<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Gas gangrene and can you explain it in depth? [/INST] Gas gangrene (also known as clostridial myonecrosis and myonecrosis) is a bacterial infection that produces tissue gas in gangrene. This deadly form of gangrene usually is caused by Clostridium perfringens bacteria. About 1,000 cases of gas gangrene are reported yearly in the United States.Myonecrosis is a condition of necrotic damage, specific to muscle tissue. It is often seen in infections with C. perfringens or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis by specific exotoxins. These microorganisms are opportunistic and, in general, enter the body through significant skin breakage. Gangrenous infection by soil-borne bacteria was common in the combat injuries of soldiers well into the 20th century, because of non-sterile field surgery and the basic nature of care for severe projectile wounds.Other causes of myonecrosis include envenomation by snakes of the genus Bothrops (family Viperidae), ischemic necrosis, caused by vascular blockage (e.g., diabetes type II), tumours that block or hoard blood supply, and disseminated intravascular coagulation or other thromboses.

Presentation
Gas gangrene can cause myonecrosis (muscle tissue death), gas production, and sepsis. Progression to toxemia and shock is often very rapid. It can easily be noticed by the large, blackened sores that form, as well as a degree of loud and distinctive crepitus caused by gas escaping the necrotic tissue.

Symptoms
A multitude of symptoms is associated with Gas gangrene. Distinctively, black lesions on the skin appear in a bubble form which allows visualization of gas-producing bacteria. Symptoms include:
Skin discoloration
"Foul, sweet" smelling discharge from lesions formed on skin
Distinctive black, bubble lesions on skin
Necrosis
Fever
Pain following site of surgery or trauma
Lightheadedness
Rapid heart rate
Numbness on affected site
Blisters
Air in subcutaneous tissues
Swelling
Jaundice

Etiology
Clostridium species produce more toxins and exhibit higher degrees of virulence than any other bacterial taxon. Clostridium infections are usually opportunistic, and occur in individuals with serious preexisting medical conditions. However, Clostridium infections are also known to occur in healthy individuals. Four species of Clostridium (Clostridium botulinum, Clostridium perfringens, Clostridium tetani, and Clostridium sordelli) are responsible for most human infections. Since Clostridium is an obligate anaerobe taxon, the bacterium infects hypoxic tissues, which had become anaerobic due to restricted blood flow, degradation of blood vessels, or atherosclerosis. Immunocompromised individuals exhibit higher susceptibility for infection and higher mortality rates.

Virulence factors
Members of the Clostridium species exhibit a plethora of virulence factors. Common virulence factors associated with gas gangrene include alpha toxin and theta toxin. Clostridium perfingens causes 80–90% of infections and produces both these toxins.
Alpha toxin (α-toxin)Clostridium perfingens alpha toxin is widely associated with gas gangrene as it is its main virulence factor whilst invading its host. Alpha toxin is associated with hemolysis, thus restricting blood flow towards the area of infection. As the surrounding circulatory system collapses, neutrophils and monocytes, eosinophils and basophils cannot reach target areas of infection. The hemolytic activity of alpha toxin produces an anaerobic environment essential for the proliferation of the bacteria. Alpha toxin also exhibits the ability to infiltrate surrounding cellular tissue and cause a cascade of aberrant biochemical activity.
Theta toxin (Θ-toxin)Theta toxin is also employed by Clostridium perfingens as a virulence factor. Theta toxin also promotes vascular degradation as its counterpart alpha toxin. A platelet-activation factor is employed which triggers an acute inflammatory response in nearby tissues. This inflammatory response leads to constriction of surrounding arteries and promotes an anaerobic environment for Clostridium perfingens growth and pathophysiology.
Beta toxin (β-toxin)Beta toxin is an integral virulence factor in promoting enterocolitics and enterotoxemia. This toxin uses pores in the cellular biolipid membrane to import a pathogenic factor into organisms.

Pathophysiology
Gas gangrene is caused by exotoxin-producing Clostridium species (most often C. perfringens, and C. novyi, but less commonly C. septicum or C. ramnosum), which are mostly found in soil, but also found as normal gut flora, and other anaerobes (e.g., Bacteroides and anaerobic streptococci).Bacterium of the Clostridial species produce two toxins: alpha and theta toxins, which cause necrotizing damage to tissues.Other organisms may occasionally cause gas gangrene (for example, Klebsiella pneumoniae in the context of diabetes).A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen, and 16.1% oxygen was reported in one clinical case.Myonecrosis differs slightly from other types of necrosis. While the underlying causes are almost identical, the type of affected tissue (in particular, muscle tissue) is significantly more important for the patients general health. Superficial necrosis is unsightly and can lead to unattractive scarring, but otherwise does not affect the patients likelihood of survival or physical capability to the same extent. However, massive myonecrosis will likely result in the loss of movement of the entire region. If the necrotic damage is allowed to continue throughout an affected limb, then often that entire limb is lost permanently.It is often difficult to identify the extent of muscle damage, as C. perfringens may be at work in deeper fascial layers below the skin.  Unlike other anaerobic infections, discharge in these infections is often not purulent (filled with pus).  Instead, the discharge is often described as "sweetly putrid" or "dishwater pus" because it is much thinner than normal pus.  This is due to the lysis of neutrophils, a type of white blood cell, caused by the lecithinases and other toxins released by Clostridium species.Soil-borne anaerobes are particularly well-adapted to surviving harsh conditions. Often, a scarcity of nutrition and competition for resources from numerous other species occurs. Changes in pH and temperature are often significant, also. Bacteria often possess the ability to create exotoxins to assist them in competing with other microbes in their natural environments. When such bacteria are able to enter a living host, they encounter a vast supply of nutrients, warm conditions, and an abundance of water. This enables the microbes to rapidly proliferate, far in excess of the immune systems capability to defend, as prokaryotic bacteria possess a far greater capacity for multiplication than the hosts immune system. The combination of bacterial load and ability to multiply is the basis for the microbes ability to cause massive infection. Alongside such rapid proliferation is a corresponding mass-production of exotoxin that causes severe damage to local tissue in the host. One such exotoxin is alpha toxin, which is produced by C. perfringens and is the key virulence factor in its pathogenesis.Massive infection, gross injury, and depletion of the hosts immune capability result in system-wide sepsis. This is partly due to the burden on the immune system, its corresponding release of inflammatory cytokines, and the distribution of bacterial toxins. Massive infection is likely to result in death from a combination of system-wide septic shock and the unintentionally damaging effects of the immune response. In animals, disability and distress caused by all of these factors markedly increase the chance of predation.

Diagnosis
Various diagnostic methods can be employed in the diagnosis of Gas gangrene. Due to low incidence of myonecrosis it is an easy-to-overlook diagnosis. As bacterial infections mostly exhibit the same symptoms, early diagnosis of gas gangrene rarely occurs. The ambiguous symptoms only contribute to a poorer prognosis. Diagnostic methods include:
Biopsy of affected tissue
Cultures of fluids from inflicted area
Magnetic resonance imaging to visualize necrotized subcutaneous tissues
X-rays for air pockets in affected tissues
Microscopy identification of strain of bacteria sampled from fluids of inflicted area
Gram stain

Treatment
Treatment is usually debridement and excision, with amputation necessary in many cases. Water-soluble antibiotics (such as penicillin) alone are not effective because they do not penetrate ischaemic muscles sufficiently to be effective. Penicillin is effective against C. perfringens. When gas gangrene occurs in such regions as the abdominal cavity, the patient can be treated in a hyperbaric chamber, which contains a pressurized oxygen-rich atmosphere. The oxygen saturates the infected tissues and thereby prevents the growth of the obligately anaerobic clostridia </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Claustrophobia and can you explain it in depth? [/INST] Claustrophobia is the fear of confined spaces. It can be triggered by many situations or stimuli, including elevators, especially when crowded to capacity, windowless rooms, and hotel rooms with closed doors and sealed windows. Even bedrooms with a lock on the outside, small cars, and tight-necked clothing can induce a response in those with claustrophobia. It is typically classified as an anxiety disorder, which often results in panic attacks. The onset of claustrophobia has been attributed to many factors, including a reduction in the size of the amygdala and classical conditioning.
One study indicates that 5–10% of the world population is affected by severe claustrophobia, but only a small percentage of these people receive some kind of treatment for the disorder.
The term claustrophobia comes from Latin claustrum "a shut in place" and Greek φόβος, phóbos, "fear".

Signs and symptoms
Claustrophobia is classified as a mental and behavioral disorder,  specifically an anxiety disorder. Symptoms generally develop during childhood or adolescence. Claustrophobia is typically thought to have one key symptom: fear of suffocation. In at least one, if not several, of the following areas: small rooms, MRI or CAT scan apparatus, cars, buses, airplanes, trains, tunnels, underwater caves, cellars, elevators and caves.
Being enclosed or thinking about being enclosed in a confined space can trigger fears of not being able to breathe properly, and running out of oxygen. It is not always the small space that triggers these emotions, but it is more the fear of the possibilities of what could happen while confined to that area. When anxiety levels start to reach a certain ppo level, the person may start to experience:

sweating and/or chills
accelerated heart rate and a rise in blood pressure
dizziness, fainting spells, lightheadedness and frozen in fear
dry mouth
hyperventilation
hot flashes
shaking or trembling and a sense of "butterflies" in the stomach
nausea
headache
numbness
a choking sensation
tightness in the chest/chest pain and difficulty breathing
an urge to use the bathroom
confusion or disorientation
fear of harm or illness

Causes
The fear of enclosed spaces is an irrational fear. Most claustrophobic people who find themselves in a room without windows consciously know that they are not in danger, yet these same people will be afraid, possibly terrified to the point of incapacitation, and many do not know why.

Amygdala
The amygdala is one of the smallest structures in the brain, but also one of the most powerful. The amygdala is needed for the conditioning of fear, or the creation of a fight-or-flight response. A fight-or-flight response is created when a stimulus is associated with a grievous situation. Cheng believes that a phobias roots are in this fight-or-flight response.
In generating a fight-or-flight response, the amygdala acts in the following way:
The amygdalas anterior nuclei associated with fear each other. Nuclei send out impulses to other nuclei, which influence respiratory rate, physical arousal, the release of adrenaline, blood pressure, heart rate, behavioral fear response, and defensive responses, which may include freezing up. These reactions constitute an autonomic failure in a panic attack.

A study done by Fumi Hayano found that the right amygdala was smaller in patients who suffered from panic disorders. The reduction of size occurred in a structure known as the corticomedial nuclear group which the CE nucleus belongs to. This causes interference, which in turn causes abnormal reactions to aversive stimuli in those with panic disorders. In claustrophobic people, this translates as panicking or overreacting to a situation in which the person finds themselves physically confined.

Classical conditioning
Claustrophobia results as the mind comes to connect confinement with danger. It often comes as a consequence of a traumatic childhood experience, although the onset can come at any point in an individuals life. Such an experience can occur multiple times, or only once, to make a permanent impression on the mind. The majority of claustrophobic participants in an experiment done by Lars-Göran Öst reported that their phobia had been "acquired as a result of a conditioning experience". In most cases, claustrophobia seems to be the result of past experiences.

Conditioning experiences
A few examples of common experiences that could result in the onset of claustrophobia in children (or adults) are as follows:

A child (or, less commonly, an adult) is shut into a pitch-black room and cannot find the door or the light-switch.
A child gets shut into a box.
A child is locked in a closet.
A child falls into a deep pool and cannot swim.
A child gets separated from their parents in a large crowd and gets lost.
A child sticks their head between the bars of a fence and then cannot get back out.
A child crawls into a hole and gets stuck, or cannot find their way back.
A child is left in their parents car, truck, or van.
A child is in a crowded area with no windows (a classroom, basement, etc.) and has run-ins with other people, or is put there as a means of punishment.The term past experiences, according to one author, can extend to the moment of birth. In John A. Speyrers "Claustrophobia and the Fear of Death and Dying", the reader is brought to the conclusion that claustrophobias high frequency is due to birth trauma, about which he says is "one of the most horrendous experiences we can have during our lifetime", and it is in this helpless moment that the infant develops claustrophobia.

Magnetic resonance imaging (MRI) can trigger claustrophobia. An MRI scan entails lying still for some time in a narrow tube. In a study involving claustrophobia and MRI, it was reported that 13% of patients experienced a panic attack during the procedure. The procedure has been linked not only to the triggering of preexisting claustrophobia, but also to the onset of the condition in some people. Panic attacks experienced during the procedure can stop the person from adjusting to the situation, thereby perpetuating the fear.

S.J. Rachman tells of an extreme example, citing the experience of 21 miners. These miners were trapped underground for 14 days, during which six of the miners died of suffocation. After their rescue, ten of the miners were studied for ten years. All but one were greatly affected by the experience, and six developed phobias to "confining or limiting situations". The only miner who did not develop any noticeable symptoms was the one who acted as leader.Another factor that could cause the onset of claustrophobia is "information received". As Aureau Walding states in "Causes of Claustrophobia", many people, especially children, learn who and what to fear by watching parents or peers. This method does not only apply to observing a teacher, but also observing victims. Vicarious classical conditioning also includes when a person sees another person exposed directly to an especially unpleasant situation. This would be analogous to observing someone getting stuck in a tight space, suffocated, or any of the other examples that were listed above.

Prepared phobia
There is research that suggests that claustrophobia is not entirely a classically conditioned or learned phobia. It is not necessarily an inborn fear, but it is very likely what is called a prepared phobia. As Erin Gersley says in "Phobias: Causes and Treatments", humans are genetically predisposed to become afraid of things that are dangerous to them. Claustrophobia may fall under this category because of its "wide distribution… early onset and seeming easy acquisition, and its non-cognitive features." The acquisition of claustrophobia may be part of a vestigial evolutionary survival mechanism, a dormant fear of entrapment and/or suffocation that was once important for the survival of humanity and could be easily awakened at any time. Hostile environments in the past would have made this kind of pre-programmed fear necessary, and so the human mind developed the capacity for "efficient fear conditioning to certain classes of dangerous stimuli".Rachman provides an argument for this theory in his article: "Phobias". He agrees with the statement that phobias generally concern objects that constitute a direct threat to human survival, and that many of these phobias are quickly acquired because of an "inherited biological preparedness". This brings about a prepared phobia, which is not quite innate, but is widely and easily learned. As Rachman explains in the article: "The main features of prepared phobias are that they are very easily acquired, selective, stable, biologically significant, and probably [non-cognitive]." Selective and biologically significant mean that they only relate to things that directly threaten the health, safety, or survival of an individual. Non-cognitive suggests that these fears are acquired unconsciously. Both factors point to the theory that claustrophobia is a prepared phobia that is already pre-programmed into the mind of a human being.

Diagnosis
Claustrophobia is the fear of being closed into a small space. It is typically classified as an anxiety disorder and often results in a rather severe panic attack. It is also confused sometimes with Cleithrophobia (the fear of being trapped).Diagnosis of claustrophobia usually transpires from a consultation about other anxiety-related conditions. Certain criteria have to be met to be diagnosed with specific phobias. This criteria includes:
an interminable obstructive or excessive fear caused by the existence or anticipation of a specific situation
anxiety response when stimulus is exhibited; can result in panic attacks in adults or, for children, an outburst, clinging, crying, etc.
acknowledgment by adult patients that their fear stems from the anticipated threat or danger
engaging in procedures to evade dreaded object or situation, or proneness to face the situation but with discomfort or anxiety
the persons evasion of the object or situation impedes with everyday life and relationships
the phobia is continuous, usually for 6 months or longer
symptoms cannot be ascribed to other underlying mental conditions, such as obsessive-compulsive disorder (OCD) or post-traumatic stress disorder (PTSD)

Scale
This method was developed in 1979 by interpreting the files of patients diagnosed with claustrophobia and by reading various scientific articles about the diagnosis of the disorder. Once an initial scale was developed, it was tested and sharpened by several experts in the field. Today, it consists of 20 questions that determine anxiety levels and desire to avoid certain situations. Several studies have proved this scale to be effective in claustrophobia diagnosis.

Questionnaire
This method was developed by Rachman and Taylor, two experts in the field, in 1993. This method is effective in distinguishing symptoms stemming from fear of suffocation. In 2001, it was modified from 36 to 24 items by another group of field experts. This study has also been proven very effective by various studies.

Treatment
Cognitive therapy
Cognitive therapy is a widely accepted form of treatment for most anxiety disorders. It is also thought to be particularly effective in combating disorders where the patient does not actually fear a situation but, rather, fears what could result from being in such a situation. The ultimate goal of cognitive therapy is to modify distorted thoughts or misconceptions associated with whatever is being feared; the theory is that modifying these thoughts will decrease anxiety and avoidance of certain situations. For example, cognitive therapy would attempt to convince a claustrophobic patient that elevators are not dangerous but are, in fact, very useful in getting you where you would like to go faster. A study conducted by S.J. Rachman shows that cognitive therapy decreased fear and negative thoughts/connotations by an average of around 30% in claustrophobic patients tested, proving it to be a reasonably effective method.

In vivo exposure
This method forces patients to face their fears by complete exposure to whatever fear they are experiencing. This is usually done in a progressive manner starting with lesser exposures and moving upward towards severe exposures. For example, a claustrophobic patient would start by going into an elevator and work up to an MRI. Several studies have proven this to be an effective method in overcoming various phobias, claustrophobia included. S.J. Rachman has also tested the effectiveness of this method in treating claustrophobia and found it to decrease fear and negative thoughts/connotations by an average of nearly 75% in his patients. Of the methods he tested in this particular study, this was by far the most significant reduction.

Interoceptive exposure
This method attempts to recreate internal physical sensations within a patient in a controlled environment and is a less intense version of in vivo exposure. This was the final method of treatment tested by S.J. Rachman in his 1992 study. It lowered fear and negative thoughts/connotations by about 25%. These numbers did not quite match those of in vivo exposure or cognitive therapy, but still resulted in significant reductions.Other forms of treatment that have also been shown to be reasonably effective are psychoeducation, counter-conditioning, regressive hypnotherapy and breathing re-training. Medications often prescribed to help treat claustrophobia include antidepressants and beta blockers, which help to relieve the heart-pounding symptoms often associated with anxiety attacks.

See also
Agoraphobia
List of phobias
Premature burial

References
Bibliography
Carlson, Neil R., et al. Psychology: the Science of Behavior, 7th ed. Allyn & Bacon, Pearson. 2010.
Cheng, Dominic T., et al. "Human Amygdala Activity During the Expression of Fear Responses". Behavioral Neuroscience. Vol. 120. American Psychological Association. 14 September 2006.
Fritscher, Lisa. "Claustrophobia: Fear of Enclosed Spaces". About.com. New York Times Company. 21 September 2009. Web. 9 September 2010.
Gersley, Erin. "Phobias: Causes and Treatments". AllPsych Journal. AllPsych Online. 17 November 2001. Web. 18 September 2010.
Hayano, Fumi PhD., et al. "Smaller Amygdala Is Associated With Anxiety in Patients With Panic Disorder". Psychiatry and Clinical Neurosciences. Vol. 63, Issue 3. Japanese Society of Psychiatry and Neurology 14 May 2009.
Öst, Lars-Göran. "The Claustrophobia Scale: A Psychometric Evaluation". Behaviour Research and Therapy 45.5 (2007): 1053–64.
Rachman, S.J. "Claustrophobia", in Phobias: A Handbook of Theory, Research, and Treatment. John Wiley and Sons, Ltd. Baffins Lane, Chichester, West Sussex, England. 1997.
Rachman, S.J. "Phobias". Education.com. The Gale Group. 2009. Web. 19 September 2010.
Speyrer, John A. "Claustrophobia and the Fear of Death and Dying". The Primal Psychotherapy Page. N.p. 3 October 1995. Web. 9 September 2010.
Thorpe, Susan, Salkovis, Paul M., & Dittner, Antonia. "Claustrophobia in MRI: the Role of Cognitions". Magnetic Resonance Imaging. Vol. 26, Issue 8. 3 June 2008.
Walding, Aureau </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Altered level of consciousness and can you explain it in depth? [/INST] An altered level of consciousness is any measure of arousal other than normal.  Level of consciousness (LOC) is a measurement of a persons arousability and responsiveness to stimuli from the environment.  A mildly depressed level of consciousness or alertness may be classed as lethargy; someone in this state can be aroused with little difficulty.  People who are obtunded have a more depressed level of consciousness and cannot be fully aroused.  Those who are not able to be aroused from a sleep-like state are said to be stuporous. Coma is the inability to make any purposeful response.   Scales such as the Glasgow coma scale have been designed to measure the level of consciousness.
An altered level of consciousness can result from a variety of factors, including alterations in the chemical environment of the brain (e.g. exposure to poisons or intoxicants), insufficient oxygen or blood flow in the brain, and excessive pressure within the skull.  Prolonged unconsciousness is understood to be a sign of a medical emergency.  A deficit in the level of consciousness suggests that both of the cerebral hemispheres or the reticular activating system have been injured.  A decreased level of consciousness correlates to increased morbidity (sickness) and mortality (death). Thus it is a valuable measure of a patients medical and neurological status. In fact, some sources consider level of consciousness to be one of the vital signs.

Definition
Scales and terms to classify the levels of consciousness differ, but in general, reduction in response to stimuli indicates an altered level of consciousness:

Altered level of consciousness is sometimes described as altered sensorium.

Glasgow Coma Scale
The most commonly used tool for measuring LOC objectively is the Glasgow Coma Scale (GCS).  It has come into almost universal use for assessing people with brain injury, or an altered level of consciousness. Verbal, motor, and eye-opening responses to stimuli are measured, scored, and added into a final score on a scale of 3–15, with a lower score being a more decreased level of consciousness.

Others
The AVPU scale is another means of measuring LOC: people are assessed to determine whether they are alert, responsive to verbal stimuli, responsive to painful stimuli, or unresponsive.  To determine responsiveness to voice, a caregiver speaks to, or, failing that, yells at the person.  Responsiveness to pain is determined with a mild painful stimulus such as a pinch; moaning or withdrawal from the stimulus is considered a response to pain.  The ACDU scale, like AVPU, is easier to use than the GCS and produces similarly accurate results.  Using ACDU, a patient is assessed for alertness, confusion, drowsiness, and unresponsiveness.The Grady Coma Scale classes people on a scale of I to V along a scale of confusion, stupor, deep stupor, abnormal posturing, and coma.

Pathophysiology
Although the neural science behind alertness, wakefulness, and arousal are not fully known, the reticular formation is known to play a role in these.  The ascending reticular activating system is a postulated group of neural connections that receives sensory input and projects to the cerebral cortex through the midbrain and thalamus from the reticular formation. Since this system is thought to modulate wakefulness and sleep, interference with it, such as injury, illness, or metabolic disturbances, could alter the level of consciousness.Normally, stupor and coma are produced by interference with the brain stem, such as can be caused by a lesion or indirect effects, such as brain herniation.  Mass lesions in the brain stem normally cause coma due to their effects on the reticular formation. Mass lesions that occur above the tentorium cerebelli normally do not significantly alter the level of consciousness unless they are very large or affect both cerebral hemispheres.

Diagnosis
Assessing LOC involves determining an individuals response to external stimuli.  Speed and accuracy of responses to questions and reactions to stimuli such as touch and pain are noted. Reflexes, such as the cough and gag reflexes, are also means of judging LOC.  Once the level of consciousness is determined, clinicians seek clues for the cause of any alteration. Usually the first tests in the ER are pulse oximetry to determine if there is hypoxia, serum glucose levels to rule out hypoglycemia. A urine drug screen may be sent. A CT head is very important to obtain to rule out bleed. In cases where meningitis is suspected, a lumbar puncture must be performed. A serum TSH is an important test to order. In select groups consider vitamin B12 levels. Checking serum ammonia is particularly advised in neonatal coma to discern inborn errors of metabolism.

Differential diagnosis
A lowered level of consciousness indicate a deficit in brain function.  Level of consciousness can be lowered when the brain receives insufficient oxygen (as occurs in hypoxia); insufficient blood (as occurs in shock, in children for example due to intussusception); or has an alteration in the brains chemistry. Metabolic disorders such as diabetes mellitus and uremia can alter consciousness. Hypo- or hypernatremia (decreased and elevated levels of sodium, respectively) as well as dehydration can also produce an altered LOC </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Diplopia and can you explain it in depth? [/INST] Diplopia is the simultaneous perception of two images of a single object that may be displaced horizontally or vertically in relation to each other. Also called double vision, it is a loss of visual focus under regular conditions, and is often voluntary. However, when occurring involuntarily, it results in impaired function of the extraocular muscles, where both eyes are still functional, but they cannot turn to target the desired object. Problems with these muscles may be due to mechanical problems, disorders of the neuromuscular junction, disorders of the cranial nerves (III, IV, and VI) that innervate the muscles, and occasionally disorders involving the supranuclear oculomotor pathways or ingestion of toxins.Diplopia can be one of the first signs of a systemic disease, particularly to a muscular or neurological process, and it may disrupt a persons balance, movement, or reading abilities.

Causes
Diplopia has a diverse range of ophthalmologic, infectious, autoimmune, neurological, and neoplastic causes:

Papilledema

Diagnosis
Diplopia is diagnosed mainly by information from the patient. Doctors may use blood tests, physical examinations, computed tomography (CT), or magnetic resonance imaging (MRI) to find the underlying cause.Classification
One of the first steps in diagnosing diplopia is often to see whether one of two major classifications may be eliminated. That involves blocking one eye to see which symptoms are evident in each eye alone. Persisting blurry or double vision with one eye closed is classified as monocular diplopia.

Binocular
Binocular diplopia is double vision arising as a result of strabismus(in laymans terms "cross-eyed"), the misalignment of the two eyes relative to each other, either esotropia (inward) or exotropia (outward). In such a case while the fovea of one eye is directed at the object of regard, the fovea of the other is directed elsewhere, and the image of the object of regard falls on an extrafoveal area of the retina. Acute diplopia is a diagnostic challenge. The most common cause of acute diplopia are ocular motor nerve palsies (OMP).The brain calculates the visual direction of an object based upon the position of its image relative to the fovea. Images falling on the fovea are seen as being directly ahead, while those falling on retina outside the fovea may be seen as above, below, right, or left of straight ahead depending upon the area of retina stimulated. Thus, when the eyes are misaligned, the brain perceives two images of one target object, as the target object simultaneously stimulates different, noncorresponding, retinal areas in either eye, thus producing double vision.This correlation of particular areas of the retina in one eye with the same areas in the other is known as retinal correspondence. This relationship also gives rise to an associated phenomenon of binocular diplopia, although one that is rarely noted by those experiencing diplopia. Because the fovea of one eye corresponds to the fovea of the other, images falling on the two foveae are projected to the same point in space. Thus, when the eyes are misaligned, two different objects will be perceived as superimposed in the same space. This phenomenon is known as visual confusion.The brain naturally guards against double vision. In an attempt to avoid double vision, the brain can sometimes ignore the image from one eye, a process known as suppression. The ability to suppress is to be found particularly in childhood when the brain is still developing. Thus, those with childhood strabismus almost never complain of diplopia, while adults who develop strabismus almost always do. While this ability to suppress might seem an entirely positive adaptation to strabismus, in the developing child, this can prevent the proper development of vision in the affected eye, resulting in amblyopia. Some adults are also able to suppress their diplopia, but their suppression is rarely as deep or as effective and takes much longer to establish,  thus they are not at risk of permanently compromising their vision. In some cases, diplopia disappears without medical intervention, but in other cases, the cause of the double vision may still be present.
Certain people with diplopia who cannot achieve fusion and yet do not suppress may display a certain type of spasm-like irregular movement of the eyes in the vicinity of the fixation point (see: Horror fusionis).

Monocular
Diplopia can also occur when viewing with only one eye; this is called monocular diplopia, or where the patient perceives more than two images, monocular polyopia.  While serious causes rarely may be behind monocular diplopia symptoms, this is much less often the case than with binocular diplopia. The differential diagnosis of multiple image perception includes the consideration of such conditions as corneal surface keratoconus, subluxation of the lens, a structural defect within the eye, a lesion in the anterior visual cortex, or nonorganic conditions, but diffraction-based (rather than geometrical) optical models have shown that common optical conditions, especially astigmatism, can also produce this symptom.

Temporary
Temporary binocular diplopia can be caused by alcohol intoxication or head injuries, such as concussion (if temporary double vision does not resolve quickly, one should see an optometrist or ophthalmologist immediately). It can also be a side effect of benzodiazepines or opioids, particularly if used in larger doses for recreation, the antiepileptic drugs phenytoin and zonisamide, and the anticonvulsant drug lamotrigine, as well as the hypnotic drug zolpidem and the dissociative drugs ketamine and dextromethorphan. Temporary diplopia can also be caused by tired or strained eye muscles. If diplopia appears with other symptoms such as fatigue and acute or chronic pain, the patient should see an ophthalmologist immediately.

Voluntary
Some people are able to consciously uncouple their eyes, either by overfocusing closely (i.e. going cross-eyed) or unfocusing.  Also, while looking at one object behind another object, the foremost objects image is doubled (for example, placing ones finger in front of ones face while reading text on a computer monitor). In this sense, double vision is neither dangerous nor harmful, and may even be enjoyable </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Thyroiditis and can you explain it in depth? [/INST] Thyroiditis is the inflammation of the thyroid gland. The thyroid gland is located on the front of the neck below the laryngeal prominence, and makes hormones that control metabolism.

Signs and symptoms
There are many different signs and symptoms for thyroiditis, none of which are exclusively limited to this disease. Many of the signs imitate symptoms of other diseases, so thyroiditis can sometimes be difficult to diagnose. Common hypothyroid symptoms manifest when thyroid cell damage is slow and chronic, and may include fatigue, weight gain, feeling "fuzzy headed", depression, dry skin, and constipation. Other, rarer symptoms include swelling of the legs, vague aches and pains, decreased concentration and so on. When conditions become more severe, depending on the type of thyroiditis, one may start to see puffiness around the eyes, slowing of the heart rate, a drop in body temperature, or even incipient heart failure. On the other hand, if the thyroid cell damage is acute, the thyroid hormone within the gland leaks out into the bloodstream causing symptoms of thyrotoxicosis, which is similar to those of hyperthyroidism. These symptoms include weight loss, irritability, anxiety, insomnia, fast heart rate, and fatigue. Elevated levels of thyroid hormone in the bloodstream cause both conditions, but thyrotoxicosis is the term used with thyroiditis since the thyroid gland is not overactive, as in the case of hyperthyroidism.

Causes
Thyroiditis is generally caused by an immune system attack on the thyroid, resulting in inflammation and damage to the thyroid cells. This disease is often considered a malfunction of the immune system and can be associated with IgG4-related systemic disease, in which symptoms of autoimmune pancreatitis, retroperitoneal fibrosis and noninfectious aortitis also occur. Such is also the case in Riedel thyroiditis, an inflammation in which the thyroid tissue is replaced by fibrous tissue which can extend to neighbouring structures. Antibodies that attack the thyroid are what causes most types of thyroiditis. It can also be caused by an infection, like a virus or bacteria, which works in the same way as antibodies to cause inflammation in the glands, such as in the case of subacute granulomatous thyroiditis (de Quervain). Certain people make thyroid antibodies, and thyroiditis can be considered an autoimmune disease, because the body acts as if the thyroid gland is foreign tissue. Some drugs, such as interferon, lithium, amiodarone and immune check point inhibitors can also cause thyroiditis.

Diagnosis
The most common and helpful way to diagnose thyroiditis is first for a physician to palpate the thyroid gland during a physical examination. Laboratory tests allow doctors to evaluate the patient for elevated erythrocyte sedimentation rates, elevated thyroglobulin levels, and depressed radioactive iodine uptake (Mather, 2007). Blood tests also help to determine the kind of thyroiditis and to see how much thyroid stimulating hormone the pituitary gland is producing and what antibodies are present in the body. In some cases, a biopsy may be needed to find out what is attacking the thyroid.

Classification
Thyroiditis is a group of disorders that all cause thyroidal inflammation. Forms of the disease are Hashimotos thyroiditis, the most common cause of hypothyroidism in the US, postpartum thyroiditis, subacute thyroiditis, silent thyroiditis, drug-induced thyroiditis, radiation-induced thyroiditis, acute thyroiditis, and Riedels thyroiditis.Each different type of this disease has its own causes, clinical features, diagnoses, durations, resolutions, conditions, and risks.

Treatment
Treatments for this disease depend on the type of thyroiditis that is diagnosed. For the most common type, which is known as Hashimotos thyroiditis, the treatment is to immediately start hormone replacement </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is West Nile fever and can you explain it in depth? [/INST] West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes. In about 80% of infections people have few or no symptoms. About 20% of people develop a fever, headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10 percent.West Nile virus (WNV) is usually spread by mosquitoes that become infected when they feed on infected birds, which often carry the disease. Rarely the virus is spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding, but it otherwise does not spread directly between people. Risks for severe disease include being over 60 years old and having other health problems. Diagnosis is typically based on symptoms and blood tests.There is no human vaccine. The best way to reduce the risk of infection is to avoid mosquito bites. Mosquito populations may be reduced by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. When mosquitoes cannot be avoided, mosquito repellent, window screens, and mosquito nets reduce the likelihood of being bitten. There is no specific treatment for the disease; pain medications may reduce symptoms.The virus was discovered in Uganda in 1937, and was first detected in North America in 1999. WNV has occurred in Europe, Africa, Asia, Australia, and North America. In the United States thousands of cases are reported a year, with most occurring in August and September. It can occur in outbreaks of disease. Severe disease may also occur in horses, for which a vaccine is available. A surveillance system in birds is useful for early detection of a potential human outbreak.

Signs and symptoms
About 80% of those infected with West Nile virus (WNV) show no symptoms and go unreported. About 20% of infected people develop symptoms. These vary in severity, and begin 3 to 14 days after being bitten. Most people with mild symptoms of WNV recover completely, though fatigue and weakness may last for weeks or months. Symptoms may range from mild, such as fever, to severe, such as paralysis and meningitis. A severe infection can last weeks and can, rarely, cause permanent brain damage. Death may ensue if the central nervous system is affected. Medical conditions such as cancer and diabetes, and age over 60 years, increase the risk of developing severe symptoms.Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, meningoencephalitis, and it may or may not be present in poliomyelitis-like syndrome. Thus, headache is not a useful indicator of neuroinvasive disease.

West Nile fever (WNF), which occurs in 20 percent of cases, is a febrile syndrome that causes flu-like symptoms. Most characterizations of WNF describe it as a mild, acute syndrome lasting 3 to 6 days after symptom onset. Systematic follow-up studies of patients with WNF have not been done, so this information is largely anecdotal. Possible symptoms include high fever, headache, chills, excessive sweating, weakness, fatigue, swollen lymph nodes, drowsiness, pain in the joints and flu-like symptoms. There may be gastrointestinal symptoms including nausea, vomiting, loss of appetite, and diarrhea. Fewer than one-third of patients develop a rash.
West Nile neuroinvasive disease (WNND), which occurs in less than 1 percent of cases, is when the virus infects the central nervous system resulting in meningitis, encephalitis, meningoencephalitis or a poliomyelitis-like syndrome. Many patients with WNND have normal neuroimaging studies, although abnormalities may be present in various cerebral areas including the basal ganglia, thalamus, cerebellum, and brainstem.
West Nile virus encephalitis (WNE) is the most common neuroinvasive manifestation of WNND. WNE presents with similar symptoms to other viral encephalitis with fever, headaches, and altered mental status. A prominent finding in WNE is muscular weakness (30 to 50 percent of patients with encephalitis), often with lower motor neuron symptoms, flaccid paralysis, and hyporeflexia with no sensory abnormalities.
West Nile meningitis (WNM) usually involves fever, headache, stiff neck and pleocytosis, an increase of white blood cells in cerebrospinal fluid. Changes in consciousness are not usually seen and are mild when present.
West Nile meningoencephalitis is inflammation of both the brain (encephalitis) and meninges (meningitis).
West Nile poliomyelitis (WNP), an acute flaccid paralysis syndrome associated with WNV infection, is less common than WNM or WNE. This syndrome is generally characterized by the acute onset of asymmetric limb weakness or paralysis in the absence of sensory loss. Pain sometimes precedes the paralysis. The paralysis can occur in the absence of fever, headache, or other common symptoms associated with WNV infection. Involvement of respiratory muscles, leading to acute respiratory failure, sometimes occurs.
West-Nile reversible paralysis, Like WNP, the weakness or paralysis is asymmetric. Reported cases have been noted to have an initial preservation of deep tendon reflexes, which is not expected for a pure anterior horn involvement. Disconnect of upper motor neuron influences on the anterior horn cells possibly by myelitis or glutamate excitotoxicity have been suggested as mechanisms. The prognosis for recovery is excellent.
Nonneurologic complications of WNV infection that may rarely occur include fulminant hepatitis, pancreatitis, myocarditis, rhabdomyolysis, orchitis, nephritis, optic neuritis and cardiac dysrhythmias and hemorrhagic fever with coagulopathy. Chorioretinitis may also be more common than previously thought.
Skin manifestations, specifically rashes, are common; however, there are few detailed descriptions in case reports, and few images are available. Punctate erythematous, macular, and papular eruptions, most pronounced on the extremities have been observed in WNV cases and in some cases histopathologic findings have shown a sparse superficial perivascular lymphocytic infiltrate, a manifestation commonly seen in viral exanthems. A literature review provides support that this punctate rash is a common cutaneous presentation of WNV infection.

Cause
Virology
WNV is one of the Japanese encephalitis antigenic serocomplex of viruses.
Image reconstructions and cryoelectron microscopy reveal a 45–50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus Flavivirus within the family Flaviviridae. The genetic material of WNV is a positive-sense, single strand of RNA, which is between 11,000 and 12,000 nucleotides long; these genes encode seven nonstructural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12-kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral membrane proteins.West Nile virus has been seen to replicate faster and spread more easily to birds at higher temperatures; one of several ways climate change could affect the epidemiology of this disease.

Transmission
The prime method of spread of the West Nile virus (WNV) is the female mosquito. In Europe, cats were identified as being hosts for West Nile virus.
The important mosquito vectors vary according to area; in the United States, Culex pipiens (Eastern United States, and urban and residential areas of the United States north of 36–39°N), Culex tarsalis (Midwest and West), and Culex quinquefasciatus (Southeast) are the main vector species.The mosquito species that are most frequently infected with WNV feed primarily on birds. Different species of mosquitos take a blood meal from different types of vertebrate hosts, Mosquitoes show further selectivity, exhibiting preference for different species of birds. In the United States, WNV mosquito vectors feed preferentially on members of the Corvidae and thrush family. Among the preferred species within these families are the American crow, a corvid, and the American robin (Turdus migratorius).Some species of birds develop sufficient viral levels (>~104.2 log PFU/ml;) after being infected to transmit the infection to biting mosquitoes that in turn go on to infect other birds. In birds that die from WNV, death usually occurs after 4 to 6 days.  In mammals and several species of birds, the virus does not multiply as readily and so does not develop high viremia during infection.  Mosquitoes biting such hosts are not believed to ingest sufficient virus to become infected, making them so-called dead-end hosts.  As a result of the differential infectiousness of hosts, the feeding patterns of mosquitoes play an important role in WNV transmission, and they are partly genetically controlled, even within a species.Direct human-to-human transmission initially was believed to be caused only by occupational exposure, such as in a laboratory setting, or conjunctival exposure to infected blood. The US outbreak identified additional transmission methods through blood transfusion, organ transplant, intrauterine exposure, and breast feeding. Since 2003, blood banks in the United States routinely screen for the virus among their donors. As a precautionary measure, the UKs National Blood Service initially ran a test for this disease in donors who donate within 28 days of a visit to the United States, Canada, or the northeastern provinces of Italy, and the Scottish National Blood Transfusion Service asks prospective donors to wait 28 days after returning from North America or the northeastern provinces of Italy before donating. There also have been reports of possible transmission of the virus from mother to child during pregnancy or breastfeeding or exposure to the virus in a lab, but these are rare cases and not conclusively confirmed.Recently, the potential for mosquito saliva to affect the course of WNV disease was demonstrated.  Mosquitoes inoculate their saliva into the skin while obtaining blood. Mosquito saliva is a pharmacological cocktail of secreted molecules, principally proteins, that can affect vascular constriction, blood coagulation, platelet aggregation, inflammation, and immunity. It clearly alters the immune response in a manner that may be advantageous to a virus. Studies have shown it can specifically modulate the immune response during early virus infection, and mosquito feeding can exacerbate WNV infection, leading to higher viremia and more severe forms of disease.

Vertical transmission
Vertical transmission, the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature. Mosquito progeny infected vertically in autumn may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring, although it likely plays little role in transmission in the summer and fall.

Risk factors
Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation.   For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene CCR5 gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of CCR5 made up 4.0 to 4.5% of a sample of people with West Nile disease, while the incidence of the gene in the general population is only 1.0%.The most at risk occupations in the U.S. are outdoor workers, for example farmers, loggers, landscapers/groundskeepers, construction workers, painters, summer camp workers and pavers. Two reports of accidental exposure by laboratory personnel working with infected fluids or tissues have been received. While this appears to be a rare occurrence, it highlights the need for proper handling of infected materials. The World Health Organization states that there are no known cases of health care workers acquiring the virus from infected patients when the appropriate infection control precautions are observed.

Diagnosis
Preliminary diagnosis is often based on the patients clinical symptoms, places and dates of travel (if patient is from a nonendemic country or area), activities, and epidemiologic history of the location where infection occurred. A recent history of mosquito bites and an acute febrile illness associated with neurologic signs and symptoms should cause clinical suspicion of WNV.Diagnosis of West Nile virus infections is generally accomplished by serologic testing of blood serum or cerebrospinal fluid (CSF), which is obtained via a lumbar puncture. Initial screening could be done using the ELISA technique detecting immunoglobulins in the sera of the tested individuals.Typical findings of WNV infection include lymphocytic pleocytosis, elevated protein level, reference glucose and lactic acid levels, and no erythrocytes.Definitive diagnosis of WNV is obtained through detection of virus-specific antibody IgM and neutralizing antibodies. Cases of West Nile virus meningitis and encephalitis that have been serologically confirmed produce similar degrees of CSF pleocytosis and are often associated with substantial CSF neutrophilia.
Specimens collected within eight days following onset of illness may not test positive for West Nile IgM, and testing should be repeated. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavivirus infection and is not by itself evidence of an acute West Nile virus infection.If cases of suspected West Nile virus infection, sera should be collected on both the acute and
convalescent phases of the illness.  Convalescent specimens should be collected 2–3 weeks after acute specimens.
It is common in serologic testing for cross-reactions to occur among flaviviruses such as dengue virus (DENV) and tick-borne encephalitis virus; this necessitates caution when evaluating serologic results of flaviviral infections.Four FDA-cleared WNV IgM ELISA kits are commercially available from different manufacturers in the U.S., each of these kits is indicated for use on serum to aid in the presumptive laboratory diagnosis of WNV infection in patients with clinical symptoms of meningitis or encephalitis. Positive WNV test results obtained via use of these kits should be confirmed by additional testing at a state health department laboratory or CDC.In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry, and virus culture of autopsy tissues can also be useful. Only a few state laboratories or other specialized laboratories, including those at CDC, are capable of doing this specialized testing.

Differential diagnosis
A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing using polymerase chain reaction (PCR) testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis.

Prevention
Many of the guidelines for preventing occupational West Nile virus exposure are common to all mosquito-borne diseases.Public health measures include taking steps to reduce mosquito populations. Personal recommendations are to reduce the likelihood of being bitten. General measures to avoid bites include:

Using insect repellent on exposed skin to repel mosquitoes. Repellents include products containing DEET and picaridin. DEET concentrations of 30% to 50% are effective for several hours. Picaridin, available at 7% and 15% concentrations, needs more frequent application. DEET formulations as high as 30% are recommended for children over two months of age. The CDC also recommends the use of: IR3535, oil of lemon eucalyptus, para-menthane-diol, or 2-undecanone.  Protect infants less than two months of age by using a carrier draped with mosquito netting with an elastic edge for a tight fit.
When using sunscreen, apply sunscreen first and then repellent. Repellent should be washed off at the end of the day before going to bed.
Wear long-sleeve shirts, which should be tucked in, long trousers, socks, and hats to cover exposed skin (although most fabrics do not totally protect against bites). Insect repellents should be applied over top of protective clothing for greater protection. Do not apply insect repellents underneath clothing.
Repellents containing permethrin (e.g., Permanone) or other insect repellents may be applied to clothing, shoes, tents, mosquito nets, and other gear. (Permethrin is not suitable for use directly on skin.) Most repellent is generally removed from clothing and gear by a single washing, but permethrin-treated clothing is effective for up to five washings.
Most mosquitoes that transmit disease are most active at dawn and in the evening dusk. A notable exception is the Asian tiger mosquito, which is a daytime feeder and is more apt to be found in, or on the periphery of, shaded areas with heavy vegetation. They are now widespread in the United States, and in Florida they have been found in all 67 counties.
In an at-risk area, staying in air-conditioned or well-screened room, or sleeping under an insecticide-treated bed net is recommended. Bed nets should be tucked under mattresses, and can be sprayed with a repellent if not already treated with an insecticide.

Monitoring and control
West Nile virus can be sampled from the environment by the pooling of trapped mosquitoes via ovitraps, carbon dioxide-baited light traps, and gravid traps, testing blood samples drawn from wild birds, dogs, and sentinel monkeys, and testing brains of dead birds found by various animal control agencies and the public.Testing of the mosquito samples requires the use of reverse-transcriptase PCR (RT-PCR) to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC) or enzyme-linked immunosorbent assay (ELISA).Dead birds, after necropsy, or their oral swab samples collected on specific RNA-preserving filter paper card, can have their virus presence tested by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate-enzyme reaction.
West Nile control is achieved through mosquito control, by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas, and targeting the adult population via lethal ovitraps and aerial spraying of pesticides.
Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives that may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern United States, Culex pipiens, is a canopy feeder.

Treatment
No specific treatment is available for WNV infection. Most people recover without treatment. In mild cases, over-the-counter pain relievers can help ease mild headaches and muscle aches in adults. In severe cases supportive care is provided, often in hospital, with intravenous fluids, pain medication, respiratory support, and prevention of secondary infections.

Prognosis
While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60 to 90 days to recover. Patients with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple somatic complaints such as tremor, and dysfunction in motor skills and executive functions for over a year. People with milder symptoms are just as likely as people with more severe symptoms to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue.  One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.

Epidemiology
WNV was first isolated from a feverish 37-year-old woman at Omogo in the West Nile District of Uganda in 1937 during research on yellow fever virus.  A series of serosurveys in 1939 in central Africa found anti-WNV positive results ranging from 1.4% (Congo) to 46.4% (White Nile region, Sudan). It was subsequently identified in Egypt (1942) and India (1953), a 1950 serosurvey in Egypt found 90% of those over 40 years in age had WNV antibodies. The ecology was characterized in 1953 with studies in Egypt and Israel. The virus became recognized as a cause of severe human meningoencephalitis in elderly patients during an outbreak in Israel in 1957. The disease was first noted in horses in Egypt and France in the early 1960s and found to be widespread in southern Europe, southwest Asia and Australia.The first appearance of WNV in the Western Hemisphere was in 1999  with encephalitis reported in humans, dogs, cats, and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus. The American outbreak began in College Point, Queens in New York City and was later spread to the neighboring states of New Jersey and Connecticut. The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence.  West Nile virus is now endemic in Africa, Europe, the Middle East, west and central Asia, Oceania (subtype Kunjin), and most recently, North America and is spreading into Central and South America.
Outbreaks of West Nile virus encephalitis in humans have occurred in Algeria (1994), Romania (1996 to 1997), the Czech Republic (1997), Congo (1998), Russia (1999), the United States (1999 to 2009), Canada (1999–2007), Israel (2000) and Greece (2010).
Epizootics of disease in horses occurred in Morocco (1996), Italy (1998), the United States (1999 to 2001), and France (2000), Mexico (2003) and Sardinia (2011).
Outdoor workers (including biological fieldworkers, construction workers, farmers, landscapers, and painters), healthcare personnel, and laboratory personnel who perform necropsies on animals are at risk of contracting WNV.In 2012, the US experienced one of its worst epidemics in which 286 people died, with the state of Texas being hard hit by this virus.

Weather
Drought has been associated with a higher number of West Nile virus cases in the following year. As drought can decrease fish and other populations that eat mosquito eggs, higher numbers of mosquitoes can result. Higher temperatures are linked to decreased time for replication and increased viral load in birds and mosquitoes.

Research
A vaccine for horses (ATCvet code: QI05AA10 (WHO)) based on killed viruses exists; some zoos have given this vaccine to their birds, although its effectiveness is unknown. Dogs and cats show few if any signs of infection. There have been no known cases of direct canine-human or feline-human transmission; although these pets can become infected, it is unlikely they are, in turn, capable of infecting native mosquitoes and thus continuing the disease cycle. AMD3100, which had been proposed as an antiretroviral drug for HIV, has shown promise against West Nile encephalitis. Morpholino antisense oligos conjugated to cell penetrating peptides have been shown to partially protect mice from WNV disease. There have also been attempts to treat infections using ribavirin, intravenous immunoglobulin, or alpha interferon. GenoMed, a U.S. biotech company, has found that blocking angiotensin II can treat the "cytokine storm" of West Nile virus encephalitis as well as other viruses.As of 2019, six vaccines had progressed to human trials but none had been licensed in the United States. Only the two live attenuated vaccines produced strong immunity after a single dose.

References
External links

De Filette M, Ulbert S, Diamond M, Sanders NN (2012). "Recent progress in West Nile virus diagnosis and vaccination" </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Obstruction and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Microscopic colitis and can you explain it in depth? [/INST] Microscopic colitis refers to two related medical conditions which cause diarrhea: collagenous colitis and lymphocytic colitis. Both conditions are characterized by the presence of chronic non-bloody watery diarrhea, normal appearances on colonoscopy and characteristic histopathology findings of inflammatory cells.

Signs and symptoms
The main symptom is persistent non-bloody watery diarrhea, which may be profuse. People may also experience abdominal pain, fecal incontinence, and unintentional weight loss. Microscopic colitis is the diagnosis in around 10% of cases investigated for chronic non-bloody diarrhea.

Associated conditions
A higher incidence of autoimmune diseases, for example arthritis, Sjögrens syndrome, thyroid disorders, and celiac disease, has been reported in people with microscopic colitis. Associations with various drugs have been found, especially proton pump inhibitors, H2 blockers, selective serotonin reuptake inhibitors (SSRIs), and non-steroidal anti-inflammatory drugs (NSAIDs). Bile acid diarrhea is found in 41% of patients with collagenous colitis and 29% with lymphocytic colitis. Additionally, cigarette smoking has been identified as a significant risk factor of microscopic colitis.

Diagnosis
Colonoscopic appearances are normal or near normal. As the changes are often patchy, an examination limited to the rectum may miss cases of microscopic colitis, and so a full colonoscopy is necessary. Multiple colonic biopsies are taken in order to make the diagnosis. Histological features of colonic biopsies indicating microscopic colitis are: greater than 20 intraepithelial lymphocytes per 100 epithelial cells and, additionally, 10-20 μm of a thickened subepithelial collagen band in collagenous colitis. Inflammation of the lamina propria, with mainly mononuclear cells, may be observed in collagenous colitis.

Pathology
Microscopic colitis is characterized by an increase in inflammatory cells, particularly lymphocytes, in colonic biopsies with an otherwise normal appearance and architecture of the colon. Inflammatory cells are increased both in the surface epithelium ("intraepithelial lymphocytes") and in the lamina propria. The key feature is more than 20 intra-epithelial lymphocytes per 100 epithelial cells. These are the principal features of lymphocytic colitis. An additional distinguishing feature of collagenous colitis is a thickened subepithelial collagen layer, which may be up to 30 micrometres thick, that occurs in addition to the features found in lymphocytic colitis. The fact that the two types of microscopic colitis share many features including epidemiology, risk factors and, response to therapy has led to the suggestion that they are actually subtypes of the same disease.

Differential diagnosis
Differential diagnoses, which should be ruled out, include bile acid diarrhea, lactose malabsorption, celiac disease, Crohns disease, ulcerative colitis, and infectious colitis.

Treatment
Lymphocytic and collagenous colitis have both been shown in randomized, placebo-controlled trials to respond well to budesonide, a glucocorticoid. Budesonide formulated to be active in the distal colon and rectum is effective for both active disease and in the prevention of relapse </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hematemesis and can you explain it in depth? [/INST] Hematemesis is the vomiting of blood. It is always an important sign. It can be confused with hemoptysis (coughing up blood) or epistaxis (nosebleed), which are more common. The source is generally the upper gastrointestinal tract, typically above the suspensory muscle of duodenum. It may be caused by ulcers, tumors of the stomach or esophagus, varices, prolonged and vigorous retching, gastroenteritis, ingested blood (from bleeding in the mouth, nose, or throat), or certain drugs.Hematemesis is treated as a medical emergency, with treatments based on the amount of blood loss. Investigations include endoscopy. Any blood loss may be corrected with intravenous fluids and blood transfusions. Patients may need to avoid taking anything by mouth.

Definition
Hematemesis is the vomiting of blood. This is usually vomit that contains bright red blood. Coffee ground vomiting is similar to hematemesis, but is distinct in not involving bright red blood.Hematemesis is always an important sign. It must be differentiated from hemoptysis (coughing up blood) and epistaxis (nosebleed). Both of these are more common conditions. These may be difficult to distinguish.

Differential diagnosis
Hematemesis may be caused by:

Peptic ulcer. This may be related to Zollinger–Ellison syndrome, which causes severe disease.
Vascular malfunctions of the gastrointestinal tract, such as bleeding gastric varices or intestinal varices.
Mallory-Weiss syndrome: bleeding tears in the esophagal mucosa, usually caused by prolonged and vigorous retching.
Vomiting of ingested blood after bleeding in the mouth, nose, or throat.
Tumors of the stomach or esophagus.
Irritation or erosion of the lining of the esophagus or stomach.
Radiation poisoning.
Viral hemorrhagic fevers.
Gastroenteritis.
Gastritis.
Chronic viral hepatitis.
Hepatic schistosomiasis, or intestinal schistosomiasis. This is caused by the parasite Schistosoma mansoni.
Iatrogenic injury (invasive procedure such as endoscopy or transesophageal echocardiography)
Atrio-oesophageal fistula.
Yellow fever.
Strongyloidiasis.
Certain drugs.
Plague, most commonly from septicemic plague.

Mechanism
The source of vomited blood is usually from the upper gastrointestinal tract. This can include the esophagus, stomach, and parts of the small intestine. This may be the suspensory muscle of duodenum. Hematemesis tends to occur only after significant blood loss.

Evaluation
Hematemesis may be investigated with endoscopy of the upper gastrointestinal tract. Barium meal may also be used.

Management
Hematemesis is treated as a medical emergency. The most vital distinction is whether there is blood loss sufficient to cause shock. Correct management is required in such conditions. It is required to perform all tests such as endoscopy before medication. A platelet test is also an important test in such conditions.  Medicines such as painkillers or antibiotics, e.g. ciprofloxacin, could decrease platelet count which can lead to thrombocytopenia (when the body does not have sufficient platelets in the blood and cannot form clots). In such conditions wrong medication or management could be deadly. Blood transfusion is required in such conditions if the body loses more than 20 percent of body blood volume. Severe loss makes it impossible for the heart to pump a sufficient amount of blood to the body. In such conditions unmaintained blood volume could lead to hypovolemic shock (hypovolemic shock could lead to damage of body organs e.g. kidney, brain, or gangrene of arms or legs). An untreated patient could develop cerebral atrophy.

Minimal blood loss
In cases that do not involve shock, treatment may involve proton pump inhibitors (such as omeprazole) to treat stomach ulcers if they are present. This is given until endoscopy can be arranged. Blood transfusions may be given if the level of hemoglobin in the blood is extremely low, that is less than 8.0 g/dL or 4.5–5.0 mmol/L. A patient may be kept nothing by mouth (or no eating or drinking). Adequate venous access (such as with large-bore cannulas or a central venous catheter) is generally obtained in case the patient develops a further bleed and becomes unstable.

Significant blood loss
In a "hemodynamically significant" case of hematemesis, there may be shock. Resuscitation is an immediate priority to prevent death </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hematuria and can you explain it in depth? [/INST] Hematuria or haematuria is defined as the presence of blood or red blood cells in the urine. “Gross hematuria” occurs when urine appears red, brown, or tea-colored due to the presence of blood. Hematuria may also be subtle and only detectable with a microscope or laboratory test. Blood that enters and mixes with the urine can come from any location within the urinary system, including the kidney, ureter, urinary bladder, urethra, and in men, the prostate. Common causes of hematuria include urinary tract infection (UTI), kidney stones, viral illness, trauma, bladder cancer, and exercise. These causes are grouped into glomerular and non-glomerular causes, depending on the involvement of the glomerulus of the kidney. But not all red urine is hematuria. Other substances such as certain medications and foods (e.g. blackberries, beets, food dyes) can cause urine to appear red. Menstruation in women may also cause the appearance of hematuria and may result in a positive urine dipstick test for hematuria. A urine dipstick test may also give an incorrect positive result for hematuria if there are other substances in the urine such as myoglobin, a protein excreted into urine during rhabdomyolysis. A positive urine dipstick test should be confirmed with microscopy, where hematuria is defined by three of more red blood cells per high power field. When hematuria is detected, a thorough history and physical examination with appropriate further evaluation (e.g. laboratory testing) can help determine the underlying cause.

Differential diagnosis
Hematuria can be classified according to visibility, anatomical origin, and timing of blood during urination.In terms of the visibility, hematuria can be visible to the naked eye (termed "gross hematuria") and may appear red or brown (sometimes referred to as tea-colored), or it can be microscopic (i.e. not visible to the eye but detected with a microscope or laboratory test). Microscopic hematuria is present when there are three or more red blood cells per high power field.
In terms of the anatomical origin, blood or red blood cells can enter and mix with urine at multiple anatomical sites within the urinary system, including the kidney, ureter, urinary bladder, and urethra, and in men, the prostate. Additionally, menstruation in women may cause the appearance of hematuria and may result in a positive urine dipstick test for hematuria. The causes corresponding to these anatomic locations can be divided into glomerular and non-glomerular causes, referring to the involvement of the glomerulus of the kidney. Non-glomerular causes can be further subdivided into upper urinary tract and lower urinary tract causes.
In terms of the timing during urination, hematuria can be initial, terminal or total, meaning blood can appear in the urine at the onset, midstream, or later. If it appears soon after the onset of urination, a distal site is suggested.  A longer delay suggests a more proximal lesion. In other words, shorter times suggest distal sites while longer times suggest proximal sites. Hematuria that occurs throughout urination suggests that bleeding is occurring above the level of the bladder. This is very significant in regards to developing a differential diagnosis and eventually for the purposes of creating a treatment plan for the patient.Many causes may present as either visible hematuria or microscopic hematuria, and so the differential diagnosis is frequently organized based upon glomerular and non-glomerular causes.

Glomerular hematuria
Glomerular causes include:

IgA nephropathy
Thin glomerular basement membrane disease
Hereditary nephritis (Alports disease)
Hemolytic uremic syndrome
Postinfectious glomerulonephritisCertain infectious agents like Group B Strep(strep pyogenes) can cause a person to get a very specific manifestation known as post-streptococcal glomerulonephritis. This manifestation results in a person having the symptom of cola-colored urine.
Membranoproliferative glomerulonephritis
Lupus nephritis
Henoch-Shonlein purpura
Nephritic syndrome
Nephrotic syndrome
Polycystic kidney disease
Idiopathic hematuria

Non-glomerular hematuria
Visible blood clots in the urine indicate a non-glomerular cause. Non-glomerular causes include:

Urinary tract infections, such as pyelonephritis, cystitis, prostatitis, and urethritis
Kidney stones
Cancers, such as renal cell carcinoma and bladder cancer (particularly transitional cell carcinoma), and in men, prostate cancer
Urinary tract strictures
Benign prostatic hyperplasia
Renal papillary necrosis
Trauma or damage to the lining of the urinary tract
Intense exercise
Increased tendency to bleed due to acquired or genetic conditions (e.g. sickle cell disease or vitamin K deficiency bleeding) or certain medications (e.g. blood thinners)

Mimickers of hematuria
Pigmenturia
Not all red or brown urine is caused by hematuria. Other substances such as certain medications and certain foods can cause urine to appear red.Medications that may cause urine to appear red include:

Phenazopyridine
Nitrofurantoin
Doxorubicin
RifampicinFoods that may cause urine to appear red include:

Blackberries
Food dyes.
Beets
Rhubarb
Fava beans

False positive urine dipstick
A urine dipstick may be falsely positive for hematuria due to other substances in the urine. While the urine dipstick test is able to recognize heme in red blood cells, it also identifies free hemoglobin and myoglobin. Free hemoglobin may be found in the urine resulting from hemolysis, and myoglobin may be found in the urine resulting from rhabdomyolysis. Thus, a positive dipstick test does not necessarily indicate hematuria; rather, microscopy of the urine showing three of more red blood cells per high power field confirms hematuria.

Menstruation
In women, menstruation may cause the appearance of hematuria and may result in a urine dipstick test positive for hematuria. Menstruation can be ruled out as a cause of hematuria by inquiring about menstruation history and ensuring the urine specimen is collected without menstrual blood.

Evaluation
The evaluation of hematuria is dependent upon the visibility of the blood in the urine (i.e. visible/gross vs microscopic hematuria). Visible hematuria must be investigated, as it may be due to a pathological cause. In those with visible hematuria, urological cancer (most frequently bladder or kidney cancer) is discovered in 20-25%. Hematuria alone without accompanying symptoms should be raise suspicion of malignancy of the urinary tract until proven otherwise. The initial evaluation of patients presenting with signs and symptoms that are consistent of hematuria include assessment of hemodynamic status, underlying cause of hematuria, and ensuring urinary drainage. These steps include assessment of the patients heart rate, blood pressure, a physician exam taken by a healthcare professional, and blood work to ensure the patients hemodynamic status is adequate. It is important to obtain a detailed history from the patient (i.e. recreational, occupational, and medication exposures) as this information can be helpful in suggesting a cause of hematuria. The physical exam can also be helpful in identifying a cause of the hematuria as certain signs found on the physical exam can suggest specific causes of the hematuria. In the event the initial evaluation of hematuria does not reveal an underlying cause  then evaluation by a physician who specializes in Urology may proceed. This medical evaluation may consist of, but is not limited too, a history and physical exam taken by healthcare personnel, laboratory studies (i.e. blood work), cystoscopy, and specialized imaging procedures (i.e. CT or MRI).

Visible hematuria
The first step in evaluation of red or brown colored urine is to confirm true hematuria with urinalysis and urine microscopy, where hematuria is defined by three of more red blood cells per high power field. Although a urine dipstick test may be used, it can give false positive or false negative results. In gathering information, it is important to inquire about recent trauma, urologic procedures, menses, and culture-documented urinary tract infection. If any of these are present, it is appropriate to repeat a urinalysis with urine microscopy in 1 to 2 weeks or after treatment of the infection. If the results of the urinalysis and urine microscopy reveal a glomerular origin of hematuria (indicated by proteinuria or red blood cell casts), consultation of a nephrologist should be made. If the results of the urinalysis indicate a non-glomerular origin, a microbiological culture of the urine should be performed, if it has not been done already. If the culture is positive, treatment of the infection should follow and urinalysis and urine microscopy should be repeated once complete. If the culture is negative or if hematuria persists after treatment, CT urogram and cystoscopy should be performed. Of note, hemodynamic stability should be monitored and a complete blood count should be ordered to assess for anemia.In summary, those with visible hematuria confirmed by urinalysis and urine microscopy and with no recent trauma, urologic procedures, menses, or urinary tract infection should undergo cystoscopy and CT urogram.

Microscopic hematuria
After detecting and confirming hematuria with urinalysis and urine microscopy, the first step in evaluation of microscopic hematuria is to rule out benign causes. Benign causes include urinary tract infection, viral illness, kidney stone, recent intense exercise, menses, recent trauma, or recent urological procedure. After benign causes have resolved or been treated, a repeat urinalysis and urine microscopy is warranted to ensure cessation of hematuria. If hematuria persists (even if there is a suspected cause), the next step is to stratify the risk of the person for urothelial cancer into low, intermediate, or high risk to determine next steps. To be in the low risk category, one must satisfy all of the following criteria: Has never smoked tobacco or smoked less than 10 pack-years; is a female less than 50 years old or a male less than 40 years old; has 3-10 red blood cells per high power field; has not had microscopic hematuria before; and has no other risk factors for urothelial cancer. To be in the intermediate risk category, one must satisfy any of the following criteria: Has smoked 10-30 pack-years; is a female 50–59 years old or a male aged 40–59 years old; has 11-25 red blood cells per high power field; or was previously a low-risk patient with persistent microscopic hematuria and has 3-25 red blood cells per high power field. To be in the high risk category, one must satisfy any of the following criteria: Has smoked more than 30 pack-years; is older than 60 years of age; or has above 25 red blood cells per high power field on any urinalysis. For the low risk category, the next step is to either repeat a urinalysis with urine microscopy in 6 months or perform a cystoscopy and renal ultrasound. For the intermediate risk category, the next step is to perform a cystoscopy and renal ultrasound. For the high risk category, the next step is to perform a cystoscopy and CT urogram. If an underlying cause for hematuria is discovered, it should be managed appropriately. However, if no underlying cause is discovered, the hematuria should be re-evaluated with urinalysis and urine microscopy within 12 months. Additionally, for all risk categories, if a nephrologic origin is suspected, consultation of a nephrologist should be made.

Pathophysiology
The pathophysiology of hematuria can often be explained by damage to the structures of the urinary system, including the kidney, ureter, urinary bladder, and urethra, and in men, the prostate. Common mechanisms include structural disruption to the glomerular basement membrane and mechanical or chemical erosion of the mucosal surfaces of the genitourinary tract.

Management
Medical Emergency: Acute clot retention
Acute clot retention is one of three emergencies that can occur with hematuria. The other two are anemia and shock. Blood clots can prevent urine outflow through either ureter or the bladder. This is known as acute urinary retention.
Blood clots that remain in the bladder are digested by urinary urokinase producing fibrin fragments. These fibrin fragments are natural anticoagulants and promote ongoing bleeding from the urinary tract. Removing all blood clots prevents the formation of this natural anticoagulant. This in turns facilitates the cessation of bleeding from the urinary tract.The acute management of obstructing clots is the placement of a large (22-24 French) urethral Foley catheter. Clots are evacuated with a Toomey syringe and saline irrigation. If this does not control the bleeding, management should escalate to continuous bladder irrigation (CBI) via a three-port urethral catheter. If both a large urethral Foley catheter and CBI fail, an urgent cystoscopy in the operating room will be necessary. Lastly, a transfusion and/or a correction of a coexisting coagulopathy may be necessary.

Medical Emergency: Urosepsis
Urosepsis is defined as sepsis caused by a urogenital tract infection and comprises about 25% of all sepsis cases. Urosepsis is the result of a systemic inflammatory response to infection and can be identified by numerous signs and symptoms (e.g. fever, hypothermia, tachycardia, and leukocytosis). Signs and symptoms that indicate a urogential tract infection is the source of the sepsis may include, but are not limited to, flank pain, costovertebral angle tenderness, pain with micturition, urinary retention, and scrotal pain. In terms of the visibility, hematuria can be visible to the naked eye (termed "gross hematuria") and may appear red or brown (sometimes referred to as tea-colored), or it can be microscopic (i.e. not visible to the eye but detected of urosepsis. In addition to imaging tests, patients may be treated with antibiotics to relieve the infection and intravenous fluids to maintain cardiovascular and renal perfusion </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Nosebleed and can you explain it in depth? [/INST] A nosebleed, also known as epistaxis, is bleeding from the nose. Blood can flow down into the stomach, and cause nausea and vomiting. In more severe cases, blood may come out of both nostrils. Rarely, bleeding may be so significant that low blood pressure occurs. Blood may also come up the nasolacrimal duct and out from the eye.Risk factors include trauma, including putting the finger in the nose, blood thinners, high blood pressure, alcoholism, seasonal allergies, dry weather, and inhaled corticosteroids. There are two types: anterior, which is more common; and posterior, which is less common but more serious. Anterior nosebleeds generally occur from Kiesselbachs plexus while posterior bleeds generally occur from the sphenopalatine artery. The diagnosis is by direct observation.Prevention may include the use of petroleum jelly in the nose. Initially, treatment is generally the application of pressure for at least five minutes over the lower half of the nose. If this is not sufficient, nasal packing may be used. Tranexamic acid may also be helpful. If bleeding episodes continue, endoscopy is recommended.About 60% of people have a nosebleed at some point in their life. About 10% of nosebleeds are serious. Nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999. Nosebleeds most commonly affect those younger than 10 and older than 50.

Cause
Nosebleeds can occur due to a variety of reasons. Some of the most common causes include trauma from nose picking, blunt trauma (such as a motor vehicle accident), or insertion of a foreign object (more likely in children). Relative humidity (including centrally heated buildings), respiratory tract infections, chronic sinusitis, rhinitis or environmental irritants can cause inflammation and thinning of the tissue in the nose, leading to a greater likelihood of bleeding from the nose.Most causes of nose bleeding are self-limiting and do not require medical attention. However, if nosebleeds are recurrent or do not respond to home therapies, an underlying cause may need to be investigated. Some rarer causes are listed below:Coagulopathy

Thrombocytopenia (thrombotic thrombocytopenic purpura, idiopathic thrombocytopenic purpura)
Von Willebrands disease
Hemophilia
Leukemia
HIV
Chronic liver disease—cirrhosis causes deficiency of factor II, VII, IX,& XDietary

Sulfur dioxide (sulphur dioxide) E220 (as a food preservative used particularly in wines, dried fruits, etc. )
Sulphites as food preservatives
Salicylates naturally occurring in some fruits and vegetablesInflammatory

Granulomatosis with polyangiitis
Systemic lupus erythematosusMedications/Drugs

Anticoagulation (warfarin, heparin, aspirin, etc.)
Insufflated drugs (particularly cocaine)
Nasal sprays (particularly prolonged or improper use of nasal steroids)Neoplastic

Squamous cell carcinoma
Adenoid cystic carcinoma
Melanoma
Nasopharyngeal carcinoma
Nasopharyngeal angiofibroma
Nosebleeds can be a sign of cancer in the sinus area, which is rare, or tumors starting at the base of the brain, such as meningioma. Due to the sensitive location, nosebleeds caused by tumors are typically associated with other symptoms, such as hearing or vision problems.Traumatic

Anatomical deformities (e.g. septal spurs)
Blunt trauma (usually a sharp blow to the face such as a punch, sometimes accompanying a nasal fracture)
Foreign bodies (such as fingers during nose-picking)
Digital trauma
Middle ear barotrauma (such as from descent in aircraft or ascent in scuba diving)
Nasal bone fracture
Septal fracture/perforation
Surgery (e.g. septoplasty and functional endoscopic sinus surgery)
Nasal bleeds may be due to fracture of facial bones namely maxilla and zygoma.Vascular

Hereditary hemorrhagic telangiectasia (Osler–Weber–Rendu disease)
Angioma
Aneurysm of the carotid artery

Pathophysiology
The nasal mucosa contains a rich blood supply that can be easily ruptured and cause bleeding. Rupture may be spontaneous or initiated by trauma. Nosebleeds are reported in up to 60% of the population with peak incidences in those under the age of ten and over the age of 50 and appear to occur in males more than females. An increase in blood pressure (e.g. due to general hypertension) tends to increase the duration of spontaneous epistaxis. Anticoagulant medication and disorders of blood clotting can promote and prolong bleeding. Spontaneous epistaxis is more common in the elderly as the nasal mucosa (lining) becomes dry and thin and blood pressure tends to be higher. The elderly are also more prone to prolonged nosebleeds as their blood vessels are less able to constrict and control the bleeding.
The vast majority of nosebleeds occur in the front anterior (front) part of the nose from the nasal septum. This area is richly endowed with blood vessels (Kiesselbachs plexus). This region is also known as Littles area. Bleeding farther back in the nose is known as a posterior bleed and is usually due to bleeding from Woodruffs plexus, a venous plexus situated in the posterior part of inferior meatus. Posterior bleeds are often prolonged and difficult to control. They can be associated with bleeding from both nostrils and with a greater flow of blood into the mouth. Sometimes blood flowing from other sources of bleeding passes through the nasal cavity and exits the nostrils. It is thus blood coming from the nose but is not a true nosebleed, that is, not truly originating from the nasal cavity. Such bleeding is called "pseudoepistaxis" (pseudo + epistaxis). Examples include blood coughed up through the airway and ending up in the nasal cavity, then dripping out.

Prevention
People with uncomplicated nosebleeds can use conservative methods to prevent future nosebleeds such as sleeping in a humidified environment or applying petroleum jelly to the nasal nares.

Treatment
Most anterior nosebleeds can be stopped by applying direct pressure, which helps by promoting blood clots. Those who have a nosebleed should first attempt to blow out any blood clots and then apply pressure for at least five minutes and up to 20 minutes. Pressure should be firm and tilting the head forward helps decrease the chance of nausea and airway obstruction as seen in the picture on the right. When attempting to stop a nosebleed at home, the head should not be tilted back. Swallowing excess blood can irritate the stomach and cause vomiting. Vasoconstrictive medications such as oxymetazoline (Afrin) or phenylephrine are widely available over the counter for treatment of allergic rhinitis and may also be used to control benign cases of epistaxis. Those with nosebleeds that last longer than 20 minutes (in the setting of direct pressure as seen in the image to the right) should seek medical attention.

Nasal packing
If pressure and chemical cauterization cannot stop bleeding, nasal packing is the mainstay of treatment. There are several forms of nasal packing that can be contrasted by anterior nasal packing and posterior nasal packing. Traditionally, nasal packing was accomplished by packing gauze into the nose, thereby placing pressure on the vessels in the nose and stopping the bleeding. Traditional gauze packing has been replaced with products such as Merocel and the Rapid Rhino. The Merocel nasal tampon is similar to gauze packing except it is a synthetic foam polymer (made of polyvinyl alcohol and expands in the nose after application of water) that provides a less hospitable medium for bacteria. The Rapid Rhino stops nosebleeds using a balloon catheter, made of carboxymethylcellulose, which has a cuff that is inflated by air to stop bleeding through extra pressure in the nasal cavity. Systematic review articles have demonstrated that the efficacy in stopping nosebleeds is similar between the Rapid Rhino and Merocel packs; however, the Rapid Rhino has been shown to have greater ease of insertion and reduced discomfort. People who receive nasal packing need to return to a medical professional in 24–72 hours in order to have packing removed. There are also several dissolvable packing materials that stop bleeding through use of thrombotic agents that promote blood clots, such as surgicel. The thrombogenic foams and gels do not require removal and dissolve after a few days. Posterior nasal packing can be achieved by using a Foley catheter, blowing up the balloon when it is in the back of the throat, and applying traction. Complications of nasal packing include abscesses, septal hematomas, sinusitis, and pressure necrosis. In rare cases toxic shock syndrome can occur with prolonged nasal packing. As a result, many forms of nasal packing involve use of topical antistaphylococcal antibiotic ointment.

Tranexamic acid
Tranexamic acid helps promote blood clotting. For nosebleeds it can be applied to the site of bleeding, taken by mouth, or injected into a vein.

Cauterization
This method involves applying a chemical such as silver nitrate to the nasal mucosa, which burns and seals off the bleeding. Eventually the nasal tissue to which the chemical is applied will undergo necrosis. This form of treatment is best for mild bleeds, especially in children, that are clearly visible. A topical anesthetic (such as lidocaine) is usually applied prior to cauterization. Silver nitrate can cause blackening of the skin due to silver sulfide deposit, though this will fade with time.

Surgery
Ongoing bleeding despite good nasal packing is a surgical emergency and can be treated by endoscopic evaluation of the nasal cavity under general anesthesia to identify an elusive bleeding point or to directly ligate (tie off) the blood vessels supplying the nose. These blood vessels include the sphenopalatine, anterior and posterior ethmoidal arteries </s>