidence of a significant amount of force and may indicate severe thoracic injuries such as pulmonary contusion </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 Thromboangiitis obliterans and can you explain it in depth? [/INST] Thromboangiitis obliterans, also known as Buerger disease (English ; German: [ˈbʏʁɡɐ]), is a recurring progressive inflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet. It is strongly associated with use of tobacco products, primarily from smoking, but is also associated with smokeless tobacco.

Signs and symptoms
There is a recurrent acute and chronic inflammation and thrombosis of arteries and veins of the hands and feet. The main symptom is pain in the affected areas, at rest and while walking (claudication). The impaired circulation increases sensitivity to cold. Peripheral pulses are diminished or absent. There are color changes in the extremities. The colour may range from cyanotic blue to reddish blue. Skin becomes thin and shiny. Hair growth is reduced. Ulcerations and gangrene in the extremities are common complications, often resulting in the need for amputation of the involved extremity.

Pathophysiology
There are characteristic pathologic findings of acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet (the lower limbs being more common). The mechanisms underlying Buergers disease are still largely unknown, but smoking and tobacco consumption are major factors associated with it. It has been suggested that the tobacco may trigger an immune response in susceptible persons or it may unmask a clotting defect, either of which could incite an inflammatory reaction of the vessel wall. This eventually leads to vasculitis and ischemic changes in distal parts of limbs.A possible role for Rickettsia in this disease has been proposed.

Diagnosis
A concrete diagnosis of thromboangiitis obliterans is often difficult as it relies heavily on exclusion of other conditions. The commonly followed diagnostic criteria are outlined below although the criteria tend to differ slightly from author to author. Olin (2000) proposes the following criteria:
Typically between 20 and 40 years old and male, although recently females have been diagnosed.
Current (or recent) history of tobacco use.
Presence of distal extremity ischemia (indicated by claudication, pain at rest, ischemic ulcers or gangrene) documented by noninvasive vascular testing such as ultrasound.
Exclusion of other autoimmune diseases, hypercoagulable states, and diabetes mellitus by laboratory tests.
Exclusion of a proximal source of emboli by echocardiography and arteriography.
Consistent arteriographic findings in the clinically involved and noninvolved limbs.Buergers disease can be mimicked by a wide variety of other diseases that cause diminished blood flow to the extremities. These other disorders must be ruled out with an aggressive evaluation, because their treatments differ substantially from that of Buergers disease, for which there is no treatment known to be effective.Some diseases with which Buergers disease may be confused include atherosclerosis (build-up of cholesterol plaques in the arteries), endocarditis (an infection of the lining of the heart), other types of vasculitis, severe Raynauds phenomenon associated with connective tissue disorders (e.g., lupus or scleroderma), clotting disorders or the production of clots in the blood.Angiograms of the upper and lower extremities can be helpful in making the diagnosis of Buergers disease. In the proper clinical setting, certain angiographic findings are diagnostic of Buergers. These findings include a "corkscrew" appearance of arteries that result from vascular damage, particularly the arteries in the region of the wrists and ankles. Collateral circulation gives "tree root" or "spider leg" appearance. Angiograms may also show occlusions (blockages) or stenosis (narrowings) in multiple areas of both the arms and legs. Distal plethysmography also yields useful information about circulatory status in digits.
To rule out other forms of vasculitis (by excluding involvement of vascular regions atypical for Buergers), it is sometimes necessary to perform angiograms of other body regions (e.g., a mesenteric angiogram).Skin biopsies of affected extremities are rarely performed because of the frequent concern that a biopsy site near an area poorly perfused with blood will not heal well.

Prevention
The cause of the disease is thought to be autoimmune in nature and heavily linked to tobacco use in patients with Buergers as primary disease.

Treatment
Smoking cessation has been shown to slow the progression of the disease and decrease the severity of amputation in most patients, but does not halt the progression.
In acute cases, drugs and procedures which cause vasodilation are effective in reducing pain experienced by patient. For example, prostaglandins like Limaprost are vasodilators and give relief of pain, but do not help in changing the course of disease. Epidural anesthesia and hyperbaric oxygen therapy also have vasodilator effect.  There is moderate certainty evidence that intravenous iloprost (prostacyclin analogue) is more effective than aspirin for relieving rest pain and healing ischemic ulcers. No difference have been detected between iloprost or clinprost (prostacyclin) and alprostadil (prostaglandin analogue) for relieving pain and healing ulcers.In chronic cases, lumbar sympathectomy may be occasionally helpful. It reduces vasoconstriction and increases blood flow to limb. It aids in healing and giving relief from pain of ischemic ulcers. Bypass can sometimes be helpful in treating limbs with poor perfusion secondary to this disease.  Use of vascular growth factor and stem cell injections have been showing promise in clinical studies. There may be a benefit of using bone marrow-derived stem cells in healing ulcers and improving pain-free walking distance, but larger, high-quality trials are needed. Debridement is done in necrotic ulcers. In gangrenous digits, amputation is frequently required. Below-knee and above-knee amputation is rarely required.Streptokinase has been proposed as adjuvant therapy in some cases.Despite the clear presence of inflammation in this disorder, anti-inflammatory agents such as corticosteroids have not been shown to be beneficial in healing, but do have significant anti-inflammatory and pain relief qualities in low dosage intermittent form. Similarly, strategies of anticoagulation have not proven effective.
physical therapy: interferential current therapy to decrease inflammation.

Prognosis
Buergers is not immediately fatal.  Amputation is common and major amputations (of limbs rather than fingers/toes) are almost twice as common in patients who continue to smoke. Prognosis markedly improves if a person quits smoking.  Female patients tend to show much higher longevity rates than men. The only known way to slow the progression of the disease is to abstain from all tobacco products.

Epidemiology
Buergers is more common among men than women </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 Dyshidrosis and can you explain it in depth? [/INST] Dyshidrosis is a type of dermatitis that is characterized by itchy blisters on the palms of the hands and bottoms of the feet. Blisters are generally one to two millimeters in size and heal over three weeks. However, they often recur. Redness is not usually present. Repeated attacks may result in fissures and skin thickening.The cause is unknown. Triggers may include allergens, physical or mental stress, frequent hand washing, or metals. Diagnosis is typically based on what it looks like and the symptoms. Allergy testing and culture may be done to rule out other problems. Other conditions that produce similar symptoms include pustular psoriasis and scabies.Avoiding triggers may be useful, as may a barrier cream. Treatment is generally with steroid cream. High strength steroid creams may be required for the first week or two. Antihistamines may be used to help with the itch. If this is not effective steroid pills, tacrolimus, or psoralen plus ultraviolet A (PUVA) may be tried.About 1 in 2,000 people are affected in Sweden. Males and females appear to be affected equally. It explains about one in five cases of hand dermatitis. The first description was in 1873. The name comes from the word "dyshidrotic", meaning "difficult sweating", as problems with sweating was once believed to be the cause.

Signs and symptoms
Dyshidrosis has been described as having the following characteristics:

Itchiness of the palms or soles, followed by the sudden development of intensely itchy small blisters on the sides of the fingers, the palms or the feet.
These blisters are often described as having a "tapioca pudding" appearance.
After a few weeks, the small blisters eventually disappear as the top layer of skin falls off.
These eruptions do not occur elsewhere on the body.
The eruptions may be symmetrical.

Causes
The exact causes of dyshidrosis are unknown. Food allergens may be involved in certain cases </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 Testicular torsion and can you explain it in depth? [/INST] Testicular torsion occurs when the spermatic cord (from which the testicle is suspended) twists, cutting off the blood supply to the testicle. The most common symptom in children is sudden, severe testicular pain. The testicle may be higher than usual in the scrotum and vomiting may occur. In newborns, pain is often absent and instead the scrotum may become discolored or the testicle may disappear from its usual place.Most of those affected have no obvious prior underlying health problems. Testicular tumor or prior trauma may increase risk. Other risk factors include a congenital malformation known as a "bell-clapper deformity" wherein the testis is inadequately attached to the scrotum allowing it to move more freely and thus potentially twist. Cold temperatures may also be a risk factor. The diagnosis should usually be made based on the presenting symptoms, but requires timely diagnosis and treatment to avoid testicular loss. An ultrasound can be useful when the diagnosis is unclear.Treatment is by physically untwisting the testicle, if possible, followed by surgery. Pain can be treated with opioids. Outcome depends on time to correction. If successfully treated within six hours onset, it is often good. However, if delayed for 12 or more hours the testicle is typically not salvageable. About 40% of people require removal of the testicle.It is most common just after birth and during puberty. It occurs in about 1 in 4,000 to 1 in 25,000 males under 25 years of age each year. Of children with testicular pain of rapid onset, testicular torsion is the cause of about 10% of cases. Complications may include an inability to have children. The condition was first described in 1840 by Louis Delasiauve.

Signs and symptoms
Testicular torsion usually presents with severe testicular pain or pain in the groin and lower abdomen. Pain generally begins suddenly and typically involves only one side. There is often associated nausea and vomiting. The testicle may lie higher in the scrotum due to twisting and subsequent shortening of the spermatic cord or may be positioned in a horizontal orientation. Mild warmth and redness of the overlying area may be present. Elevation of the testicle may worsen the pain. Urinary symptoms, such as pain or increased frequency of urination are also typically absent. Symptom onset often follows physical activity or trauma to the testes or scrotum. Children with testicular torsion may awaken with testicular or abdominal pain in the middle of the night or in the morning. There may be a history of previous, similar episodes of scrotal pain due to prior transient testicular torsion with spontaneous resolution.

Complications
Testicular infarction: Testicular damage occurs as a consequence of decreased blood flow, and therefore decreased oxygen and nutrient supply, to the testicle. If the testicle is not viable during surgical exploration, it must be removed to prevent further necrosis, or tissue death.
Infertility: The impact of testicular torsion on long-term fertility is not yet fully understood. However, testicular torsion may cause abnormal sperm function on semen analysis, although these abnormalities are more likely to be found in adolescents and in adults. Torsion does not seem to affect long-term sperm function in neonates. The cause of abnormal sperm function is thought to be due to the following mechanisms:
Immunological theory, also known as "sympathetic orchidopathia": It is thought that following injury to the testicle, the bodys immune system is activated to clean up damaged cells. In the process, it creates anti-testicular cell antibodies, or proteins that cross the injured blood-testis barrier and damage both the affected and contralateral testicles.
Abnormalities in microcirculation within the testicle
Reperfusion injury: This type of injury is seen in tissues that have been deprived of blood supply for a prolonged period.
Gangrene, or a type of tissue damage caused by lack of blood supply, of the testis.
Sepsis, in extremely rare cases (0,03%), if not treated for a long period of time, it could lead to sepsis and cause severe life-threatening infections and injuries through the blood and organs, which could lead to death.
Recurrence of torsion may occur even after surgical fixation, although this is very unlikely.
Psychological impact of losing a testicle.

Risk factors
Most of those affected with testicular torsion have no prior underlying health problems or predisposing conditions. However, there are certain factors that may increase risk of testicular torsion. A larger testicle either due to normal variation or testicular tumor increases the risk of torsion. Similarly, the presence of a mass or malignancy involving the spermatic cord can also predispose to torsion.Age is also an important risk factor for torsion. Torsion most commonly occurs either in the newborn or just before or during puberty. Testicular torsion often occurs before or during puberty, prior to complete testicular descent. Epididymitis is more commonly a postpubertal condition.Several congenital anatomic malformations or variations in the testicle or the surrounding structures may allow for increased scrotal rotation and increase the risk of testicular torsion. A congenital malformation of the processus vaginalis known as "bell-clapper deformity" accounts for 90% of all cases. In this condition, rather than the testes attaching posteriorly to the inner lining of the scrotum by the mesorchium, the mesorchium terminates early and the testis is free floating in the tunica vaginalis. Other anatomic risk factors include horizontal lie of the testicle or a spermatic cord with a long intrascrotal portion. Cryptorchidisim is also a risk factor for torsion with some studies proposing a 10-fold higher risk.
Testicular torsion may also be caused by trauma to the scrotum or exercise (in particular, bicycle riding), however only about 4-8% of cases are the result of trauma. There is thought to be a possible genetic basis for predisposition to torsion, based on multiple published reports of familial testicular torsion. There is controversy whether cold weather months are associated with an increased risk.

Pathophysiology
Testicular torsion occurs when there is mechanical twisting of the spermatic cord, which suspends the testicle within the scrotum and contains the testicular artery and vein. Twisting of the cord reduces or eliminates blood flow to the testicle. The degree of arterial and venous obstruction depends on the duration and severity of the torsion event. Typically, venous blood flow is compromised first. The increase in venous pressure subsequently causes decreased arterial blood flow, leading to decreased oxygen supply to the testicle, and if untreated, testicular infarction.It is also believed that torsion occurring during fetal development can lead to so-called neonatal torsion or vanishing testis, and is one of the causes of an infant being born with monorchism (one testicle).

Intermittent testicular torsion
Intermittent testicular torsion (ITT) is a less serious but chronic variant of torsion. It is characterized by intermittent scrotal or testicular pain, followed by eventual spontaneous detorsion and resolution of pain. Nausea and vomiting may also occur.: 150  Though less pressing, such individuals are at significant risk of complete torsion and possible subsequent orchiectomy and the recommended treatment is elective bilateral orchiopexy.  Ninety-seven percent of patients who undergo such surgery experience complete relief from their symptoms.: 316

Extravaginal testicular torsion
Torsion occurring outside of the tunica vaginalis, when the testis and gubernaculum can rotate freely, is termed an extravaginal testicular torsion. This type occurs exclusively in newborns, however, newborns can be affected by other testicular torsion variants as well. Neonates experiencing such a torsion typically present with painless scrotal swelling, discoloration, and a firm, painless mass in the scrotum. Such testes are usually necrotic from birth and must be removed surgically.: 315  The exact cause of or specific risk factors for extravaginal torsion in this population remain unclear.

Intravaginal testicular torsion
Intravaginal testicular torsion occurs when the testicle rotates on the spermatic cord within the tunica vaginalis. This variant more commonly occurs in older children and adults. The "bell-clapper deformity," in which there is inappropriately high attachment of the tunica vaginalis over the spermatic cord and failure of the normal posterior attachment of the testicle to the inner scrotum, which allows the testicle to move freely within the tunica vaginalis and predisposes to intravaginal testicular torsion.

Torsion of the testicular appendix
The testicular appendix is located in the upper pole of the testicle. It is an embryonic remnant that has no known function, but is at risk for torsion events. This type of torsion is the most common cause of acute scrotal pain in boys ages 7–14. Its appearance is similar to that of testicular torsion but the onset of pain is typically more gradual. Palpation reveals a small firm nodule on the upper portion of the testis which displays a characteristic "blue dot sign".  This is the appendix of the testis which has become discolored and is noticeably blue through the skin. Unlike other torsions, however, the cremasteric reflex is still active.  Typical treatment involves the use of over-the-counter analgesics and the condition resolves within 2–3 days.: 316

Torsion of the undescended testicle
The undescended testis is at increased risk of testicular torsion. The mechanism for torsion in the undescended testicle is not fully understood, though it may be due to abnormal contractions of the cremaster muscle, which covers the testicle and spermatic cord and is responsible for raising and lowering the testicle to regulate scrotal temperature. The undescended testicle is also at higher risk for testicular tumor, which due to the increased weight and size compared to a healthy testicle can predispose to torsion.

Diagnosis
The diagnosis should generally be made based on the presenting symptoms. An ultrasound can be useful when the diagnosis is unclear. However, imaging should not delay surgical intervention as complications develop with prolonged ischemia. Immediate surgery is recommended regardless of imaging findings if there is a high degree of suspicion based on history and physical examination.Given the treatment implications of testicular torsion, it is important to distinguish testicular torsion from other causes of testicular pain, such as epididymitis, which can present similarly. While both conditions can cause testicular pain, the pain of epididymitis is typically localized to the epididymis at the rear pole of the testicle. Epididymitis may also be characterized by discoloration and swelling of the testis, and fever. The cremasteric reflex in epididymitis is usually present. Testicular torsion, or more probably impending testicular infarction, can also produce a low-grade fever. There is often an absent or decreased cremasteric reflex.

Clinical exam
The absence of the cremasteric reflex in an acutely painful testicle is most indicative of testicular torsion (the twisting of the spermatic cord of the testicle makes reflexive responses all but impossible). The cremasteric reflex normally causes elevation of the testicle by stroking the inner thigh. Absence is especially common in children, but its presence does not exclude a diagnosis of testicular torsion.On physical examination, the testis can be swollen, tender, high-riding, and with an abnormal transverse lie.Prehns sign, a classic physical exam finding, has not been reliable in distinguishing torsion from other causes of testicular pain such as epididymitis. The individual will not usually have a fever, though nausea is common.

Imaging
A doppler ultrasound scan of the scrotum can identify the absence of blood flow in the twisted testicle and is nearly 90% accurate in diagnosis. It can also help distinguish torsion from epididymitis.Radionuclide scanning (scintigraphy) of the scrotum is the most accurate imaging technique, but it is not routinely available, particularly with the urgency that might be required. The agent of choice for this purpose is technetium-99m pertechnetate. Initially it provides a radionuclide angiogram, followed by a static image after the radionuclide has perfused the tissue. In the healthy patient, initial images show symmetric flow to the testes, and delayed images show uniformly symmetric activity. In testicular torsion, the images may show heterogenous activity within the affected testicle.

Treatment
Testicular torsion is a surgical emergency that requires immediate intervention to restore the flow of blood to the testicle. If treated either manually or surgically within six hours, there is a high chance (approximately 90%) of saving the testicle. At 12 hours the rate decreases to 50%; at 24 hours it drops to 10%, and after 24 hours the ability to save the testicle approaches 0, although salvage of the testicle has been reported beyond 24 hours </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 Pelvic inflammatory disease and can you explain it in depth? [/INST] Pelvic inflammatory disease, also known as pelvic inflammatory disorder (PID), is an infection of the upper part of the female reproductive system, namely the uterus, fallopian tubes, and ovaries, and inside of the pelvis. Often, there may be no symptoms. Signs and symptoms, when present, may include lower abdominal pain, vaginal discharge, fever, burning with urination, pain with sex, bleeding after sex, or irregular menstruation. Untreated PID can result in long-term complications including infertility, ectopic pregnancy, chronic pelvic pain, and cancer.The disease is caused by bacteria that spread from the vagina and cervix. Infections by Neisseria gonorrhoeae or Chlamydia trachomatis are present in 75 to 90 percent of cases. Often, multiple different bacteria are involved. Without treatment, about 10 percent of those with a chlamydial infection and 40 percent of those with a gonorrhea infection will develop PID. Risk factors are generally similar to those of sexually transmitted infections and include a high number of sexual partners and drug use. Vaginal douching may also increase the risk. The diagnosis is typically based on the presenting signs and symptoms. It is recommended that the disease be considered in all women of childbearing age who have lower abdominal pain. A definitive diagnosis of PID is made by finding pus involving the fallopian tubes during surgery. Ultrasound may also be useful in diagnosis.Efforts to prevent the disease include not having sex or having few sexual partners and using condoms. Screening women at risk for chlamydial infection followed by treatment decreases the risk of PID. If the diagnosis is suspected, treatment is typically advised. Treating a womans sexual partners should also occur. In those with mild or moderate symptoms, a single injection of the antibiotic ceftriaxone along with two weeks of doxycycline and possibly metronidazole by mouth is recommended. For those who do not improve after three days or who have severe disease, intravenous antibiotics should be used.Globally, about 106 million cases of chlamydia and 106 million cases of gonorrhea occurred in 2008. The number of cases of PID, however, is not clear. It is estimated to affect about 1.5 percent of young women yearly. In the United States, PID is estimated to affect about one million people each year. A type of intrauterine device (IUD) known as the Dalkon shield led to increased rates of PID in the 1970s. Current IUDs are not associated with this problem after the first month.

Signs and symptoms
Symptoms in PID range from none to severe. If there are symptoms, fever, cervical motion tenderness, lower abdominal pain, new or different discharge, painful intercourse, uterine tenderness, adnexal tenderness, or irregular menstruation may be noted.Other complications include endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis, periappendicitis, and perihepatitis.

Complications
PID can cause scarring inside the reproductive system, which can later cause serious complications, including chronic pelvic pain, infertility, ectopic pregnancy (the leading cause of pregnancy-related deaths in adult females), and other complications of pregnancy. Occasionally, the infection can spread to the peritoneum causing inflammation and the formation of scar tissue on the external surface of the liver (Fitz-Hugh–Curtis syndrome).

Cause
Chlamydia trachomatis and Neisseria gonorrhoeae are usually the main cause of PID. Data suggest that PID is often polymicrobial. Isolated anaerobes and facultative microorganisms have been obtained from the upper genital tract. N. gonorrhoeae has been isolated from fallopian tubes, facultative and anaerobic organisms were recovered from endometrial tissues.The anatomical structure of the internal organs and tissues of the female reproductive tract provides a pathway for pathogens to ascend from the vagina to the pelvic cavity thorough the infundibulum. The disturbance of the naturally occurring vaginal microbiota associated with bacterial vaginosis increases the risk of PID.N. gonorrhoea and C. trachomatis are the most common organisms. The least common were infections caused exclusively by anaerobes and facultative organisms. Anaerobes and facultative bacteria were also isolated from 50 percent of the patients from whom Chlamydia and Neisseria were recovered; thus, anaerobes and facultative bacteria were present in the upper genital tract of nearly two-thirds of the PID patients. PCR and serological tests have associated extremely fastidious organism with endometritis, PID, and tubal factor infertility.  Microorganisms associated with PID are listed below.Rarely cases of PID have developed in people who have stated they have never had sex.

Bacteria
Diagnosis
Upon a pelvic examination, cervical motion, uterine, or adnexal tenderness will be experienced.  Mucopurulent cervicitis and or urethritis may be observed. In severe cases more testing may be required such as laparoscopy, intra-abdominal bacteria sampling and culturing, or tissue biopsy.Laparoscopy can visualize "violin-string" adhesions, characteristic of Fitz-Hugh–Curtis perihepatitis and other abscesses that may be present.Other imaging methods, such as ultrasonography, computed tomography (CT), and magnetic imaging (MRI), can aid in diagnosis. Blood tests can also help identify the presence of infection: the erythrocyte sedimentation rate (ESR), the C-reactive protein (CRP) level, and chlamydial and gonococcal DNA probes.Nucleic acid amplification tests (NAATs), direct fluorescein tests (DFA), and enzyme-linked immunosorbent assays (ELISA) are highly sensitive tests that can identify specific pathogens present. Serology testing for antibodies is not as useful since the presence of the microorganisms in healthy people can confound interpreting the antibody titer levels, although antibody levels can indicate whether an infection is recent or long-term.Definitive criteria include histopathologic evidence of endometritis, thickened filled Fallopian tubes, or laparoscopic findings. Gram stain/smear becomes definitive in the identification of rare, atypical and possibly more serious organisms. Two thirds of patients with laparoscopic evidence of previous PID were not aware they had PID, but even asymptomatic PID can cause serious harm.
Laparoscopic identification is helpful in diagnosing tubal disease; a 65 percent to 90 percent positive predictive value exists in patients with presumed PID.Upon gynecologic ultrasound, a potential finding is tubo-ovarian complex, which is edematous and dilated pelvic structures as evidenced by vague margins, but without abscess formation.

Differential diagnosis
A number of other causes may produce similar symptoms including appendicitis, ectopic pregnancy, hemorrhagic or ruptured ovarian cysts, ovarian torsion, and endometriosis and gastroenteritis, peritonitis, and bacterial vaginosis among others.Pelvic inflammatory disease is more likely to reoccur when there is a prior history of the infection, recent sexual contact, recent onset of menses, or an IUD (intrauterine device) in place or if the partner has a sexually transmitted infection.Acute pelvic inflammatory disease is highly unlikely when recent intercourse has not taken place or an IUD is not being used. A sensitive serum pregnancy test is typically obtained to rule out ectopic pregnancy. Culdocentesis will differentiate hemoperitoneum (ruptured ectopic pregnancy or hemorrhagic cyst) from pelvic sepsis (salpingitis, ruptured pelvic abscess, or ruptured appendix).Pelvic and vaginal ultrasounds are helpful in the diagnosis of PID. In the early stages of infection, the ultrasound may appear normal. As the disease progresses, nonspecific findings can include free pelvic fluid, endometrial thickening, uterine cavity distension by fluid or gas. In some instances the borders of the uterus and ovaries appear indistinct. Enlarged ovaries accompanied by increased numbers of small cysts correlates with PID.Laparoscopy is infrequently used to diagnose pelvic inflammatory disease since it is not readily available.  Moreover, it might not detect subtle inflammation of the fallopian tubes, and it fails to detect endometritis.  Nevertheless, laparoscopy is conducted if the diagnosis is not certain or if the person has not responded to antibiotic therapy after 48 hours.No single test has adequate sensitivity and specificity to diagnose pelvic inflammatory disease. A large multisite U.S. study found that cervical motion tenderness as a minimum clinical criterion increases the sensitivity of the CDC diagnostic criteria from 83 percent to 95 percent. However, even the modified 2002 CDC criteria do not identify women with subclinical disease.

Prevention
Regular testing for sexually transmitted infections is encouraged for prevention. The risk of contracting pelvic inflammatory disease can be reduced by the following:

Using barrier methods such as condoms; see human sexual behaviour for other listings.
Seeking medical attention if you are experiencing symptoms of PID.
Using hormonal combined contraceptive pills also helps in reducing the chances of PID by thickening the cervical mucosal plug & hence preventing the ascent of causative organisms from the lower genital tract.
Seeking medical attention after learning that a current or former sex partner has, or might have had a sexually transmitted infection.
Getting a STI history from your current partner and strongly encouraging they be tested and treated before intercourse.
Diligence in avoiding vaginal activity, particularly intercourse, after the end of a pregnancy (delivery, miscarriage, or abortion) or certain gynecological procedures, to ensure that the cervix closes.
Reducing the number of sexual partners.
Sexual monogamy.
Abstinence

Treatment
Treatment is often started without confirmation of infection because of the serious complications that may result from delayed treatment. Treatment depends on the infectious agent and generally involves the use of antibiotic therapy although there is no clear evidence of which antibiotic regimen is more effective and safe in the management of PID. If there is no improvement within two to three days, the patient is typically advised to seek further medical attention. Hospitalization sometimes becomes necessary if there are other complications.  Treating sexual partners for possible STIs can help in treatment and prevention.For women with PID of mild to moderate severity, parenteral and oral therapies appear to be effective.  It does not matter to their short- or long-term outcome whether antibiotics are administered to them as inpatients or outpatients. Typical regimens include cefoxitin or cefotetan plus doxycycline, and clindamycin plus gentamicin. An alternative parenteral regimen is ampicillin/sulbactam plus doxycycline. Erythromycin-based medications can also be used. A single study suggests superiority of azithromycin over doxycycline. Another alternative is to use a parenteral regimen with ceftriaxone or cefoxitin plus doxycycline </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 Yersinia and can you explain it in depth? [/INST] Yersinia is a genus of bacteria in the family Yersiniaceae. Yersinia species are Gram-negative, coccobacilli bacteria, a few micrometers long and fractions of a micrometer in diameter, and are facultative anaerobes. Some members of Yersinia are pathogenic in humans; in particular, Y. pestis is the causative agent of the plague. Rodents are the natural reservoirs of Yersinia; less frequently, other mammals serve as the host. Infection may occur either through blood (in the case of Y. pestis) or in an alimentary fashion, occasionally via consumption of food products (especially vegetables, milk-derived products, and meat) contaminated with infected urine or feces.
Speculations exist as to whether or not certain Yersinia can also be spread by  protozoonotic mechanisms, since Yersinia species are known to be facultative intracellular parasites; studies and discussions of the possibility of amoeba-vectored (through the cyst form of the protozoan) Yersinia propagation and proliferation are now in progress.

Microbial physiology
An interesting feature peculiar to some of the Yersinia bacteria is the ability to not only survive, but also to actively proliferate at temperatures as low as 1–4 °C (e.g., on cut salads and other food products in a refrigerator). Yersinia bacteria are relatively quickly inactivated by oxidizing agents such as hydrogen peroxide and potassium permanganate solutions.

Genetics
Database
The creation of YersiniaBase, a data and tools collection for the reporting and comparison of Yersinia species genome sequence data, was reported in January 2015.  The provisional representation of species addressed by the resource has been indicated in the TaxBox on this page by a superscript yb beside the species name.  Development of YersiniaBase was funded by the University of Malaya and the Ministry of Education, Malaysia.

Pathogenesis
Y. pestis is the causative agent of plague </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 Post-nasal drip and can you explain it in depth? [/INST] Post-nasal drip (PND), also known as upper airway cough syndrome (UACS), occurs when excessive mucus is produced by the nasal mucosa. The excess mucus accumulates in the back of the nose, and eventually in the throat once it drips down the back of the throat. It can be caused by rhinitis, sinusitis, gastroesophageal reflux disease (GERD), or by a disorder of swallowing (such as an esophageal motility disorder). Other causes can be allergy, cold, flu, and side effects from medications.
However, some researchers argue that the flow of mucus down the back of the throat from the nasal cavity is a normal physiologic process that occurs in all healthy individuals. Some researchers challenge post-nasal drip as a syndrome and instead view it as a symptom, also taking into account variation across different societies. Furthermore, this rebuttal is reinforced because of the lack of an accepted definition, pathologic tissue changes, and available biochemical tests.

Signs and symptoms
PND may present itself through the constant presence of discomfort in the upper airways. It is classically described as the sensation of a substance "dripping down the throat" and may also present with rhinorrhea, constant throat clearing, and cough, although its symptoms can be very nonspecific.  PND is one of the most common etiologies for chronic cough, defined as a cough persisting beyond 8 weeks.GERD is often associated with a high prevalence of upper-respiratory symptoms similar to those of PND, such as coughing, throat clearing, hoarseness and change in voice. Reflux causes throat irritation, leading to a sensation of increased mucus in the throat, which is believed to aggravate and, in some cases, cause post-nasal drip.Post-nasal drip can be a cause of laryngeal inflammation and hyperresponsiveness, leading to symptoms of vocal cord dysfunction.

Causes
There are multiple causes of PND, which can be acute or chronic.

Allergic rhinitis
Allergic rhinitis (AR) is a common condition where exposure to allergens results in the release of inflammatory mediators, such as histamine, that causes sneezing, rhinorrhea, itchy eyes, and nasal congestion. The increased rhinorrhea and mucus production can result in PND.

Non-allergic rhinitis
Non-allergic rhinitis (NAR) is a condition in which there are symptoms of rhinitis, including rhinorrhea and nasal obstruction, but with negative skin and serum allergy testing results. It can be further categorized into:
Non-allergic rhinitis with eosinophilia (NARES)
Hormonal rhinitis (such as during pregnancy)
Medication-induced rhinitis
Atrophic rhinitis
Irritant and occupational rhinitis (including tobacco smoke, cleaning supplies, etc.)
Idiopathic nonallergic rhinitis

Rhinosinusitis
Rhinosinusitis is inflammation or infection of the sinus cavities. Acute rhinosinusitis has symptoms lasting less than four weeks, while chronic rhinosinusitis lasts greater than 12 weeks. This persistent irritation can lead to increased mucus production as a result of pro-inflammatory pathways, producing symptoms of PND.

Mechanism
The exact mechanism of PND depends on its etiology, but usually involves increased production of mucus from the nasal mucosa. In addition to providing sense of smell, the nasal cavity serves to filter and regulate the temperature and humidity of inspired air. The nasal mucosa can produce secretions, or mucus, that provides lubrication and protection for the nasal cavity. This mucus production is activated by the autonomic nervous system; specifically, cholinergic neuropeptides are responsible for increasing mucus production. Excess mucus can drain posteriorly into the upper and lower airways, which, along with other physical and chemical irritants, can activate receptors in the respiratory tract that results in a protective physiological cough.

Diagnosis
Diagnosis of PND depends on both a detailed history and clinical examination to help determine its etiology. The history may begin with feelings of obstructed nasal breathing or "stuffy nose" with or without nasal discharge. If allergic rhinitis is suspected, a family history of allergic conditions as well as a personal history of other associated conditions such as food allergy, asthma, and atopic dermatitis can be evaluated.  Allergic rhinitis classically has more symptoms of sneezing attacks, itchy eyes, and respiratory problems, although it is difficult to distinguish the different types of rhinitis by symptomology alone. Visual inspection can reveal mouth breathing, which is suggestive of nasal obstruction, or a horizontal crease across the nose (caused by the "allergic salute").In the absence of any specific diagnostic tests, it may be difficult to diagnose PND from history of symptoms alone, as the etiology is broad and the symptoms may be very general. As such, suggestive procedures that highlight rhinitis and mucopurulent secretions, such as nasoendoscopy, may instead be utilized because of the vague nature of information available to directly attribute specific symptoms to the syndrome.

Treatment
Treatment options depend on the nature of an individual’s post-nasal drip and its cause </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 Rotator cuff tear and can you explain it in depth? [/INST] A rotator cuff tear is an injury where one or more of the tendons or muscles of the rotator cuff of the shoulder get torn. Symptoms may include shoulder pain, which is often worse with movement, limited range of motion, or weakness. This may limit peoples ability to brush their hair or put on clothing. Clicking may also occur with movement of the arm.Tears may occur as the result of a sudden force or gradually over time. Risk factors include certain repetitive activities, smoking, and a family history of the condition. Diagnosis is based on symptoms, examination, and medical imaging. The rotator cuff is made up of the supraspinatus, infraspinatus, teres minor, and subscapularis. The supraspinatus is the most commonly affected.Treatment may include pain medication such as NSAIDs and specific exercises. It is recommended that people who are unable to raise their arm above 90 degrees after 2 weeks should be further assessed. In severe cases surgery may be tried, however benefits of surgery are unclear as of 2019. Rotator cuff tears are common. Those over the age of 40 are most often affected. The condition has been described since at least the early 1800s.

Signs and symptoms
Many rotator cuff tears have no symptoms. Both partial and full thickness tears have been found on post mortem and MRI studies in those without any history of shoulder pain or symptoms. However, the most common presentation is shoulder pain or discomfort. This may occur with activity, particularly shoulder activity above the horizontal position, but may also be present at rest in bed. Pain-restricted movement above the horizontal position may be present, as well as weakness with shoulder flexion and abduction.Abnormal mobility or function of the scapula (scapular dyskinesia) may be present and is related to lower functional scores; it unclear whether scapular dyskinesia is a cause, effect or compensation for rotator cuff pathology.

Risk factors
Epidemiological studies strongly support a relationship between age and cuff tear prevalence, with the most common cause being age-related degeneration and, less frequently, sports injuries or trauma.Those most prone to failed rotator cuff syndrome are people 65 years of age or older; and those with large, sustained tears. Smokers, people with diabetes, individuals with muscle atrophy or fatty infiltration, and those who do not follow postoperative-care recommendations also are at greater risk. In a 2008 study the frequency of such tears increased from 13% in the youngest group (aged 50–59 y) to 20% (aged 60–69 y), 31% (aged 70–79 y), and 51% in the oldest group (aged 80–89 y).Some risk factors such as increased age and height cannot be changed. Increased body mass index is also associated with tearing. Recurrent lifting and overhead motions are at risk for rotator cuff injury as well. This includes jobs that involve repetitive overhead work, such as carpenters, painters, custodians, and servers. People who play sports that involve overhead motions, such as swimming, water polo, volleyball, baseball, tennis, and American football quarterbacks, are at a greater risk of experiencing a rotator cuff tear. Striking-based combat sports, such as boxing, also account for severe rotator cuff injuries of competitors, typically when their punches miss the target, or overusing the shoulder by throwing excessively large amounts of punches. Certain track-and-field activities, such as shot put, javelin throw are also of considerable risk, especially when performing outdoors under cold weather conditions or neglecting warming-up procedures, for proper warm-up of the throwing and/or swinging arm can help reduce the stress on the musculature of the shoulder girdle. Corticosteroid injections around the tendons increases the risk of tendon tear and delay tendon healing.

Mechanisms of injury
The shoulder is a complex mechanism involving bones, ligaments, joints, muscles, and tendons.
The two main causes are acute injury or chronic and cumulative degeneration of the shoulder joint. Mechanisms can be extrinsic, intrinsic or a combination of both.The cuff is responsible for stabilizing the glenohumeral joint to allow abduction and rotation of the humerus. When trauma occurs, these functions can be compromised. Because individuals are dependent on the shoulder for many activities, overuse can lead to tears, with the vast majority being in the supraspinatus tendon.The role of the supraspinatus is to resist downward motion, both while the shoulder is relaxed and carrying weight. Supraspinatus tears usually occurs at its insertion on the humeral head at the greater tubercle. Though the supraspinatus is the most commonly injured tendon in the rotator cuff, the other three can also be injured at the same time.

Acute tears
The amount of stress needed to acutely tear a rotator cuff tendon will depend on the underlying condition of the tendon. If healthy, the stress needed will be high, such as with a fall on the outstretched arm. This stress may occur coincidentally with other injuries such as a dislocation of the shoulder or separation of the acromioclavicular joint. In the case of a tendon with pre-existing degeneration, the force may be more modest, such as with a sudden lift, particularly with the arm above the horizontal position.  The type of loading involved with injury is usually eccentric, such as when two people are carrying a load and one lets go, forcing the other to maintain force while the muscle elongates.

Chronic tears
Chronic tears are indicative of extended use in conjunction with other factors such as poor biomechanics or muscular imbalance.  Ultimately, most are the result of wear that occurs slowly over time as a natural part of aging. They are more common in the dominant arm, but a tear in one shoulder signals an increased risk of a tear in the opposing shoulder.Several factors contribute to degenerative, or chronic, rotator cuff tears of which repetitive stress is the most significant. This stress consists of repeating the same shoulder motions frequently, such as overhead throwing, rowing, and weightlifting.  Many jobs that require frequent shoulder movement such as lifting and overhead movements also contribute. In older populations impairment of blood supply can also be an issue.  With age, circulation to the rotator cuff tendons decreases, impairing natural ability to repair, increasing risk for tear. Another potential contributing cause is impingement syndrome, the most common non-sports related injury and which occurs when the tendons of the rotator cuff muscles become irritated and inflamed while passing through the subacromial space beneath the acromion. This relatively small space becomes even smaller when the arm is raised in a forward or upward position. Repetitive impingement can inflame the tendons and bursa, resulting in the syndrome.

Extrinsic factors
Well-documented anatomic factors include the morphologic characteristics of the acromion, a bony projection from the scapula that curves over the shoulder joint.  Hooked, curved, and laterally sloping acromia are strongly associated with cuff tears and may cause damage through direct traction on the tendon. Conversely, flat acromia may have an insignificant involvement in cuff disease and consequently may be best treated conservatively. The development of these different acromial shapes is likely both genetic and acquired. In the latter case, there can be a progression from flat to curved or hooked with increasing age.  Repetitive mechanical activities such as sports and exercise may contribute to flattening and hooking of the acromion. Cricket bowling, swimming, tennis, baseball, and kayaking are often implicated.  Progression to a hooked acromion could be an adaptation to an already damaged, poorly balanced rotator cuff with resultant stress on the coracoacromial arch. Other anatomical factors include an os acromiale and acromial spurs. Environmental factors include age, shoulder overuse, smoking, and medical conditions that affect circulation or impair the inflammatory and healing response, such as diabetes mellitus.

Intrinsic factors
Intrinsic factors refer to injury mechanisms that occur within the rotator cuff itself. The principal is a degenerative-microtrauma model, which supposes that age-related tendon damage compounded by chronic microtrauma results in partial tendon tears that then develop into full rotator cuff tears. As a result of repetitive microtrauma in the setting of a degenerative rotator cuff tendon, inflammatory mediators alter the local environment, and oxidative stress induces tenocyte apoptosis causing further rotator cuff tendon degeneration. A neural theory also exists that suggests neural overstimulation leads to the recruitment of inflammatory cells and may also contribute to tendon degeneration.

Surgical considerations
Depending upon the diagnosis, several treatment alternatives are available. They include revision repair, non-anatomic repair, tendon transfer and arthroplasty. When possible, surgeons make tension-free repairs in which they use grafted tissues rather than stitching to reconnect tendon segments. This can result in a complete repair. Other options are a partial repair, and reconstruction involving a bridge of biologic or synthetic substances. Partial repairs typically are performed on retracted cuff tears.Tendon transfers are prescribed for young, active cuff-tear individual who experience weakness and decreased range of motion, but little pain. The technique is not considered appropriate for older people, or those with pre-operative stiffness or nerve injuries. People diagnosed with glenohumeral arthritis and rotator cuff anthropathy have the alternative of total shoulder arthroplasty, if the cuff is largely intact or repairable. If the cuff is incompetent then a reverse shoulder arthroplasty is available and, although not as robust a prosthesis, does not require an intact cuff to maintain a stable joint.

Diagnosis
Diagnosis is based upon physical assessment and history, including description of previous activities and acute or chronic symptoms.  A systematic, physical examination of the shoulder comprises inspection, palpation, range of motion,  provocative tests to reproduce the symptoms, neurological examination, and strength testing.  The shoulder should also be examined for tenderness and deformity.  Since pain arising from the neck is frequently referred to the shoulder, the examination should include an assessment of the cervical spine looking for evidence suggestive of a pinched nerve, osteoarthritis, or rheumatoid arthritis.
Neer promoted the concept of three stages of rotator cuff disease. Stage I, according to Neer, occurred in those younger than 25 years and involved edema and hemorrhage of the tendon and bursa. Stage II involved tendinitis and fibrosis of the rotator cuff in 25- to 40-year-olds. Stage III involved tearing of the rotator cuff (partial or full thickness) and occurred in those older than 40 years.  For surgical purposes, tears are also described by location, size or area, and depth. Further subclasses include the acromiohumeral distance, acromial shape, fatty infiltration or degeneration of muscles, muscle atrophy, tendon retraction, vascular proliferation, chondroid metaplasia, and calcification.  Again, in surgical planning, age-related degeneration of thinning and disorientation of the collagen fibers, myxoid degeneration, and hyaline degeneration are considered.Diagnostic modalities, dependent on circumstances, include X-ray, MRI, MR arthrography, double-contrast arthrography, and ultrasound. Although MR arthrography is currently considered the gold standard, ultrasound may be most cost-effective.  Usually, a tear will be undetected by X-ray, although bone spurs, which can impinge upon the rotator cuff tendons, may be visible.  Such spurs suggest chronic severe rotator cuff disease.  Double-contrast arthrography involves injecting contrast dye into the shoulder joint to detect leakage out of the injured rotator cuff  and its value is influenced by the experience of the operator. The most common diagnostic tool is magnetic resonance imaging (MRI), which can sometimes indicate the size of the tear, as well as its location within the tendon.  Furthermore, MRI enables the detection or exclusion of complete rotator cuff tears with reasonable accuracy and is also suitable to diagnose other pathologies of the shoulder joint.The logical use of diagnostic tests is an important component of effective clinical practice.Clinical judgement, rather than over reliance on MRI or any other modality, is strongly advised in determining the cause of shoulder pain, or planning its treatment, since rotator cuff tears are also found in some without pain or symptoms. The role of X-ray, MRI, and ultrasound, is adjunctive to clinical assessment and serves to confirm a diagnosis provisionally made by a thorough history and physical examination. Over-reliance on imaging may lead to overtreatment or distract from the true dysfunction causing symptoms.

Symptoms
Symptoms may occur immediately after trauma (acute) or develop over time (chronic).
Acute injury is less frequent than chronic disease, but may follow bouts of forcefully raising the arm against resistance, as occurs in weightlifting, for example.  In addition, falling forcefully on the shoulder can cause acute symptoms.  These traumatic tears predominantly affect the supraspinatus tendon or the rotator interval and symptoms include severe pain that radiates through the arm, and limited range of motion, specifically during abduction of the shoulder.
Chronic tears occur among individuals who constantly participate in overhead activities, such as pitching or swimming, but can also develop from shoulder tendinitis or rotator cuff disease. Symptoms arising from chronic tears include sporadic worsening of pain, debilitation, and atrophy of the muscles, noticeable pain during rest, crackling sensations (crepitus) when moving the shoulder, and inability to move or lift the arm sufficiently, especially during abduction and flexion motions.Pain in the anterolateral aspect of the shoulder is not specific to the shoulder, and may arise from, and be referred from, the neck, heart or gut.
Symptoms will often include pain or ache over the front and outer aspect of the shoulder, pain aggravated by leaning on the elbow and pushing upwards on the shoulder (such as leaning on the armrest of a reclining chair), intolerance of overhead activity, pain at night when lying directly on the affected shoulder, pain when reaching forward (e.g. unable to lift a gallon of milk from the refrigerator). Weakness may be reported, but is often masked by pain and is usually found only through examination. With longer-standing pain, the shoulder is favored and gradually loss of motion and weakness may develop, which, due to pain and guarding, are often unrecognized and only brought to attention during the physical exam.Primary shoulder problems may cause pain over the deltoid muscle intensified by abduction against resistance – the impingement sign. This signifies pain arising from the rotator cuff, but cannot distinguish between inflammation, strain, or tear. Individuals may report that they are unable to reach upwards to brush their hair or to lift a food can from an overhead shelf.

Signs
No single physical examination test distinguishes reliably between bursitis, partial-thickness, and full-thickness tears. The most useful single test for infraspinatous tendon tears is the drop sign (the examiner lifts the arm straight out from the body with the palm up, the person then needs to hold it there for 10 seconds) and the external rotation lag sign (with the arm by the side and the elbow bent to 90 degrees the person tries to rotate outwards against resistance).A combination of tests seems to provide the most accurate diagnosis. For impingement, these tests include the Hawkins-Kennedy impingement sign in which an examiner medially rotates the injured individuals flexed arm, forcing the supraspinatus tendon against the coracoacromial ligament and so producing pain if the test is positive a positive painful arc sign, and weakness in external rotation with the arm at the side.
For the diagnosis of full-thickness rotator cuff tear, the best combination appears to include once more the painful arc and weakness in external rotation, and in addition, the drop arm sign. This test is also known as Codmans test. The arm is raised to the side to 90° by the examiner.  The injured individual then attempts to look to lower the arm back to neutral, palm down. If the arm drops suddenly or pain is experienced, the test is considered positive.

MRI
Magnetic resonance imaging (MRI) and ultrasound are comparable in efficacy and helpful in diagnosis although both have a false positive rate of 15–20%.  MRI can reliably detect most full-thickness tears although very small pinpoint tears may be missed. In such situations, an MRI combined with an injection of contrast material, an MR-arthrogram, may help to confirm the diagnosis.  It should be realized that a normal MRI cannot fully rule out a small tear (a false negative) while partial-thickness tears are not as reliably detected. While MRI is sensitive in identifying tendon degeneration (tendinopathy), it may not reliably distinguish between a degenerative tendon and a partially torn tendon. Again, magnetic resonance arthrography can improve the differentiation. An overall sensitivity of 91% (9% false negative rate) has been reported indicating that magnetic resonance arthrography is reliable in the detection of partial-thickness rotator cuff tears. However, its routine use is not advised, since it involves entering the joint with a needle with potential risk of infection. Consequently, the test is reserved for cases in which the diagnosis remains unclear.

Ultrasound
Musculoskeletal ultrasound has been advocated by experienced practitioners, avoiding the radiation of X-ray and the expense of MRI while demonstrating comparable accuracy to MRI for identifying and measuring the size of full-thickness and partial-thickness rotator cuff tears. This modality can also reveal the presence of other conditions that may mimic rotator cuff tear at clinical examination, including tendinosis, calcific tendinitis, subacromial subdeltoid bursitis, greater tuberosity fracture, and adhesive capsulitis. However, MRI provides more information about adjacent structures in the shoulder such as the capsule, glenoid labrum muscles and bone and these factors should be considered in each case when selecting the appropriate study.

Xray
X-ray projectional radiography cannot directly reveal tears of the rotator cuff, a soft tissue, and consequently, normal X-rays cannot exclude a damaged cuff. However, indirect evidence of pathology may be seen in instances where one or more of the tendons have undergone degenerative calcification (calcific tendinitis). The humeral head may migrate upwards (high-riding humeral head) secondary to tears of the infraspinatus, or combined tears of the supraspinatus and infraspinatus. The migration can be measured by the distance between:

A line crossing the center of a line between the superior and inferior rims of the glenoid articular surface (blue in image).
The center of a "best-fit" circle positioned over the humeral articular surface (green in image)Normally, the former is positioned inferiorly to the latter, and a reversal is therefore indicating a rotator cuff tear. Prolonged contact between a high-riding humeral head and the acromion above it, may lead to X-rays findings of wear on the humeral head and acromion and secondary degenerative arthritis of the glenohumeral joint (the ball and socket joint of the shoulder), called cuff arthropathy, may follow. Incidental X-ray findings of bone spurs at the adjacent acromioclavicular joint may show a bone spur growing from the outer edge of the clavicle downwards towards the rotator cuff. Spurs may also be seen on the underside of the acromion, once thought to cause direct fraying of the rotator cuff from contact friction, a concept currently regarded as controversial.

In-office testing
As part of clinical decision-making, a simple, minimally invasive, in-office procedure may be performed, the rotator cuff impingement test. A small amount of a local anesthetic and an injectable corticosteroid are injected into the subacromial space to block pain and to provide anti-inflammatory relief. If pain disappears and shoulder function remains good, no further testing is pursued. The test helps to confirm that the pain arises from the shoulder primarily rather than referred from the neck, heart, or gut.
If pain is relieved, the test is considered positive for rotator-cuff impingement, of which tendinitis and bursitis are major causes. However, partial rotator-cuff tears may also demonstrate good pain relief, so a positive response cannot rule out a partial rotator-cuff tear. However, with demonstration of good, pain-free function, treatment will not change, so the test is useful in helping to avoid overtesting or unnecessary surgery.

Classification
Tears of the rotator cuff tendon are described as partial or full thickness, and full thickness with complete detachment of the tendons from bone.

Partial-thickness tears often appear as fraying of an intact tendon.
Full-thickness tears are "through-and-through". These tears can be small pinpoint, larger buttonhole, or involve the majority of the tendon where it still remains substantially attached to the humeral head and thus maintains function.
Full-thickness tears may also involve complete detachment of the tendon(s) from the humeral head and may result in significantly impaired shoulder motion and function.Shoulder pain is variable and may not be proportional to the size of the tear.
Tears are also sometimes classified based on the trauma that caused the injury:

Acute, as a result of a sudden, powerful movement which might include falling onto an outstretched hand at speed, making a sudden thrust with a paddle in kayaking, or following a powerful pitch/throw
Subacute, arising in similar situations but occurring in one of the five layers of the shoulder anatomy
Chronic, developing over time, and usually occurring at or near the tendon (as a result of the tendon rubbing against the overlying bone), and usually associated with an impingement syndrome

Prevention
Long-term overuse/abuse of the shoulder joint is generally thought to limit range of motion and productivity due to daily wear and tear of the muscles, and many public web sites offer preventive advice. (See external links)
The recommendations usually include:

regular shoulder exercises to maintain strength and flexibility
using proper form when lifting or moving heavy weights
resting the shoulder when experiencing pain
application of cold packs and heat pads to a painful, inflamed shoulder
strengthening program to include the back and shoulder girdle muscles as well as the chest, shoulder and upper arm
adequate rest periods in occupations that require repetitive lifting and reaching

Size
According to a study which measured tendon length against the size of the injured rotator cuff, researchers learned that as rotator cuff tendons decrease in length, the average rotator cuff tear severity is proportionally decreased, as well.  This shows that larger individuals are more likely to develop a severe rotator cuff tear if they do not "tighten the shoulder muscles around the joint".

Position
Another study observed 12 different positions of movements and their relative correlation with injuries occurred during those movements.  The evidence shows that putting the arm in a neutral position relieves tension on all ligaments and tendons.

Stretching
One article observed the influence of stretching techniques on preventive methods of shoulder injuries.  Increased velocity of exercise increases injury, but beginning a fast-movement exercise with a slow stretch may cause muscle/tendon attachment to become more resistant to tearing.

Muscle groups
When exercising, exercising the shoulder as a whole and not one or two muscle groups is also found to be imperative.  When the shoulder muscle is exercised in all directions, such as external rotation, flexion, and extension, or vertical abduction, it is less likely to develop a tear of the tendon.

Treatment
A rotator cuff tear can be treated operatively or non-operatively. No benefit is seen from early rather than delayed surgery, and many with partial tears and some with complete tears will respond to nonoperative management. Consequently, an individual may begin with nonsurgical management. However, early surgical treatment may be considered in significant (>1 cm – 1.5 cm) acute tears, or in young individuals with full-thickness tears who have a significant risk for the development of irreparable rotator cuff damage.Rotator-cuff surgery appears to result in similar benefits as nonoperative management. As a conservative approach has less complications and is less expensive it is recommended as initial treatment.

Non-operative treatment
Those with pain but reasonably maintained function are suitable for nonoperative management. This includes medications that provide pain relief such as anti-inflammatory agents, topical pain relievers such as cold packs, and if warranted, subacromial corticosteroid or local anesthetic injection. Topical glyceryl trinitrate appears effective at relieving acute symptoms however, headaches were reported as a side effect. A sling may be offered for short-term comfort, with the understanding that undesirable shoulder stiffness can develop with prolonged immobilization. Early physical therapy may afford pain relief with modalities (e.g. iontophoresis) and help to maintain motion. Ultrasound treatment is not efficacious. As pain decreases, strength deficiencies and biomechanical errors can be corrected.Shock wave therapy has seen widespread use since the 1990s to treat various musculoskeletal disorders including rotator cuff disease, but evidence of its efficacy remains dubious. In a review of 2020, the benefits and harms of shock wave therapy for rotator cuff disease, with or without calcificationcurrently, were investigated. They found low to moderate certainty evidence, that there were very few clinically important benefits of shock wave therapy, and uncertainty regarding its safety.A conservative physical therapy program begins with preliminary rest and restriction from engaging in activities which gave rise to symptoms. Normally, inflammation can usually be controlled within one to two weeks, using a nonsteroidal anti-inflammatory drug and subacromial steroid injections to decrease inflammation, to the point that pain has been significantly decreased to make stretching tolerable. After this short period, rapid stiffening and an increase in pain can result if sufficient stretching has not been implemented.
A gentle, passive range-of-motion program should be started to help prevent stiffness and maintain range of motion during this resting period. Stiffness negatively affects the tendon-bone healing process, a critical part of recovery. Stiffness during rehabilitation is related to worse clinical outcomes, so it is important for the patient to understand the importance of a proactive regimen. Strain induced tendon remodeling, which is part of an accelerated rehabilitation protocol, has been shown to speed up the time to return to daily activities. Exercises, for the anterior, inferior, and posterior shoulder, should be part of this program. Codman exercises (giant, pudding-stirring), to "permit the patient to abduct the arm by gravity, the supraspinatus remains relaxed, and no fulcrum is required" are widely used. The use of NSAIDs, hot and cold packs, and physical therapy modalities, such as ultrasound, phonophoresis, or iontophoresis, can be instituted during this stretching period, if effective.  Corticosteroid injections are recommended two to three months apart with a maximum of three injections. Multiple injections (four or more) have been shown to compromise the results of rotator cuff surgery which result in weakening of the tendon. Kinesio taping was compared to sham taping and other conservative treatment for the approach of the rotator cuff disease and has uncertain effects in terms of self‐reported pain, function, pain on motion and active range of motion.Rockwood coined the term orthotherapy to describe the program which is aimed at creating an exercise regimen that initially gently improves motion, then gradually improves strength in the shoulder girdle. This program involves a home therapy kit which includes elastic bands of six different colors and strengths, a pulley set, and a three-piece, one-meter-long stick. The program is individually customized. Participants are asked to use their exercise program whether at home, work, or traveling.

Surgery
Benefits of surgery are unclear as of 2019. Several instances when surgery may be recommended include:

20 to 30-year-old active person with an acute tear and severe functional deficit from a specific event
30 to 50-year-old person with an acute rotator cuff tear secondary to a specific event
a highly competitive athlete who is primarily involved in overhead or throwing sportsThese individuals more often benefit from operative treatment because they are willing to tolerate the risks of surgery to return to their preoperative level of function, and have higher likelihood of a successful outcome. Those who do not respond to, or are unsatisfied with, conservative treatment can seek a surgical opinion.The three general surgical approaches are arthroscopic, mini open, and open-surgical repair.
In the past, small tears were treated arthroscopically, while larger tears would usually require an open procedure.  Advances in arthroscopy now allow arthroscopic repair of even the largest tears, and arthroscopic techniques are now required to mobilize many retracted tears. The results match open surgical techniques, while permitting a more thorough evaluation of the shoulder at time of surgery, increasing the diagnostic value of the procedure, as other conditions may simultaneously cause shoulder pain. Arthroscopic surgery also allows for shorter recovery time although differences in postoperative pain or pain medication use are not seen between arthroscopic- and open-surgery. A 2019 review found that the evidence does not support decompression surgery in those with more than 3 months of shoulder pain without a history of trauma.Even for full-thickness rotator cuff tears, conservative care (i.e., nonsurgical treatment) outcomes are usually reasonably good.If a significant bone spur is present, any of the approaches may include an acromioplasty, a subacromial decompression, as part of the procedure.  Subacromial decompression, removal of a small portion of the acromion that overlies the rotator cuff, aims to relieve pressure on the rotator cuff in certain conditions and promote healing and recovery.  Although subacromial decompression may be beneficial in the management of partial and full-thickness tear repair, it does not repair the tear itself and arthroscopic decompression has more recently been combined with "mini-open" repair of the rotator cuff, allowing for the repair of the cuff without disruption of the deltoid origin.  The results of decompression alone tend to degrade with time, but the combination of repair and decompression appears to be more enduring. Subacromial decompression may not improve pain, function, or quality of life.Repair of a complete, full-thickness tear involves tissue suture. The method currently in favor is to place an anchor in the bone at the natural attachment site, with resuture of torn tendon to the anchor. If tissue quality is poor, mesh (collagen, Artelon, or other degradable material) may be used to reinforce the repair. Repair can be performed through an open incision, again requiring detachment of a portion of the deltoid, while a mini-open technique approaches the tear through a deltoid-splitting approach. The latter may cause less injury to muscle and produce better results.  Contemporary techniques now use an all arthroscopic approach.
Recovery can take as long as three–six months, with a sling being worn for the first one–six weeks. In the case of partial thickness tears, if surgery is undertaken, tear completion (converting the partial tear to a full tear) and then repair, is associated with better early outcomes than transtendinous repairs (where the intact fibres are preserved) and no difference in failure rates.Biceps tenotomy and tenodesis are often performed concomitantly with rotator cuff repair or as separate procedures, and can also cause shoulder pain. Tenodesis, which may be performed as an arthroscopic or open procedure, generally restores pain free motion it the biceps tendon, or attached portion of the labrum, but can cause pain. Tenotomy is a shorter surgery requiring less rehabilitation, that is more often performed in older patients, though after surgery there can be a cosmetic popeye sign visible in thin arms.In a small minority of cases where extensive arthritis has developed, an option is shoulder joint replacement (arthroplasty). Specifically, this is a reverse shoulder replacement, a more constrained form of shoulder arthroplasty that allows the shoulder to function well even in the presence of large full thickness rotator cuff tears.

Shoulder Replacement
The latest systematic reviews suggests (with low quality evidence) that total shoulder arthroplasty does not provide important benefits over hemiarthroplasty for glenohumeral osteoarthritis and rotator cuff tears. It highlighted the current lack of high-quality evidence and need for randomized controlled trials.

Biologics
The main goal in biological augmentation is to enhance healing. There are a number of potential options. These include injecting an individuals own stem cells, growth factors or platelet rich plasma (PRP) into the repair site, and installing scaffolds as biological or synthetic supports to maintain tissue contour. A 2014 Cochrane review evaluated PRP and found insufficient evidence to make recommendations. Mesenchymal stem cells have no convincing evidence for their use overall, with quality human trials lacking. The greater tuberosity can also be microfractured to create a small blood clot just lateral to the repair site.

Rehabilitation
Rehabilitation after surgery consists of three stages. First, the arm is immobilized so that the muscle can heal. Second, when appropriate, a therapist assists with passive exercises to regain range of motion. Third, the arm is gradually exercised actively, with a goal of regaining and enhancing strength. The empty can and full can exercises are amongst the most effective at isolating and strengthening the supraspinatus.Following arthroscopic rotator-cuff repair surgery, individuals need rehabilitation and physical therapy. Exercise decreases shoulder pain, strengthens the joint, and improves range of motion. Therapists, in conjunction with the surgeon, design exercise regimens specific to the individual and their injury.Traditionally, after injury the shoulder is immobilized for six weeks before rehabilitation. However, the appropriate timing and intensity of therapy are subject to debate. Most surgeons advocate using the sling for at least six weeks, though others advocate early, aggressive rehabilitation. The latter group favors the use of passive motion, which allows an individual to move the shoulder without physical effort. Alternatively, some authorities argue that therapy should be started later and carried out more cautiously. Theoretically, that gives tissues time to heal; though there is conflicting data regarding the benefits of early immobilization. A study of rats suggested that it improved the strength of surgical repairs, while research on rabbits produced contrary evidence. Individuals with a history of rotator cuff injury, particularly those recovering from tears, are prone to reinjury. Rehabbing too soon or too strenuously might increase the risk of retear or failure to heal. However, no research has proven a link between early therapy and the incidence of re-tears.  In some studies, those who received earlier and more aggressive therapy reported reduced shoulder pain, less stiffness and better range of motion. Other research has shown that accelerated rehab results in better shoulder function.
There is consensus amongst orthopaedic surgeons and physical therapists regarding rotator cuff repair rehabilitation protocols. The timing and duration of treatments and exercises are based on biologic and biomedical factors involving the rotator cuff. For approximately two to three weeks following surgery, an individual experiences shoulder pain and swelling; no major therapeutic measures are instituted in this window other than oral pain medicine and ice. Those at risk of failure should usually be more conservative with rehabilitations.That is followed by the "proliferative" and "maturation and remodeling" phases of healing, which ensues for the following six to ten weeks. The effect of active or passive motion during any of the phases is unclear, due to conflicting information and a shortage of clinical evidence.  Gentle physical therapy guided motion is instituted at this phase, only to prevent stiffness of the shoulder; the rotator cuff remains fragile. At three months after surgery, physical therapy intervention changes substantially to focus on scapular mobilization and stretching of the glenohumeral joint.  Once full passive motion is regained (at usually about four to four and a half months after surgery) strengthening exercises are the focus.  The strengthening focuses on the rotator cuff and the upper back/scapular stabilizers.  Typically at about six months after surgery, most have made a majority of their expected gains.The objective in repairing a rotator cuff is to enable an individual to regain full function. Surgeons and therapists analyze outcomes in several ways. Based on examinations, they compile scores on tests; some examples are those created by the University of California at Los Angeles and the American Shoulder and Elbow Surgeons. Other outcome measures include the Constant score; the Simple Shoulder Test; and the Disabilities of the Arm, Shoulder and Hand score. The tests assess range of motion and the degree of shoulder function.Due to the conflicting information about the relative benefits of rehab conducted early or later, an individualized approach is necessary. The timing and nature of therapeutic activities are adjusted according to age and tissue integrity of the repair. Management is more complex in those who have had multiple tears.

Prognosis
While people with rotator cuff tears may not have any noticeable symptoms, studies have shown that, those with age related tears,  over time 40% will have enlargement of the tear over a five-year period. Of those whose tears enlarge, 20% have no symptoms while 80% eventually develop symptoms.Most usually regain function and experience less pain following surgery. For some, however, the joint continues to hurt. Weakness and a limited range of motion also may persist. Those who report such symptoms frequently are diagnosed with failed rotator cuff syndrome. There is no irrefutable evidence that rotator cuff surgery benefits more than non-surgical management and a percentage of individuals never regain full range of motion after surgery.Arthroscopic procedures produce "satisfactory results" more than 90 percent of the time. However, 6-8 percent of patients have "incompetent" rotator cuffs because their repaired tendons either fail to heal or develop additional tears. In some cases, persistent rotator cuff type pain after surgery can be due to disease elsewhere. For example, cervical spine disease and can involve neck pain radiating into the shoulder. Suprascapular neuropathy, shoulder impingement, superior labral anterior-posterior (SLAP) tears and arthritis can all mimic rotator cuff disease and cause persistent pain that does not respond to rotator cuff surgery.

Epidemiology
Rotator cuff tears are among the most common conditions affecting the shoulder.A rotator cuff tear can be caused by the weakening of the rotator cuff tendons. This weakening can be caused by age or how often the rotator cuff is used. Adults over the age of 60 are more susceptible to a rotator cuff tear, with the overall frequency of tears increasing with age. By the age of 50 10% of people with normal shoulders have a rotator cuff tear.In an autopsy study of rotator cuff tears, the incidence of partial tears was 28%, and of complete rupture 30%. Frequently, tears occurred on both sides and occurred more often with females and with increasing age. Other cadaver studies have noted intratendinous tears to be more frequent (7.2%) than bursal-sided (2.4%) or articular-sided tears (3.6%). However, clinically, articular-sided tears are found to be 2 to 3 times more common than bursal-sided tears and among a population of young athletes, articular-sided tears constituted 91% of all partial-thickness tears. Rotator cuff tears may be more common in men between the ages of 50–60, though between 70 and 80 there is minimal difference across genders.In terms of the size of tears, a study compared the ages of patient to the size of tears. It was emphasized the older you are, the more massive of a tear you will have </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 Aortic regurgitation and can you explain it in depth? [/INST] Aortic regurgitation (AR), also known as aortic insufficiency (AI), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. As a consequence, the cardiac muscle is forced to work harder than normal.

Signs and symptoms
Symptoms of aortic regurgitation are similar to those of heart failure and include the following:
Dyspnea on exertion
Orthopnea
Paroxysmal nocturnal dyspnea
Palpitations
Angina pectoris
Cyanosis (in acute cases)

Causes
In terms of the cause of aortic regurgitation, is often due to the aortic root dilation (annuloaortic ectasia), which is idiopathic in over 80% of cases, but otherwise may result from aging, syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behçets disease, reactive arthritis and systemic hypertension. Aortic root dilation is the most common cause of aortic regurgitation in developed countries. Additionally, aortic regurgitation has been linked to the use of some medications, specifically medications containing fenfluramine or dexfenfluramine isomers and dopamine agonists. Other potential causes that affect the valve directly include Marfan syndrome, Ehlers–Danlos syndrome, ankylosing spondylitis, and systemic lupus erythematosus. In acute cases of aortic regurgitation, the main causes are infective endocarditis, aortic dissection or trauma.

Pathophysiology
The mechanism of aortic regurgitation, comprises the pressure in the left ventricle falling below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. This means that some of the blood that was already ejected from the heart is regurgitating back into the heart. The percentage of blood that regurgitates back through the aortic valve due to AR is known as the regurgitant fraction. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure. Since some of the blood that is ejected during systole regurgitates back into the left ventricle during diastole, there is decreased effective forward flow in AR.While diastolic blood pressure is diminished and the pulse pressure widens, systolic blood pressure generally remains normal or can even be slightly elevated, this is because sympathetic nervous system and the renin-angiotensin-aldosterone axis of the kidneys compensate for the decreased cardiac output. Catecholamines will increase the heart rate and increase the strength of ventricular contraction, directly increasing cardiac output. Catecholamines will also cause peripheral vasoconstriction, which causes increased systemic vascular resistance and ensures that organs are adequately perfused. Renin, a proteolytic enzyme, cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II. In the case of chronic aortic  with resultant cardiac remodeling, heart failure will develop, and it is possible to see systolic pressures diminish. Aortic regurgitation causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart.The volume overload, due to elevated pulse pressure and the systemic effects of neuroendocrine hormones causes left ventricular hypertrophy (LVH).  There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the increased left ventricular pressure overload associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.Physiologically, in individuals with a normally functioning aortic valve, the valve is only open when the pressure in the left ventricle is higher than the pressure in the aorta. This allows the blood to be ejected from the left ventricle into the aorta during ventricular systole. The amount of blood that is ejected by the heart is known as the stroke volume. Under normal conditions,  >50% of the blood in a filled left ventricle is ejected into the aorta to be used by the body. After ventricular systole, the pressure in the left ventricle decreases as it relaxes and begins to fill up with blood from the left atrium.  This relaxation of the left ventricle (early ventricular diastole) causes a fall in its pressure. When the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve will close, preventing blood in the aorta from going back into the left ventricle.

Diagnosis
In terms of the diagnosis of aortic regurgitation a common test for the evaluation of the severity is transthoracic echocardiography, which can provide two-dimensional views of the regurgitant jet, allow measurement of velocity, and estimate jet volume. The findings in severe aortic regurgitation, based on the 2012 American College of Cardiology/American Heart Association guidelines include:

Chest X-ray can assist in making the diagnosis, showing left ventricular hypertrophy and dilated aorta. ECG typically indicates left ventricular hypertrophy. Cardiac chamber catheterization assists in assessing the severity of regurgitation and any left ventricular dysfunction.

Physical examination
The physical examination of an individual with aortic regurgitation involves auscultation of the heart to listen for the murmur of aortic regurgitation and the S3 heart sound (S3 gallop correlates with development of LV dysfunction). The murmur of chronic aortic regurgitation is typically described as early diastolic and decrescendo, which is best heard in the third left intercostal space and may radiate along the left sternal border.

If there is increased stroke volume of the left ventricle due to volume overload, an ejection systolic flow murmur may also be present when auscultating the same aortic area. Unless there is concomitant aortic valve stenosis, the murmur should not start with an ejection click. There may also be an Austin Flint murmur, a soft mid-diastolic rumble heard at the apical area; it appears when a regurgitant jet of blood from severe aortic regurgitation partially closes the anterior mitral leaflet. Peripheral physical signs of aortic regurgitation are related to the high pulse pressure and the rapid decrease in blood pressure during diastole due to blood returning to the heart from the aorta through the incompetent aortic valve, although the usefulness of some of the eponymous signs has been questioned: Phonocardiograms detect AI by having electric voltage mimic the sounds the heart makes.Characteristics- indicative of aortic regurgitation are as follow:

Classification
The hemodynamic sequelae of AI are dependent on the rate of onset of AI. Therefore, can be acute or chronic as follows:

Acute aortic regurgitation In acute AR, as may be seen with acute perforation of the aortic valve due to endocarditis, there will be a sudden increase in the volume of blood in the left ventricle. The ventricle is unable to deal with the sudden change in volume. The filling pressure of the left ventricle will increase. This causes pressure in the left atrium to rise, and the individual will develop pulmonary edema. Severe acute aortic regurgitation is considered a medical emergency. There is a high mortality rate if the individual does not undergo immediate surgery for aortic valve replacement.Acute AR usually presents as florid congestive heart failure, and will not have any of the signs associated with chronic AR since the left ventricle had not yet developed the eccentric hypertrophy and dilatation that allow an increased stroke volume, which in turn cause bounding peripheral pulses.  On auscultation, there may be a short diastolic murmur and a soft S1.  S1 is soft because the elevated filling pressures close the mitral valve in diastole.Chronic aortic regurgitation If the individual survives the initial hemodynamic derailment that acute AR presents, the left ventricle adapts by its eccentric hypertrophy and dilatation with a subsequent compensated volume overload. The left ventricular filling pressures will revert to normal and the individual will no longer have overt heart failure. In this compensated phase, the individual may be totally asymptomatic and may have normal exercise tolerance. Eventually (typically after a latency period) the left ventricle will become decompensated, and filling pressures will increase. Some individuals enter this decompensated phase asymptomatically, treatment for AR involves aortic valve replacement prior to this decompensation phase.

Treatment
Aortic regurgitation can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction. Surgical treatment in asymptomatic patients has been recommended if the ejection fraction falls to 50% or below, in the face of progressive and severe left ventricular dilatation, or with symptoms or abnormal response to exercise testing. For both groups of patients, surgery before the development of worsening ejection fraction/LV dilatation is expected to reduce the risk of sudden death, and is associated with lower peri-operative mortality. Also, surgery is optimally performed immediately in acute cases.

Medical treatment
Medical therapy of chronic aortic regurgitation that is stable and asymptomatic involves the use of vasodilators. Trials have shown a short-term benefit in the use of ACE inhibitors or angiotensin II receptor antagonists, nifedipine, and hydralazine in improving left ventricular wall stress, ejection fraction, and mass. The goal in using these pharmacologic agents is to decrease the afterload so that the left ventricle is somewhat spared. The regurgitant fraction may not change significantly, since the gradient between the aortic and left ventricular pressures is usually fairly low at the initiation of treatment. Other rather conservative medical treatments for stable and asymptomatic cases include low sodium diet, diuretics, digoxin, calcium blockers and avoiding very strenuous activity.As of 2007, the American Heart Association no longer recommends antibiotics for endocarditis prophylaxis before certain procedures in patients with aortic regurgitation. Antibiotic prophylaxis to prevent endocarditis before gastrointestinal or genitourinary procedures is no longer recommended for any patient with valvular disease. Cardiac stress test is useful in identifying individuals that may be best suited for surgical intervention. Radionuclide angiography is recommended and useful when the systolic wall stress is calculated and combined to the results.

Surgery
A surgical treatment for AR is aortic valve replacement;  this is currently an open-heart procedure. In the case of severe acute aortic regurgitation, all individuals should undergo surgery, if there are no absolute contraindications (for surgery).  Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with the acute AI. Replacement with an aortic valve homograft should be performed if feasible.

Prognosis
The risk of death in individuals with aortic regurgitation, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year.  Risk increases if the ejection fraction decreases or if the individual develops symptoms.Individuals with  chronic (severe) aortic regurgitation follow a course that once symptoms appear, surgical intervention is needed. AI is fatal in 10 to 20% of individuals who do not undergo surgery for this condition. Left ventricle dysfunction determines to an extent the outlook for severity of aortic regurgitation cases.

References
Further reading
Hamirani, Yasmin S.; Dietl, Charles A.; Voyles, Wyatt; Peralta, Mel; Begay, Darlene; Raizada, Veena (2012-08-28). "Acute Aortic Regurgitation". Circulation. 126 (9): 1121–1126 </s>