<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Amnesia and explain in detail? [/INST] Amnesia is a deficit in memory caused by brain damage or disease, but it can also be caused temporarily by the use of various sedatives and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that was caused. There are two main types of amnesia: retrograde amnesia and anterograde amnesia. Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation. In some cases the memory loss can extend back decades, while in others the person may lose only a few months of memory. Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store. People with anterograde amnesia cannot remember things for long periods of time. These two types are not mutually exclusive; both can occur simultaneously.Case studies also show that amnesia is typically associated with damage to the medial temporal lobe. In addition, specific areas of the hippocampus (the CA1 region) are involved with memory. Research has also shown that when areas of the diencephalon are damaged, amnesia can occur. Recent studies have shown a correlation between deficiency of RbAp48 protein and memory loss. Scientists were able to find that mice with damaged memory have a lower level of RbAp48 protein compared to normal, healthy mice. In people with amnesia, the ability to recall immediate information is still retained, and they may still be able to form new memories. However, a severe reduction in the ability to learn new material and retrieve old information can be observed. People can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge. Individuals with amnesia also retain substantial intellectual, linguistic, and social skill despite profound impairments in the ability to recall specific information encountered in prior learning episodes.The term is from Ancient Greek forgetfulness; from  ἀ- (a-) without, and  μνήσις (mnesis) memory.

Signs and symptoms
Individuals with amnesia can learn new information, particularly if the information is non-declarative knowledge. However, in some situations, people with dense anterograde amnesia do not remember the episodes during which they previously learned or observed the information. Some people with amnesia show abnormal amounts of memory loss, confusion, and difficulty recalling other people or places. People who recover often do not remember having amnesia.

Declarative information
Declarative memory can be broken down into semantic memory and episodic memory, semantic memory being that of facts, episodic memory being that of memory related to events.
While a patient with amnesia might have a loss of declarative memory, this loss might vary in severity as well as the declarative information that it affects, depending on many factors. For example, LSJ was a patient that had retrograde declarative memory loss as the result of bilateral medial temporal lobe damage, but she was still able to remember how to perform some declarative skills. She was able to remember how to read music and the techniques used in art. She had preserved skill-related declarative memory for some things even though she had deficits in other declarative memory tasks. She even scored higher on skill-related declarative memory than the control in watercolor techniques, a technique that she used in her professional career before she acquired amnesia.

Semantic Information
The loss of semantic information in amnesia is most closely related with damage to the medial temporal lobe or to the neocortex.Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. There is evidence that the hippocampus and the medial temporal lobe may help to consolidate semantic memories, but then they are more correlated with the neocortex. While lesions of the hippocampus normally lead to the loss of episodic memory, if there is any effect on semantic memory, it is more varied and usually does not last as long.

Episodic Information
One reason that patients could not form new episodic memories is likely because the CA1 region of the hippocampus has a lesion, and thus the hippocampus could not make connections to the cortex. After an ischemic episode (an interruption of the blood flow to the brain), an MRI of patient R.B. following surgery showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells. In one instance, transient global amnesia was caused by a hippocampal CA1 lesion. While this was a temporary case of amnesia, it still shows the importance of the CA1 region of the hippocampus in memory. Episodic memory loss is most likely to occur when there has been damage to the hippocampus. There is evidence that damage to the medial temporal lobe correlates to a loss of autobiographical episodic memory.

Non-declarative information
Some retrograde and anterograde amnesiacs are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment just as healthy people; therefore, procedural learning can proceed independently of the brain system required for declarative memory. Some patients with amnesia are able to remember skills that they had learned without being able to consciously recall where they had learned that information. For example, they may learn to do a task and then be able to perform the task later without any recollection of learning the task. According to fMRI studies, the acquisition of procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor area, regions which are not normally associated with the formation of declarative memories. This type of dissociation between declarative and procedural memory can also be found in patients with diencephalic amnesia such as Korsakoffs syndrome. Another example demonstrated by some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming. Priming was accomplished in many different experiments of amnesia, and it was found that the patients can be primed; they have no conscious recall of the event, but the response is there. Those patients did well in the word fragment completion task. There is some evidence that non-declarative memory can be held onto in the form of motor skills. This idea was disputed, though, because it is argued that motor skills require both declarative and non-declarative information.

Causes
There are three generalized categories in which amnesia could be acquired by a person. The three categories are head trauma (example: head injuries), traumatic events (example: seeing something devastating to the mind), or physical deficiencies (example: atrophy of the hippocampus). The majority of amnesia and related memory issues derive from the first two categories as these are more common and the third could be considered a subcategory of the first.

Head trauma is a very broad range as it deals with any kind of injury or active action toward the brain which might cause amnesia. Retrograde and anterograde amnesia is more often seen from events like this, an exact example of a cause of the two would be electroconvulsive therapy, which would cause both briefly for the receiving patient.
Traumatic events are more subjective. What is traumatic is dependent on what the person finds to be traumatic. Regardless, a traumatic event is an event where something so distressing occurs that the mind chooses to forget rather than deal with the stress. A common example of amnesia that is caused by traumatic events is dissociative amnesia, which occurs when the person forgets an event that has deeply disturbed them. An example would be a person forgetting a fatal and graphic car accident involving their loved ones.
Physical deficiencies are different from head trauma because physical deficiencies lean more toward passive physical issues. Examples of physical deficiencies include Alzheimers disease, neurological paraneoplastic syndromes such as anti-NMDA receptor encephalitis, and vitamin B12 deficiency.Among specific causes of amnesia are the following:

Electroconvulsive therapy in which seizures are electrically induced in patients for therapeutic effect can have acute effects including both retrograde and anterograde amnesia.
Alcohol can both cause blackouts and have deleterious effects on memory formation.

Diagnosis
Types
Anterograde amnesia is the inability to create new memories due to brain damage, while long-term memories from before the event remain intact. The brain damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke, head trauma, encephalitis, surgery, Wernicke–Korsakoff syndrome, cerebrovascular events, anoxia or other trauma. The two brain regions related with this condition are medial temporal lobe and medial diencephalon. Anterograde amnesia cannot be treated with pharmacological methods due to neuronal loss. However, treatment exists in educating patients to define their daily routines and after several steps they begin to benefit from their procedural memory. Procedural memory can be intact even when other forms of memory is not, although not always the case. Likewise, social and emotional support is critical to improving quality of life for those with anterograde amnesia. Fentanyl use by opioid users has been identified as a potential cause in a cluster of cases that occurred in Boston, MA.
 Retrograde amnesia is inability to recall memories before onset of amnesia. One may be able to encode new memories after the incident. Retrograde is usually caused by head trauma or brain damage to parts of the brain besides the hippocampus. The hippocampus is responsible for encoding new memory. Episodic memory is more likely to be affected than semantic memory. The damage is usually caused by head trauma, cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or chronic alcoholism. People with retrograde amnesia are more likely to remember general knowledge rather than specifics. Recent memories are less likely to be recovered, but older memories will be easier to recall due to strengthening over time. Retrograde amnesia is usually temporary and can be treated by exposing them to memories from the loss. Another type of consolidation (process by which memories become stable in the brain) occurs over much longer periods of time/days, weeks, months and years and likely involves transfer of information from the hippocampus to more permanent storage site in the cortex. The operation of this longer-term consolidation process is seen in the retrograde amnesia of patients with hippocampal damage who can recall memories from childhood relatively normally, but are impaired when recalling experiences that occurred just a few years prior to the time they became amnesic. (Kirwan et al.,2008)In the case of LSJ, her case shows that retrograde amnesia can affect many different parts of knowledge. LSJ was not able to remember things from her child or adult life. She was not able to remember things that most people pick up in everyday life such as logos or the names of common songs.
Post-traumatic amnesia is generally due to a head injury (example: a fall, a knock on the head). Traumatic amnesia is often transient, but may be permanent or either anterograde, retrograde, or mixed type. The extent of the period covered by the amnesia is related to the degree of injury and may give an indication of the prognosis for recovery of other functions. Mild trauma, such as a car accident that results in no more than mild whiplash, might cause the occupant of a car to have no memory of the moments just before the accident due to a brief interruption in the short/long-term memory transfer mechanism. The patient may also lose knowledge of who people are. Having longer periods of amnesia or consciousness after an injury may be an indication that recovery from remaining concussion symptoms will take much longer.
Dissociative amnesia results from a psychological cause as opposed to direct damage to the brain caused by head injury, physical trauma or disease, which is known as organic amnesia. Individuals with organic amnesia have difficulty with emotion expression as well as undermining the seriousness of their condition. The damage to the memory is permanent. Dissociative amnesia can include:
Repressed memory is the inability to recall information, usually about stressful or traumatic events in persons lives, such as a violent attack or disaster. The memory is stored in long-term memory, but access to it is impaired because of psychological defense mechanisms. Persons retain the capacity to learn new information and there may be some later partial or complete recovery of memory. Formerly known as "Psychogenic Amnesia".
Dissociative fugue (formerly psychogenic fugue) is also known as fugue state. It is caused by psychological trauma, is usually temporary and unresolved, and therefore, may return. It must exist outside the influence of pre-existing medical conditions, such as a lobotomy, and immediate influence of any mind-altering substances, such as alcohol or drugs. An individual with dissociative fugue disorder either completely forgets or is confused about their identity, and may even assume a new one. They can travel hundreds miles from their home or work; they can also engage in other uncharacteristic, and occasionally unsafe, behavior. For example, two men in a study of five individuals with dissociative fugue had engaged in criminal activity while in their fugue state, having had no criminal record before the episodes. While popular in fiction, this type of amnesia is extremely rare.
Posthypnotic amnesia occurs when events during hypnosis are forgotten, or where memories are unable to be recalled. The failure to remember those events is induced by suggestions made during the hypnosis. Some characteristics of posthypnotic amnesia include inability to remember specific events while under hypnotic influence, reversibility, and having no relation between the implicit and explicit memory. Research has shown that there could be selectivity with amnesia when posthypnotic amnesia occurs.
Lacunar amnesia  is the loss of memory about one specific event. It is a type of amnesia that leaves a lacuna (a gap) in the record of memory in the cortex region of the brain. The cause of this type of amnesia is the result of brain damage to the limbic system which control our memories and emotions.
Childhood amnesia (also known as infantile amnesia) is the common inability to remember events from ones own childhood. Sigmund Freud notoriously attributed this to sexual repression, while modern scientific approaches generally attribute it to aspects of brain development or developmental psychology, including language development, which may be why people do not easily remember pre-language events. Some research states that most adults cannot remember memories as early as two or three years old. Research suggests there are cultural influences that affect memories that are recalled. Researchers have found that implicit memories cannot be recalled or described. Remembering how to play the piano is a common example of implicit memory, as are walking, speaking, and other everyday activities that would be difficult to focus on if they had to be relearned every time one got up in the morning. Explicit memories, on the other hand, can be recalled and described in words. Remembering the first time meeting a teacher is an example of an explicit memory.
Transient global amnesia is a well-described medical and clinical phenomenon. This form of amnesia is distinct in that abnormalities in the hippocampus can sometimes be visualized using a special form of magnetic resonance imaging of the brain known as diffusion-weighted imaging (DWI). Symptoms typically last for less than a day and there is often no clear precipitating factor or any other neurological deficits. The cause of this syndrome is not clear. The hypothesis of the syndrome includes transient reduced blood flow, possible seizure or an atypical type of a migraine. Patients are typically amnestic of events more than a few minutes in the past, though immediate recall is usually preserved.
Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge. When individuals are unable to remember, false memories can occur and cause great confusion.
Korsakoffs syndrome can result from long-term alcoholism or malnutrition. It is caused by brain damage due to a vitamin B1 deficiency and will be progressive if alcohol intake and nutrition pattern are not modified. Other neurological problems are likely to be present in combination with this type of Amnesia, such as problems with the medial temporal lobe and frontal lobe dysfunction. Korsakoffs syndrome is also known to be connected with confabulation. The persons short-term memory may appear to be normal, but the person may have a difficult time attempting to recall a past story, or with unrelated words, as well as complicated patterns. Korsakoffs syndrome is unique because it involves both anterograde and retrograde amnesia.
Drug-induced amnesia is intentionally caused by injection of an amnestic drug to help a patient forget surgery or medical procedures, particularly those not performed under full anesthesia, or likely to be particularly traumatic. Such drugs are also referred to as "premedicants". Most commonly, a 2-halogenated benzodiazepine such as midazolam or flunitrazepam is the drug of choice, although other strongly amnestic drugs such as propofol or scopolamine may also be used for this application. Memories of the short time-frame in which the procedure was performed are permanently lost or at least substantially reduced, but once the drug wears off, memory is no longer affected.
Situation-specific amnesia can arise in a variety of circumstances (for example, committing an offence, child sexual abuse) resulting in PTSD. It has been claimed that it involves a narrowing of consciousness with attention focused on central perceptual details and/or that the emotional or traumatic events are processed differently from ordinary memories.
Transient epileptic amnesia is a rare and unrecognized form of temporal lobe epilepsy, which is typically an episodic isolated memory loss. It has been recognized as a treatment-responsive syndrome congenial to anti-epileptic drugs.
Semantic amnesia affects semantic memory and primarily expresses itself in the form of problems with language use and acquisition. Semantic amnesia can lead to dementia.
Pseudodementia (otherwise known as depression-related cognitive dysfunction) is a condition where mental cognition can be temporarily decreased. The term pseudodementia is applied to the range of functional psychiatric conditions such as depression and schizophrenia, that may mimic organic dementia, but are essentially reversible on treatment. Pseudodementia typically involves three cognitive components: memory issues, deficits in executive functioning, and deficits in speech and language. Specific cognitive symptoms might include trouble recalling words or remembering things in general, decreased attentional control and concentration, difficulty completing tasks or making decisions, decreased speed and fluency of speech, and impaired processing speed. People with pseudodementia are typically very distressed about the cognitive impairment they experience. With in this condition, there are two specific treatments that have been found to be effective for the treatment of depression, and these treatments may also be beneficial in the treatment of pseudodementia. Cognitive behavioral therapy (CBT) involves exploring and changing thought patterns and behaviors in order to improve ones mood. Interpersonal therapy focuses on the exploration of an individuals relationships and identifying any ways in which they may be contributing to feelings of depression.

Treatment
Many forms of amnesia fix themselves without being treated. However, there are a few ways to cope with memory loss if treatment is needed. Since there are a variety of causes that form different amnesia, it is important to note that there are different methods that response better with the certain type of amnesia. Emotional support and love as well as medication and psychological therapy have been proven effective.One technique for amnesia treatment is cognitive or occupational therapy. In therapy, amnesiacs will develop the memory skills they have and try to regain some they have lost by finding which techniques help retrieve memories or create new retrieval paths. This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.Another coping mechanism is taking advantage of technological assistance, such as a personal digital device to keep track of day-to-day tasks. Reminders can be set up for appointments when to take medications, birthdays and other important events. Many pictures can also be stored to help amnesiacs remember names of friends, family, and co-workers. Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.While there are no medications available to treat amnesia, underlying medical conditions can be treated to improve memory. Such conditions include but are not limited to low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder and blood clots in the brain. Wernicke–Korsakoff syndrome involves a lack of thiamin and replacing this vitamin by consuming thiamin-rich foods such as whole-grain cereals, legumes (beans and lentils), nuts, lean pork, and yeast. Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.Although improvements occur when patients receive certain treatments, there is still no actual cure remedy for amnesia so far. To what extent the patient recovers and how long the amnesia will continue depends on the type and severity of the lesion.

History
French psychologist Theodule-Armand Ribot was among the first scientists to study amnesia. He proposed Ribots Law which states that there is a time gradient in retrograde amnesia. The law follows a logical progression of memory loss due to disease. First, a patient loses the recent memories, then personal memories, and finally intellectual memories. He implied that the most recent memories were lost first.Case studies have played a large role in the discovery of amnesia and the parts of the brain that were affected. The studies gave important insight into how amnesia affects the brain. The studies also gave scientists the resources into improving their knowledge about amnesia and insight into a cure or prevention. There are several extremely important case studies: Henry Molaison, R.B, and G.D.

Henry Molaison
Henry Molaison, formerly known as H.M., changed the way people thought of memory. The case was first reported in a paper by William Beecher Scoville and Brenda Milner in 1957. He was a patient who had  severe epilepsy attributed to a bicycle accident at the age of nine. Physicians were unable to control his seizures with drugs, so the neurosurgeon Scoville tried a new approach involving brain surgery. He removed his medial temporal lobe bilaterally by doing a temporal lobectomy. His epilepsy did improve, but Molaison lost the ability to form new long-term memories (anterograde amnesia). He exhibited normal short-term memory ability. If he was given a list of words, he would forget them in about a minutes time. In fact, he would forget that he had even been given a list in the first place. However, H.M.s working and short-term memory seemed to be intact. He had a normal digit span and could hold a conversation that did not require him to recall past parts of the conversation. Once Molaison stopped thinking about the lists he was unable to recall them again from long-term memory. This gave researchers evidence that short-term and long-term memory are in fact two different processes. Even though he forgot about the lists, he was still able to learn things through his implicit memory. The psychologists would ask him to draw something on a piece of paper, but to look at the paper using a mirror. Though he could never remember ever doing that task, he would improve after doing it over and over again. This showed the psychologists that he was learning and remembering things unconsciously. In some studies it was found that H.M.s perceptual learning was intact and that his other cognitive skills were working appropriately. It was also found that some people with declarative information amnesia are able to be primed.Studies were completed consistently throughout Molaisons lifetime to discover more about amnesia. Researchers did a 14-year follow-up study on Molaison. They studied him for a period of two weeks to learn more about his amnesia. After 14 years, Molaison still could not recall things that had happened since his surgery. However, he could still remember things that had happened prior to the operation. Researchers also found that, when asked, Molaison could answer questions about national or international events, but he could not remember his own personal memories. After his death Molaison donated his brain to science, where they were able to discover the areas of the brain that had the lesions which caused his amnesia, particularly the medial temporal lobe. This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works. H.M.s case showed us that memory processes are consolidated into different parts of the brain and that short-term and working memory are not usually impaired in cases of amnesia.

Clive Wearing
Another famous historical case of amnesia was that of Clive Wearing. Clive Wearing was a conductor and musician who contracted herpes simplex virus. This virus affected the hippocampal regions of the brain. Because of this damage, Wearing was unable to remember information for more than a few moments. Wearings non-declarative memory was still functioning but his declarative memory was impaired. To him, he felt that he had just come to consciousness for the first time every time he was unable to hold on to information. This case also can be used as evidence that there are different memory systems for declarative and non-declarative memory. This case was more evidence that the hippocampus is an important part of the brain in remembering past events and that declarative and non-declarative memories have different processes in different parts of the brain.

Patient R.B.
Patient R.B. was a normally functioning man until the age of 52. At age 50, he had been diagnosed with angina and had surgery for heart problems on two occasions. After an ischemic episode (reduction of blood to the brain) that was caused from a heart bypass surgery, R.B. demonstrated a loss of anterograde memory, but almost no loss of retrograde memory, with the exception of a couple of years before his surgery, and presented no sign of any other cognitive impairment. It wasnt until after his death that researchers had the chance to examine his brain, when they found his lesions were restricted to the CA1 portion of the hippocampus. This case study led to important research involving the role of the hippocampus and the function of memory.

Patient G.D.
Patient G.D. was a white male born in 1940 who served in the Navy. He was diagnosed with chronic kidney failure and received hemodialysis treatment for the rest of his life. In 1983, he went to the hospital for elective parathyroidectomy. He also had a left thyroid lobectomy because of the severe loss of blood in his left lobe. He began having cardiac problems as a result of the surgery and became very agitated. Even five days after being released from the hospital he was unable to remember what had happened to him </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Ovarian torsion and explain in detail? [/INST] Ovarian torsion (OT) or adnexal torsion is an abnormal condition where an ovary twists on its attachment to other structures, such that blood flow is decreased. Symptoms typically include pelvic pain on one side. While classically the pain is sudden in onset, this is not always the case. Other symptoms may include nausea. Complications may include infection, bleeding, or infertility.Risk factors include ovarian cysts, ovarian enlargement, ovarian tumors, pregnancy, fertility treatment, and prior tubal ligation. The diagnosis may be supported by an ultrasound done via the vagina or CT scan, but these do not completely rule out the diagnosis. Surgery is the most accurate method of diagnosis.Treatment is by surgery to either untwist and fix the ovary in place or to remove it. The ovary will often recover, even if the condition has been present for some time. In those who have had a prior ovarian torsion, there is a 10% chance the other will also be affected. The diagnosis is relatively rare, affecting about 6 per 100,000 women per year. While it most commonly occurs in those of reproductive age, it can occur at any age.

Signs and symptoms
Patients with ovarian torsion often present with sudden onset of sharp and usually unilateral lower abdominal pain, in 70% of cases accompanied by nausea and vomiting.

Pathophysiology
The development of an ovarian mass is related to the development of torsion. In the reproductive years, regular growth of large corpus luteal cysts are a risk factor for rotation. The mass effect of ovarian tumors is also a common cause of torsion. Torsion of the ovary usually occurs with torsion of the fallopian tube as well on their shared vascular pedicle around the broad ligament, although in rare cases the ovary rotates around the mesovarium or the fallopian tube rotates around the mesosalpinx. In 80%, torsion happens unilaterally, with slight predominance on the right. In ovarian torsion, the ovary rotates around both the infundibulopelvic ligament (ie, suspensory ligament) and the utero-ovarian ligament (i.e. ovarian ligament), disrupting blood flow to the ovary.

Diagnosis
Ovarian torsion is difficult to diagnose accurately, and operation is often performed before certain diagnosis is made. A study at an  obstetrics and gynaecology department found that preoperative diagnosis of ovarian torsion was confirmed in only 46% of people.

Ultrasound
Gynecologic ultrasonography is the imaging modality of choice. Use of doppler ultrasound  in the diagnosis has been suggested. However, doppler flow is not always absent in torsion – the definitive diagnosis is often made in the operating room.Lack of ovarian blood flow on doppler sonography seems to be a good predictor of ovarian torsion. Women with pathologically low flow are more likely to have torsion. The sensitivity and specificity of abnormal ovarian flow are 44% and 92%, respectively, with a positive and negative predictive value of 78% and 71%, respectively. Specific flow features on Doppler sonography include:
Little or no intra-ovarian venous flow </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hyperchloremia and explain in detail? [/INST] Hyperchloremia is an electrolyte disturbance in which there is an elevated level of chloride ions in the blood. The normal serum range for chloride is 96 to 106 mEq/L, therefore chloride levels at or above 110 mEq/L usually indicate kidney dysfunction as it is a regulator of chloride concentration. As of now there are no specific symptoms of hyperchloremia; however, it can be influenced by multiple abnormalities that cause a loss of electrolyte-free fluid,  loss of hypotonic fluid, or increased administration of sodium chloride. These abnormalities are caused by diarrhea, vomiting, increased sodium chloride intake, renal dysfunction, diuretic use, and diabetes. Hyperchloremia should not be mistaken for hyperchloremic metabolic acidosis as hyperchloremic metabolic acidosis is characterized by two major changes: a decrease in blood pH and bicarbonate levels, as well as an increase in blood chloride levels. Instead those with hyperchloremic metabolic acidosis are usually predisposed to hyperchloremia.
Hyperchloremia prevalence in hospital settings has been researched in the medical field since one of the major sources of treatment at hospitals is administering saline solution.  Previously, animal models with elevated chloride have displayed more inflammation markers, changes in blood pressure, increased renal vasoconstriction, and less renal blood flow as well at glomerulus filtration, all of which are prompting researchers to investigate if these changes or others may exist in patients. Some studies have reported a possible relationship between increased chloride levels and death or acute kidney injury in severely ill patients that may frequent the hospital or have prolonged visits. There are other studies that have found no relationship.

Symptoms
Hyperchloremia does not have many noticeable symptoms and can only be confirmed with testing, yet, the causes of hyperchloremia do have symptoms.
Symptoms of the above stated abnormalities may include:
Dehydration - due to diarrhea, vomiting, sweating
Hypertension - due to increased sodium chloride intake
Cardiovascular dysfunction - due to increased sodium chloride intake
Edema - due to influx in sodium in the body
Weakness - due to loss of fluids
Thirst - due to loss of fluids
Kussmaul breathing - due to high ion concentrations, loss of fluids, or kidney failure
High blood sugar - due to diabetes
Hyperchloremic metabolic acidosis - due to severe diarrhea and/or kidney failure
Respiratory alkalosis - due to renal dysfunction

Causes
There are many scenarios which may results in hyperchloremia. The first instance is when there is a loss of electrolyte-free fluid. This simply means that the body is losing increased amounts of fluids that do not contain electrolytes, like chloride, resulting in high concentration of these ions in the body. This loss of fluids can be due to sweating (due to exercise or fever), skin burns, lack of adequate water intake, hyper-metabolic state, and diabetes insipidus. Losing fluids can lead to feelings of dehydration and dry mucous membrane.The second scenario that may lead to hyperchloremia is known as loss of hypotonic fluid which can be a direct result of loss of electrolyte fluid. Normally, water in the body is moving from an area of low ion concentration to an area of high ion concentration. In this case, the water is being excreted in the urine, therefore, less water is available to dilute these areas of high ion concentration. This can be due to diuretic use, diarrhea, vomiting, burns, kidney disease, kidney failure, and renal tubular acidosis . This may also lead to feeling of dehydration.The third scenarios that may lead to hyperchloremia is an increase in sodium chloride intake. This can be due to dietary intake or intravenous fluid administration in hospital settings. This can lead to the body experiencing hypertension, edema, and cardiovascular dysfunction.

Mechanism
The nephrons in the kidney are responsible for regulating the level of chloride in the blood. The general mechanism is that as filtrate fluid passes through the nephrons varying concentrations of ions will be secreted into the interstitial fluid or absorbed into the lumen. All along the nephrons are blood capillaries waiting to reabsorb ions from the interstitial fluid to circulate in the body. The amount of chloride to be released in the urine is due to the receptors lining the nephrons and the glomerulus filtration.
Normally, chloride reabsorption begins in the proximal tubule and nearly 60% of chloride is filtered here. In a person with hyperchloremia, the absorption of chloride into the interstitial fluid and subsequently into the blood capillaries is increased. This means the concentration of chloride in the filtrate is decreased, therefore, a decreased amount of chloride is being excreted as waste in the urine. In the proximal tubule chloride reabsorption occurs in two parts. In the 1st phase, organic solutes (such as phosphates, amino acids, glucose and anions), sodium ions, and hydronium ions are reabsorbed from the filtrate fluid into the interstitial fluid.  This is an important step because this creates the concentration gradient in which chloride concentration in the lumen will increase in comparison to the chloride concentration in the interstitial fluid. In phase 2, chloride will diffuse along the concentration gradient, which means chloride ions will travel from areas of high concentration to areas of low concentration.One suggested mechanism leading to hyperchloremia, there is a decrease in chloride transporter proteins along the nephron. These proteins may include sodium-potassium-2 chloride co-transporter, chloride anion exchangers, and chloride channels.  Another suggested mechanism is a depletion in concentration gradient as a result of the reduced activity in these transporters.  Such concentration gradient depletion would allow for the passive diffusion of chloride in and out the tubule.

Diagnosis
Elevated levels of chloride in the blood can be tested simply by requesting a serum chloride test. A doctor would request this test if there are signs their patient is experiencing an imbalance in acid-base levels for a prolonged period of time. For the test to occur a healthcare provider must draw a sample of blood from the patient.  The sample will then be sent to a laboratory and results will be provided to the patients physician. As mentioned earlier a normal serum chloride range is from 96 to 106 mEq/L, and hyperchloremic patients will have levels above this range.

Treatment
As with most types of electrolyte imbalance, the treatment of high blood chloride levels is based on correcting the underlying cause.

If the patient is dehydrated, therapy consists of establishing and maintaining adequate hydration such as drinking 2-3 quarts of water daily. Also, to alleviate symptoms of dehydration like diarrhea or vomiting, it is suggested to take medication.
If the condition is caused or exacerbated by medications or treatments, these may be altered or discontinued, if deemed prudent.
If there is underlying kidney disease (which is likely if there are other electrolyte disturbances), then the patient will be referred to a nephrologist for further care.
If there is an underlying dysfunction of the endocrine or hormone system, the patient will likely be referred to an endocrinologist for further assessment.
If the electrolyte imbalance is due to influx of sodium chloride in the body, then it has been suggested to make dietary changes or reduce the rate of administering intravenous fluids.

Recent research
In patients with sepsis or septic shock they are more susceptible to experience acute kidney injury (AKI) and the factors that may contribute to AKI are still being investigated. In a study conducted by Suetrong et al., (2016) using patients admitted to St. Paul Hospital in Vancouver with sepsis or septic shock had their body concentration of chloride checked over the course of 48 hours to determine if there is a relation between hyperchloremia and AKI. This is an important relationship to study because many times a form of therapy to treat sepsis and septic shock is to administer saline solution, which is a solution containing sodium chloride. Saline has a much higher concentration of chloride than blood. In this study they defined hyperchloremia as concentration of chloride greater than 110 mmol/L. This research demonstrated that hyperchloremia will influence a patient developing AKI </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hypoventilation and explain in detail? [/INST] Hypoventilation (also known as respiratory depression) occurs when ventilation is inadequate (hypo meaning "below") to perform needed respiratory gas exchange. By definition it causes an increased concentration of carbon dioxide (hypercapnia) and respiratory acidosis. Hypoventilation is not synonymous with respiratory arrest, in which breathing ceases entirely and death occurs within minutes due to hypoxia and leads rapidly into complete anoxia, although both are medical emergencies. Hypoventilation can be considered a precursor to hypoxia and its lethality is attributed to hypoxia with carbon dioxide toxicity.

Causes
Hypoventilation may be caused by:

A medical condition such as stroke affecting the brainstem
Voluntary breath-holding or underbreathing, for example, hypoventilation training or the Buteyko method.
Medication or drugs, typically when taken in accidental or intentional overdose. Opioids and benzodiazepines in particular are known to cause respiratory depression </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Henoch–Schönlein purpura and explain in detail? [/INST] Henoch–Schönlein purpura (HSP), also known as IgA vasculitis, is a disease of the skin, mucous membranes, and sometimes other organs that most commonly affects children. In the skin, the disease causes palpable purpura (small, raised areas of bleeding underneath the skin), often with joint pain and abdominal pain. With kidney involvement, there may be a loss of small amounts of blood and protein in the urine (hematuria and proteinuria), but this usually goes unnoticed; in a small proportion of cases, the kidney involvement proceeds to chronic kidney disease. HSP is often preceded by an infection, such as a throat infection.
HSP is a systemic vasculitis (inflammation of blood vessels) and is characterized by deposition of immune complexes containing the antibody immunoglobulin A (IgA); the exact cause for this phenomenon is unknown. In children, it usually resolves within several weeks and requires no treatment apart from symptom control but may relapse in a third of cases and cause irreversible kidney damage in about one in a hundred cases. In adults, the prognosis is different from in children. The average duration of cutaneous lesions is 27.9 months. For many, it tends to be relapsing–remitting over a long period of time, rather than self-limiting and there tend to be more complications.

Signs and symptoms
Purpura, arthritis, and abdominal pain are known as the "classic triad" of Henoch–Schönlein purpura. Purpura occur in all cases, joint pains and arthritis in 80%, and abdominal pain in 62%. Some include gastrointestinal hemorrhage as a fourth criterion; this occurs in 33% of cases, sometimes, but not necessarily always, due to intussusception. The purpura typically appear on the legs and buttocks, but may also be seen on the arms, face and trunk. The abdominal pain is colicky in character, and may be accompanied by nausea, vomiting, constipation or diarrhea. There may be blood or mucus in the stools. The joints involved tend to be the ankles, knees, and elbows, but arthritis in the hands and feet is possible; the arthritis is nonerosive and hence causes no permanent deformity. Forty percent have evidence of kidney involvement, mainly in the form of hematuria (blood in the urine), but only a quarter will have this in sufficient quantities to be noticeable without laboratory tests. Problems in other organs, such as the central nervous system (brain and spinal cord) and lungs may occur, but is much less common than in the skin, bowel and kidneys.Of the 40% of patients who develop kidney involvement, almost all have evidence (visible or on urinalysis) of blood in the urine. More than half also have proteinuria (protein in the urine), which in one eighth is severe enough to cause nephrotic syndrome (generalised swelling due to low protein content of the blood). While abnormalities on urinalysis may continue for a long time, only 1% of all HSP patients develop chronic kidney disease. Hypertension (high blood pressure) may occur. Protein loss and high blood pressure, as well as the features on biopsy of the kidney if performed, may predict progression to advanced kidney disease. Adults are more likely than children to develop advanced kidney disease.

Pathophysiology
Henoch–Schönlein purpura is a small-vessel vasculitis in which complexes of immunoglobulin A (IgA) and complement component 3 (C3) are deposited on arterioles, capillaries, and venules (hence it is a type III hypersensitivity reaction). The activation of the alternative complement pathway results in the deposition of IgA aggregates or IgA complexes in target organs (with deposition of C3). This leads to the production of inflammatory mediators, including vascular prostaglandins like prostacyclin, which may play a key role in the development of IgAV and its organ-specific clinical manifestations. As with IgA nephropathy, serum levels of IgA are high in HSP and there are identical findings on renal biopsy; however, IgA nephropathy has a predilection for young adults while HSP is more predominant among children. Further, IgA nephropathy typically only affects the kidneys while HSP is a systemic disease. HSP involves the skin and connective tissues, scrotum, joints, gastrointestinal tract and kidneys. The genetic basis remains unclear except for involvement of the human leukocyte antigen region of the genome.
It is hypothesized to involve autoimmunity triggered by infections. Streptococcus strains and Parainfluenza virus are the most commonly associated pathogens, and in children Human Parvovirus B19 is a frequent viral trigger

Diagnosis
The diagnosis is based on the combination of the symptoms, as very few other diseases cause the same symptoms together. Blood tests may show elevated creatinine and urea levels (in kidney involvement), raised IgA levels (in about 50%), and raised C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) results; none are specific for Henoch–Schönlein purpura. The platelet count may be raised, and distinguishes it from diseases where low platelets are the cause of the purpura, such as idiopathic thrombocytopenic purpura and thrombotic thrombocytopenic purpura.If there is doubt about the cause of the skin lesions, a biopsy of the skin may be performed to distinguish the purpura from other diseases that cause it, such as vasculitis due to cryoglobulinemia; on microscopy, the appearances are of a hypersensitivity vasculitis, and immunofluorescence demonstrates IgA and C3 (a protein of the complement system) in the blood vessel wall. However, overall serum complement levels are normal.
On the basis of symptoms, it is possible to distinguish HSP from hypersensitivity vasculitis (HV). In a series comparing 85 HSP patients with 93 HV patients, five symptoms were found to be indicative of HSP: palpable purpura, abdominal angina, digestive tract hemorrhage (not due to intussussception), hematuria and age less than 20. The presence of three or more of these indicators has an 87% sensitivity for predicting HSP.Biopsy of the kidney may be performed both to establish the diagnosis or to assess the severity of already suspected kidney disease. The main findings on kidney biopsy are increased cells and Ig deposition in the mesangium (part of the glomerulus, where blood is filtered), white blood cells, and the development of crescents. The changes are indistinguishable from those observed in IgA nephropathy.

HSP can develop after infections with streptococci (β-haemolytic, Lancefield group A), hepatitis B, herpes simplex virus, parvovirus B19, Coxsackievirus, adenovirus, Helicobacter pylori, measles, mumps, rubella, Mycoplasma and numerous others. Drugs linked to HSP, usually as an idiosyncratic reaction, include the antibiotics vancomycin and cefuroxime, ACE inhibitors enalapril and captopril, anti-inflammatory agent diclofenac, as well as ranitidine and streptokinase. Several diseases have been reported to be associated with HSP, often without a causative link. Only in about 35% of cases can HSP be traced to any of these causes.The exact cause of HSP is unknown, but most of its features are due to the deposition of abnormal antibodies in the wall of blood vessels, leading to vasculitis. These antibodies are of the subclass IgA1 in polymers; it is uncertain whether the main cause is overproduction (in the digestive tract or the bone marrow) or decreased removal of abnormal IgA from the circulation. It is suspected that abnormalities in the IgA1 molecule may provide an explanation for its abnormal behaviour in both HSP and the related condition IgA nephropathy. One of the characteristics of IgA1 (and IgD) is the presence of an 18 amino acid-long "hinge region" between complement-fixating regions 1 and 2. Of the amino acids, half is proline, while the others are mainly serine and threonine. The majority of the serines and the threonines have elaborate sugar chains, connected through oxygen atoms (O-glycosylation). This process is thought to stabilise the IgA molecule and make it less prone to proteolysis. The first sugar is always N-acetyl-galactosamine (GalNAc), followed by other galactoses and sialic acid. In HSP and IgAN, these sugar chains appear to be deficient. The exact reason for these abnormalities is not known.

Classification
Multiple standards exist for defining Henoch–Schönlein purpura, including the 1990 American College of Rheumatology (ACR) classification and the 1994 Chapel Hill Consensus Conference (CHCC). Some have reported the ACR criteria to be more sensitive than those of the CHCC.More recent classifications, the 2006 European League Against Rheumatism (EULAR) and Pediatric Rheumatology Society (PReS) classification, include palpable purpura as a mandatory criterion, together with at least one of the following findings: diffuse abdominal pain, predominant IgA deposition (confirmed on skin biopsy), acute arthritis in any joint, and renal involvement (as evidenced by the presence of blood and/or protein in the urine).

Differential diagnosis
Henoch–Schönlein purpura may present with an atypical manifestation, which can be confused with papular urticaria, systemic lupus erythematosus, meningococcemia, dermatitis herpetiformis, and  acute hemorrhagic edema of infancy.

Treatment
As of 2017, the optimal way to treat Henoch–Schönlein purpura remains controversial. Analgesics may be needed for the abdominal and joint pains. Wound care is warranted if the skin death and ulcerations occur. It is uncertain as to whether HSP needs treatment beyond controlling the symptoms. Most people do not receive therapy because of the high spontaneous recovery rate. Experts disagree on whether to routinely use corticosteroids as treatment for HSP. However, if they are given early in the disease episode, the duration of symptoms may be shortened, and abdominal pain can improve significantly. Moreover, the chance of severe kidney problems may be reduced. A systematic review did not find any evidence that steroid treatment (prednisone) is effective at decreasing the likelihood of developing long-term kidney disease.Evidence of worsening kidney damage would normally prompt a kidney biopsy. Treatment may be indicated on the basis of the appearance of the biopsy sample; various treatments may be used, ranging from steroids by mouth to a combination of intravenous methylprednisolone (steroid), cyclophosphamide and dipyridamole followed by prednisone. Other regimens include steroids/azathioprine, and steroids/cyclophosphamide (with or without heparin and warfarin). Intravenous immunoglobulin (IVIG) is occasionally used.There is no good evidence that treating children who have HSP with antiplatelet agent prevents persistent kidney disease. There is also no evidence that treating children or adults with cyclophosphamide prevents severe kidney disease. Heparin treatment is not justified.

Prognosis
Overall prognosis is good in most patients, with one study showing recovery occurring in 94% and 89% of children and adults, respectively (some having needed treatment). In children under ten, the condition recurs in about a third of all cases, usually within the four months of the initial attack. Recurrence is more common in older children and adults.

Kidney involvement
In adults, kidney involvement progresses to end-stage kidney disease (ESKD) more often than in children. In a UK series of 37 patients, 10 (27%) developed advanced kidney disease </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Bacterial vaginosis and explain in detail? [/INST] Bacterial vaginosis (BV) is a disease of the vagina caused by excessive growth of bacteria. Common symptoms include increased vaginal discharge that often smells like fish. The discharge is usually white or gray in color. Burning with urination may occur. Itching is uncommon. Occasionally, there may be no symptoms. Having BV approximately doubles the risk of infection by a number of sexually transmitted infections, including HIV/AIDS. It also increases the risk of early delivery among pregnant women.BV is caused by an imbalance of the naturally occurring bacteria in the vagina. There is a change in the most common type of bacteria and a hundred to thousand fold increase in total numbers of bacteria present. Typically, bacteria other than Lactobacilli become more common. Risk factors include douching, new or multiple sex partners, antibiotics, and using an intrauterine device, among others. However, it is not considered a sexually transmitted infection and, unlike gonorrhoea and chlamydia, sexual partners are not treated. Diagnosis is suspected based on the symptoms, and may be verified by testing the vaginal discharge and finding a higher than normal vaginal pH, and large numbers of bacteria. BV is often confused with a vaginal yeast infection or infection with Trichomonas.Usually treatment is with an antibiotic, such as clindamycin or metronidazole. These medications may also be used in the second or third trimesters of pregnancy. However, the condition often recurs following treatment. Probiotics may help prevent re-occurrence. It is unclear if the use of probiotics or antibiotics affects pregnancy outcomes.BV is the most common vaginal infection in women of reproductive age. The percentage of women affected at any given time varies between 5% and 70%. BV is most common in parts of Africa and least common in Asia and Europe. In the United States about 30% of women between the ages of 14 and 49 are affected. Rates vary considerably between ethnic groups within a country. While BV-like symptoms have been described for much of recorded history, the first clearly documented case occurred in 1894.

Signs and symptoms
Although about 50% of women with BV are asymptomatic, common symptoms include increased vaginal discharge that usually smells like fish. The discharge is often white or gray in color. There may be burning with urination. Occasionally, there may be no symptoms.The discharge coats the walls of the vagina, and is usually without significant irritation, pain, or erythema (redness), although mild itching can sometimes occur. By contrast, the normal vaginal discharge will vary in consistency and amount throughout the menstrual cycle and is at its clearest at ovulation—about two weeks before the period starts. Some practitioners claim that BV can be asymptomatic in almost half of affected women, though others argue that this is often a misdiagnosis.

Complications
Although previously considered a mere nuisance infection, untreated bacterial vaginosis may cause increased susceptibility to sexually transmitted infections, including HIV, and pregnancy complications.It has been shown that HIV-infected women with bacterial vaginosis (BV) are more likely to transmit HIV to their sexual partners than those without BV.
There is evidence of an association between BV and increased rates of sexually transmitted infections such as HIV/AIDS. BV is associated with up to a six-fold increase in HIV shedding. BV is a risk factor for viral shedding and herpes simplex virus type 2 infection. BV may increase the risk of infection with or reactivation of human papillomavirus (HPV).In addition, bacterial vaginosis as either pre-existing, or acquired, may increase the risk of pregnancy complications, most notably premature birth or miscarriage.
Pregnant women with BV have a higher risk of chorioamnionitis, miscarriage, preterm birth, premature rupture of membranes, and postpartum endometritis. Women with BV who are treated with in vitro fertilization have a lower implantation rate and higher rates of early pregnancy loss.

Causes
Healthy vaginal microbiota consists of species that neither cause symptoms or infections, nor negatively affect pregnancy. It is dominated mainly by Lactobacillus species. BV is defined by the disequilibrium in the vaginal microbiota, with decline in the number of lactobacilli. While the infection involves a number of bacteria, it is believed that most infections start with Gardnerella vaginalis  creating a biofilm, which allows other opportunistic bacteria to thrive.One of the main risks for developing BV is douching, which alters the vaginal microbiota and predisposes women to developing BV. Douching is strongly discouraged by the U.S. Department of Health and Human Services and various medical authorities, for this and other reasons.BV is a risk factor for pelvic inflammatory disease, HIV, sexually transmitted infections (STIs), and reproductive and obstetric disorders or negative outcomes. Although BV can be associated with sexual activity, there is no clear evidence of sexual transmission. It is possible for sexually inactive persons to develop bacterial vaginosis.Also, subclinical iron deficiency may correlate with bacterial vaginosis in early pregnancy. A longitudinal study published in February 2006, in the American Journal of Obstetrics and Gynecology, showed a link between psychosocial stress and bacterial vaginosis persisted even when other risk factors were taken into account. Exposure to the spermicide nonoxynol-9 does not affect the risk of developing bacterial vaginosis.

Diagnosis
To make a diagnosis of bacterial vaginosis, a swab from inside the vagina should be obtained. These swabs can be tested for:

Gram stain which shows the depletion of lactobacilli and overgrowth of Gardnerella vaginalis  bacteria. Bacterial vaginosis is usually confirmed by  a Gram stain of vaginal secretions.
A characteristic "fishy" odor on wet mount. This test, called the whiff test, is performed by adding a small amount of potassium hydroxide to a microscope slide containing the vaginal discharge. A characteristic fishy odor is considered a positive whiff test and is suggestive of bacterial vaginosis.
Loss of acidity. To control bacterial growth, the vagina is normally slightly acidic with a pH of 3.8–4.2. A swab of the discharge is put onto litmus paper to check its acidity. A pH greater than 4.5 is considered alkaline and is suggestive of bacterial vaginosis.
The presence of clue cells on wet mount. Similar to the whiff test, the test for clue cells is performed by placing a drop of sodium chloride solution on a slide containing vaginal discharge. If present, clue cells can be visualized under a microscope. They are so-named because they give a clue to the reason behind the discharge. These are epithelial cells that are coated with bacteria.Differential diagnosis for bacterial vaginosis includes the following:
Normal vaginal discharge.
Candidiasis (thrush, or a yeast infection).
Trichomoniasis, an infection caused by Trichomonas vaginalis.
Aerobic vaginitisThe Center for Disease Control (CDC) defines STIs as "a variety of clinical syndromes and infections caused by pathogens that can be acquired and transmitted through sexual activity." But the CDC does not specifically identify BV as sexually transmitted infection.

Amsel criteria
In clinical practice BV can be diagnosed using the Amsel criteria:
Thin, white, yellow, homogeneous discharge
Clue cells on microscopy
pH of vaginal fluid >4.5
Release of a fishy odor on adding alkali—10% potassium hydroxide (KOH) solution.At least three of the four criteria should be present for a confirmed diagnosis.
A modification of the Amsel criteria accepts the presence of two instead of three factors and is considered equally diagnostic.

Gram stain
An alternative is to use a Gram-stained vaginal smear, with the Hay/Ison criteria or the Nugent criteria. The Hay/Ison criteria are defined as follows:
Grade 1 (Normal): Lactobacillus morphotypes predominate.
Grade 2 (Intermediate): Some lactobacilli present, but Gardnerella or Mobiluncus morphotypes also present.
Grade 3 (Bacterial Vaginosis): Predominantly Gardnerella and/or Mobiluncus morphotypes. Few or absent lactobacilli. (Hay et al., 1994)Gardnerella vaginalis is the main culprit in BV. Gardnerella vaginalis is a short, Gram-variable rod (coccobacillus). Hence, the presence of clue cells and gram variable coccobacilli are indicative or diagnostic of bacterial vaginosis.

Nugent score
The Nugent score is now rarely used by physicians due to the time it takes to read the slides and requires the use of a trained microscopist. A score of 0-10 is generated from combining three other scores.  The scores are as follows:
0–3 is considered negative for BV
4–6 is considered intermediate
7+ is considered indicative of BV.At least 10–20 high power (1000× oil immersion) fields are counted and an average determined.
DNA hybridization testing with Affirm VPIII was compared to the Gram stain using the Nugent criteria. The Affirm VPIII test may be used for the rapid diagnosis of BV in symptomatic women but uses expensive proprietary equipment to read results, and does not detect other pathogens that cause BV, including Prevotella spp, Bacteroides spp, and Mobiluncus spp. The cervicovaginal microbiome measured using 16S rRNA sequencing has the capacity to increase throughput of the Nugent Score and has demonstrate to be directly comparable to clinical Nugent Score measurement.

Screening
Screening during pregnancy is not recommended in the United States as of 2020.

Prevention
Some steps suggested to lower the risk include: not douching, avoiding sex, or limiting the number of sex partners.One review concluded that probiotics may help prevent re-occurrence. Another review found that, while there is tentative evidence, it is not strong enough to recommend their use for this purpose.Early evidence suggested that antibiotic treatment of male partners could re-establish the normal microbiota of the male urogenital tract and prevent the recurrence of infection. However, a 2016 Cochrane review found high-quality evidence that treating the sexual partners of women with bacterial vaginosis had no effect on symptoms, clinical outcomes, or recurrence in the affected women. It also found that such treatment may lead treated sexual partners to report increased adverse events.

Treatment
Antibiotics
Treatment is typically with the antibiotics metronidazole or clindamycin. They can be either given by mouth or applied inside the vagina with similar efficacy. About 10% to 15% of people, however, do not improve with the first course of antibiotics and recurrence rates of up to 80% have been documented. Recurrence rates are increased with sexual activity with the same pre-/posttreatment partner and inconsistent condom use although estrogen-containing contraceptives decrease recurrence. When clindamycin is given to pregnant women symptomatic with BV before 22 weeks of gestation the risk of pre-term birth before 37 weeks of gestation is lower.Other antibiotics that may work include macrolides, lincosamides, nitroimidazoles, and penicillins.Bacterial vaginosis is not considered a sexually transmitted infection, and treatment of a male sexual partner of a woman with bacterial vaginosis is not recommended.

Probiotics
A 2009 Cochrane review found tentative but insufficient evidence for probiotics as a treatment for BV. A 2014 review reached the same conclusion. A 2013 review found some evidence supporting the use of probiotics during pregnancy. The preferred probiotics for BV are those containing high doses of lactobacilli (around 109 CFUs) given in the vagina. Intravaginal administration is preferred to taking them by mouth. Prolonged repetitive courses of treatment appear to be more promising than short courses.The lack of effectiveness of commercially available Lactobacillus probiotics may be because most do not actually contain vaginal lactobacilli strains </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Thyroid adenoma and explain in detail? [/INST] A thyroid adenoma is a benign tumor of the thyroid gland, that may be inactive or active (functioning autonomously) as a toxic adenoma.

Signs and symptoms
A thyroid adenoma may be clinically silent ("cold" adenoma), or it may be a functional tumor, producing excessive thyroid hormone ("warm" or "hot" adenoma). In this case, it may result in symptomatic hyperthyroidism, and may be referred to as a toxic thyroid adenoma.

Diagnosis
Morphology
Thyroid follicular adenoma ranges in diameter from  3 cm on an average, but sometimes is larger (up to 10 cm) or smaller. The typical thyroid adenoma is solitary, spherical and encapsulated lesion that is well demarcated from the surrounding parenchyma. The color ranges from gray-white to red-brown, depending upon

the cellularity of the adenoma
the colloid content.Areas of hemorrhage, fibrosis, calcification, and cystic change, similar to what is found in multinodular goiters, are common in thyroid (follicular) adenoma, particularly in larger lesions.

Types
Almost all thyroid adenomata are follicular adenomata </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Lymphadenopathy and explain in detail? [/INST] Lymphadenopathy or adenopathy is a disease of the lymph nodes, in which they are abnormal in size or consistency. Lymphadenopathy of an inflammatory type (the most common type) is lymphadenitis,  producing swollen or enlarged lymph nodes. In clinical practice, the distinction between lymphadenopathy and lymphadenitis is rarely made and the words are usually treated as synonymous. Inflammation of the lymphatic vessels is known as lymphangitis. Infectious lymphadenitis affecting lymph nodes in the neck is often called scrofula.
Lymphadenopathy is a common and nonspecific sign. Common causes include infections (from minor causes such as the common cold and post-vaccination swelling to serious ones such as HIV/AIDS), autoimmune diseases, and cancer. Lymphadenopathy is frequently idiopathic and self-limiting.

Causes
Lymph node enlargement is recognized as a common sign of infectious, autoimmune, or malignant disease. Examples may include:

Reactive: acute infection (e.g., bacterial, or viral), or chronic infections (tuberculous lymphadenitis, cat-scratch disease).
The most distinctive sign of bubonic plague is extreme swelling of one or more lymph nodes that bulge out of the skin as "buboes." The buboes often become necrotic and may even rupture.
Infectious mononucleosis is an acute viral infection usually caused by Epstein-Barr virus and may be characterized by a marked enlargement of the cervical lymph nodes.
It is also a sign of cutaneous anthrax and Human African trypanosomiasis
Toxoplasmosis, a parasitic disease, gives a generalized lymphadenopathy (Piringer-Kuchinka lymphadenopathy).
Plasma cell variant of Castlemans disease - associated with HHV-8 infection and HIV infection
Mesenteric lymphadenitis after viral systemic infection (particularly in the GALT in the appendix) can commonly present like appendicitis.Infectious causes of lymphadenopathy may include bacterial infections such as cat scratch disease, tularemia, brucellosis, or prevotella, as well as fungal infections such as paracoccidioidomycosis.
Tumoral:
Primary: Hodgkin lymphoma and non-Hodgkin lymphoma give lymphadenopathy in all or a few lymph nodes.
Secondary: metastasis, Virchows Node, neuroblastoma, and chronic lymphocytic leukemia.
Autoimmune: systemic lupus erythematosus and rheumatoid arthritis may have a generalized lymphadenopathy.
Immunocompromised: AIDS. Generalized lymphadenopathy is an early sign of infection with human immunodeficiency virus (HIV), the virus that causes acquired immunodeficiency syndrome (AIDS).  "Lymphadenopathy syndrome" has been used to describe the first symptomatic stage of HIV progression, preceding a diagnosis of AIDS.
Bites from certain venomous snakes such as the pit viper
Unknown: Kikuchi disease, progressive transformation of germinal centers, sarcoidosis, hyaline-vascular variant of Castlemans disease, Rosai-Dorfman disease, Kawasaki disease, Kimura disease

Benign (reactive) lymphadenopathy
Benign lymphadenopathy is a common biopsy finding, and may often be confused with malignant lymphoma. It may be separated into major morphologic patterns, each with its own differential diagnosis with certain types of lymphoma. Most cases of reactive follicular hyperplasia are easy to diagnose, but some cases may be confused with follicular lymphoma. There are seven distinct patterns of benign lymphadenopathy:
Follicular hyperplasia: This is the most common type of reactive lymphadenopathy.
Paracortical hyperplasia/Interfollicular hyperplasia: It is seen in viral infections, skin diseases, and nonspecific reactions.
Sinus histiocytosis: It is seen in lymph nodes draining limbs, inflammatory lesions, and malignancies.
Nodal extensive necrosis
Nodal granulomatous inflammation
Nodal extensive fibrosis (Connective tissue framework)
Nodal deposition of interstitial substanceThese morphological patterns are never pure </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pseudohyperaldosteronism and explain in detail? [/INST] Pseudohyperaldosteronism (also pseudoaldosteronism) is a medical condition which mimics the effects of elevated aldosterone (hyperaldosteronism) by presenting with high blood pressure (hypertension), low blood potassium levels (hypokalemia), metabolic alkalosis, and low levels of plasma renin activity (PRA). However, unlike hyperaldosteronism, this conditions exhibits low or normal levels of aldosterone in the blood. Causes include genetic disorders (e.g. Apparent mineralocorticoid excess syndrome, Liddles syndrome, and types of Congenital adrenal hyperplasia), acquired conditions (e.g. Cushings syndrome and mineralocorticoid-producing adrenal tumors), metabolic disorders, and dietary imbalances including excessive consumption of licorice. Confirmatory diagnosis depends on the specific root cause and may involve blood tests, urine tests, or genetic testing; however, all forms of this condition exhibit abnormally low concentrations of both plasma renin activity (PRA) and plasma aldosterone concentration (PAC) which differentiates this group of conditions from other forms of secondary hypertension. Treatment is tailored to the specific cause and focuses on symptom control, blood pressure management, and avoidance of triggers.

Presentation
The presentation of pseudohyperaldosteronism varies depending on the cause. The genetic conditions such as Liddles syndrome and Congenital adrenal hyperplasia present in childhood or earlier in life than the acquired causes which can present at any age. Adult patients present with clinical history of resistant hypertension despite typical medical therapy and lifestyle changes. Hypertension may be asymptomatic or may lead to symptoms such as headache, dizziness, vision changes, or kidney disease. Symptoms of hypokalemia include fatigue, muscular weakness, and increased urine production.

Causes
This condition has several known causes including genetic disorders, acquired conditions, metabolic derangements, and dietary imbalances. All causes mimic the effects of elevated aldosterone without raising aldosterone levels but achieve this through varying mechanisms.

Genetic forms
Genetic disorders that lead to this condition include Liddles syndrome, Apparent mineralocorticoid excess (AME), and two types of Congenital adrenal hyperplasia (CAH).
Liddles syndrome is autosomal dominant disorder affecting epithelial sodium channels (ENaC) in the distal tubules of the kidneys. In this disorder, a gain of function mutation decreases ENaC degradation leading to increased renal absorption of sodium and water.
Apparent mineralocorticoid excess genetic forms include autosomal recessive disorders with mutations lowering the activity of the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (11-β-HSD2). These mutations limit the ability of 11-β-HSD2 to transform active cortisol to the less active cortisone. Excess cortisol is then able to bind and activate mineralocorticoid receptors due to receptor cross-reactivity leading to aldosterone-like effects.
Congenital Adrenal Hyperplasia is an autosomal recessive disorder with multiple types, two of which lead to pseudohyperaldosteronism. Deficiency of 11-beta-hydroxylase blocks the conversion of 11-deoxycorticosterone (DOC) to corticosterone leading to an excess of DOC which acts as a mineralocorticoid similar to aldosterone. Deficiency of 17-alpha-hydroxylase blocks the conversion of pregnenolone and progesterone to their 17-a-hydroxy forms leading to increased mineralocorticoid production.

Acquired forms
Some causes of pseudohyperaldosteronism can be acquired throughout life with examples including adrenal tumors and Ectopic ACTH syndrome.
Adrenal tumor subtypes include adrenal adenomas that produce 11-deoxycorticosterone (DOC) leading to increased mineralocorticoid activity without elevated aldosterone.
Ectopic ACTH syndrome describes conditions leading to excess production of adrenocorticotropic hormone (ACTH) subsequently leading to mineralocorticoid production. This can arise in ectopic forms of Cushings syndrome associated with small-cell lung cancers and other ACTH-producing tumors. The excess ACTH can saturate the 11-β-HSD2 enzyme leading to decreased conversion of cortisol to cortisone and increased mineralocorticoid effects.

Metabolic and dietary forms
Metabolic causes include conditions of glucocorticoid resistance and from mineralocorticoid excess which can occur following high-dose corticosteroid therapy. Dietary causes include overconsumption of licorice-containing products. Glycyrrhetinic acid in licorice inhibits the 11-β-HSD2 enzyme resulting in inappropriate stimulation of the mineralocorticoid receptor by cortisol leading to aldosterone-like effects.

Diagnosis
In patients with hypertension, diagnostic clues pointing to pseudohyperaldosteronism can be found on routine labwork. These include low serum potassium (hypokalemia), elevated serum sodium (hypernatremia), and elevated serum bicarbonate (metabolic alkalosis). Urine studies may show elevated urine potassium (kaliuresis). To further differentiate between hyperaldosteronism and pseudohyperaldosteronism, studies including plasma renin activity (PRA) and plasma aldosterone concentration (PAC) can be obtained. Pseudohyperaldosteronism will exhibit low levels of both PRA and PAC while hyperaldosteronism will demonstrate elevated PAC. Confirmatory tests to diagnose the specific forms of pseudohyperaldosteronism vary depending on the cause. The genetic conditions such as Liddles syndrome and CAH can be confirmed with genetic tests for the affected genes </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Vaginal bleeding and explain in detail? [/INST] Vaginal bleeding is any expulsion of blood from the vagina. This bleeding may originate from the uterus, vaginal wall, or cervix. Generally, it is either part of a normal menstrual cycle or is caused by hormonal or other problems of the reproductive system, such as abnormal uterine bleeding.
Vaginal bleeding during pregnancy can be normal, especially in early pregnancy. However, bleeding may also indicate a pregnancy complication that needs to be medically addressed. During pregnancy bleeding is usually, but not always, related to the pregnancy itself.
Regular monthly vaginal bleeding during the reproductive years, menstruation, is a normal physiologic process. During the reproductive years, bleeding that is excessively heavy (menorrhagia or heavy menstrual bleeding), occurs between monthly menstrual periods (intermenstrual bleeding), occurs more frequently than every 21 days (abnormal uterine bleeding), occurs too infrequently (oligomenorrhea), or occurs after vaginal intercourse (postcoital bleeding) should be evaluated.The causes of abnormal vaginal bleeding vary by age, and such bleeding can be a sign of specific medical conditions ranging from hormone imbalances or anovulation to malignancy (cervical cancer, vaginal cancer or uterine cancer).  In young children, or elderly adults with cognitive impairment, the source of bleeding may not be obvious, and may be from the urinary tract (hematuria) or the rectum rather than the vagina, although most adult women can identify the site of bleeding. When vaginal bleeding occurs in prepubertal children or in postmenopausal women, it always needs medical attention.

Differential diagnosis
The parameters for normal menstruation have been defined as a result of an international process designed to simplify terminologies and definitions for abnormalities of menstrual bleeding.  The causes of abnormal vaginal bleeding vary by age.

In children
Bleeding in children is of concern if it occurs before the expected time of menarche and in the absence of appropriate pubertal development. Bleeding before the onset of pubertal development deserves evaluation. It could result from local causes or from hormonal factors. In children, it may be challenging to determine the source of bleeding, and "vaginal" bleeding may actually arise from the bladder or urethra, or from the rectum.Vaginal bleeding in the first week of life after birth is a common observation, and pediatricians typically discuss this with new mothers at the time of hospital discharge. During childhood, other possible causes include the presence of a foreign body in the vagina, trauma (either accidental or non accidental, i.e. child sexual abuse or molestation), urethral prolapse, vaginal infection (vaginitis), vulvar ulcers, vulvar skin conditions such as lichen sclerosus, and rarely, a tumor (benign or malignant vaginal tumors, or hormone-producing ovarian tumors). Hormonal causes include central precocious puberty, or peripheral precocious puberty (McCune–Albright syndrome), or primary hypothyroidism.While the symptom is typically alarming to parents, most causes are benign, although sexual abuse or tumor are particularly important to exclude. An examination under anesthesia (EUA) may be necessary to exclude a vaginal foreign body or tumor, although instruments designed for office hysteroscopy can sometimes be used in children with topical anesthesia for office vaginoscopy, precluding the need for sedation or general anesthesia and operating room time.

Premenopausal
Background
In premenopausal women, bleeding can be from the uterus, from vulvar or vaginal lesions, or from the cervix. A gynecologic examination can be performed to determine the source of bleeding. Bleeding may also occur as a result of a pregnancy complication, such as a spontaneous abortion (miscarriage), ectopic pregnancy, or abnormal growth of the placenta, even if the woman is not aware of the pregnancy. This possibility must be kept in mind with regard to diagnosis and management.
Generally, the causes of abnormal uterine bleeding in premenopausal women who are not pregnant include fibroids, polyps, hormonal disorders such as polycystic ovary syndrome (PCOS), blood clotting disorders, and cancer. Infections such as cervicitis or pelvic inflammatory disease (PID) can also result in vaginal bleeding. Postcoital bleeding is bleeding that occurs after sexual intercourse. Lastly, a normal and common side effect of birth control includes vaginal spotting or bleeding.

Clinical guidelines (FIGO classification)
A more specific clinical guideline, called the PALM-COEIN system, has been developed by FIGO (International Federation of Gynecology and Obstetrics) to classify the causes of abnormal uterine bleeding. This acronym stands for Polyp, Adenomyosis, Leiomyoma, Malignancy and Hyperplasia, Coagulopathy, Ovulatory Disorders, Endometrial Disorders, Iatrogenic Causes, and Not Classified. The FIGO Menstrual Disorders Group, with input from international experts, recommended a simplified description of abnormal bleeding that discarded imprecise terms such as menorrhagia, metrorrhagia, hypermenorrhea, and dysfunctional uterine bleeding (DUB) in favor of plain English descriptions of bleeding that describe the vaginal bleeding in terms of cycle regularity, frequency, duration, and volume.The PALM causes are related to uterine structural, anatomic, and histolopathologic causes that can be assessed with imaging techniques such as ultrasound or biopsy to view the histology of a lesion. The COEIN causes of abnormal bleeding are not related to structural causes.
Polyps: Endometrial polyps are benign growths that are typically detected during gynecologic ultrasonography and confirmed using saline infusion sonography or hysteroscopy, often in combination with an endometrial biopsy providing histopathologic confirmation. Endocervical polyps are visible at the time of a gynecologic examination using a vaginal speculum, and can often be removed with a minor office procedure.
Adenomyosis: Adenomyosis is a condition in which endometrial glands are present within the muscle of the uterus (myometrium), and the pathogenesis and mechanism by which it causes abnormal bleeding have been debated.
Leiomyoma (fibroids): Uterine leiomyoma, commonly termed uterine fibroids, are common, and most fibroids are asymptomatic. The presence of leiomyomas may not be the cause of abnormal bleeding, although fibroids that are submucosal in location are the most likely to cause abnormal bleeding.
Malignancy (pre-cancer and cancer): The Malignancy and Hyperplasia category of the PALM-COEIN system includes malignancies of the genital tract, including cancers of the vulva, the vagina, the cervix, and the uterus. Endometrial hyperplasia, included in this PALM category of abnormal bleeding, is more common in women who are obese or who have a history of chronic anovulation. When endometrial hyperplasia is associated with atypical cells, it can progress to cancer or occur concurrently with it. While endometrial hyperplasia and endometrial cancer occur most commonly among post-menopausal women, most patients with endometrial cancer have abnormal bleeding, and thus the diagnosis must be considered in women during the reproductive years.
Coagulopathies (blood clotting disorders): Heavy menstrual bleeding can be related to coagulopathies. Von Willebrand disease is the most common coagulopathy, and most women with von Willebrand disease have heavy menstrual bleeding.  Of women with heavy menstrual bleeding, up to 20% will have a bleeding disorder. Heavy menstrual bleeding since menarche is a common symptom for women with bleeding disorders, and in retrospective studies, bleeding disorders have been found in up to 62% of adolescents with heavy menstrual bleeding.
Ovulatory dysfunction: Ovulatory dysfunction or anovulation is a common cause of abnormal bleeding that may lead to irregular and unpredictable bleeding, as well as variations in the amount of flow including heavy bleeding. Endocrine, or hormonal, causes of ovulatory disorders include polycystic ovary syndrome (PCOS), thyroid disorders, hyperprolactinemia, obesity, eating disorders including anorexia nervosa or bulimia,  or to an imbalance between exercise and caloric intake.
Endometrial: Endometrial causes of abnormal bleeding include infection of the endometrium, endometritis, which may occur after a miscarriage (spontaneous abortion) or a delivery, or may be related to a sexually-transmitted infection of the uterus, fallopian tubes or pelvis generally termed pelvic inflammatory disease (PID).  Other endometrial causes of abnormal bleeding may relate to the ways that the endometrium heals itself or develops blood vessels.
Iatrogenic (caused by medical treatment or procedures): The most common Iatrogenic cause of abnormal bleeding relates to treatment with hormonal medications such as birth control pills, patches, rings, injections, implants, and intrauterine devices (IUDs).  Hormone therapy for treatment of menopausal symptoms can also cause abnormal bleeding. Unscheduled bleeding that occurs during such hormonal treatment is termed "breakthrough bleeding" (BTB)  Breakthrough bleeding may result from inconsistent use of hormonal treatment, although in the initial months after initiation of a method, it may occur even with perfect use, and may ultimately affect adherence to the medication regimen.  The risk of breakthrough bleeding with oral contraceptives is greater if pills are missed.
Not classified: The Not Classified category of the PALM-COEIN system includes conditions that may be rare, or whose contribution to abnormal bleeding has not been well established or understood.

Pregnancy
Vaginal bleeding occurs during 15–25% of first trimester pregnancies. Of these, half go on to miscarry and half bring the fetus to term. There are a number of causes including complications to the placenta, such as placental abruption and placenta previa. Other causes include miscarriage, ectopic pregnancy, molar pregnancy, incompetent cervix, uterine rupture, and preterm labor. Bleeding in early pregnancy may be a sign of a threatened or incomplete miscarriage.
In the second or third trimester a placenta previa (a placenta partially or completely overlying the cervix) may bleed quite severely. Placental abruption is often associated with uterine bleeding as well as uterine pain.

Postmenopausal
Endometrial atrophy, uterine fibroids, and endometrial cancer are common causes of postmenopausal vaginal bleeding. About 10% of cases are due to endometrial cancer. Uterine fibroids are benign tumors made of muscle cells and other tissues located in and around the wall of the uterus. Women with fibroids do not always have symptoms, but some experience vaginal bleeding between periods, pain during sex, and lower back pain.

Diagnostic evaluation
The cause of the bleeding can often be discerned on the basis of the bleeding history, physical examination, and other medical tests as appropriate. The physical examination for evaluating vaginal bleeding typically includes visualization of the cervix with a speculum, a bimanual exam, and a rectovaginal exam. These are focused on finding the source of the bleeding and looking for any abnormalities that could cause bleeding. In addition, the abdomen is examined and palpated to ascertain if the bleeding is abdominal in origin. Typically a pregnancy test is performed as well. If bleeding was excessive or prolonged, a CBC may be useful to check for anemia. Abnormal endometrium may have to be investigated by a hysteroscopy with a biopsy or a dilation and curettage.

Postmenopausal bleeding
In postmenopausal vaginal bleeding, the primary goal of any diagnostic evaluations is to exclude endometrial hyperplasia and malignancy. Transvaginal ultrasonography and endometrial sampling are common methods for an initial evaluation. Guidelines from the American College of Obstetricians and Gynecologists (ACOG) recommend transvaginal ultrasonography as an appropriate first-line procedure to identify which patients are at higher risk of endometrial cancer. Endometrial sampling is indicated if having the following findings and/or symptoms:
Endometrial thickness greater than 4 mm
Diffuse or focal increased echogenicity (heterogeneity)
Failure to visualize the endometrium
Persistent or recurrent bleeding regardless of endometrial thicknessEndometrial sampling can be obtained either by an endometrial biopsy using an endometrium sampling device such as a pipelle or by dilation and curettage (D&C) with or without a hysteroscopy.

FIGO classification
In 2011, the International Federation of Gynaecology and Obstetrics (FIGO) recognized two systems designed to aid research, education, and clinical care of women with abnormal uterine bleeding (AUB) in the reproductive years.

Complications
Severe acute bleeding, such as caused by ectopic pregnancy and post-partum hemorrhage, leads to hypovolemia (the depletion of blood from the circulation), progressing to shock. This is a medical emergency and requires hospital attendance and intravenous fluids, usually followed by blood transfusion. Once the circulating volume has been restored, investigations are performed to identify the source of bleeding and address it </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Aphonia and explain in detail? [/INST] Aphonia is defined as the inability to produce voiced sound. Damage to the nerve may be the result of surgery (e.g., thyroidectomy) or a tumor.Aphonia means "no sound" </s>