<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Color blindness and explain in detail? [/INST] Color blindness (color vision deficiency) is the decreased ability to see color or differences in color. It can impair tasks such as selecting ripe fruit, choosing clothing, and reading traffic lights. Color blindness may make some academic activities more difficult. However, issues are generally minor, and the colorblind automatically develop adaptations and coping mechanisms. People with total color blindness (achromatopsia) may also be uncomfortable in bright environments and have decreased visual acuity.
The most common cause of color blindness is an inherited problem or variation in the functionality of one or more of the three classes of cone cells in the retina, which mediate color vision. Males are more likely to be color blind than females, because the genes responsible for the most common forms of color blindness are on the X chromosome. Non-color-blind females can carry genes for color blindness and pass them on to their children. Color blindness can also result from physical or chemical damage to the eye, the optic nerve, or parts of the brain. Screening for color blindness is typically done with the Ishihara color test.There is no cure for color blindness. Diagnosis may allow an individual, or their parents/teachers to actively accommodate the condition. Special lenses such as EnChroma glasses or X-chrom contact lenses may help people with red–green color blindness at some color tasks, but they do not grant the wearer "normal color vision". Mobile apps can help people identify colors.Red–green color blindness is the most common form, followed by blue–yellow color blindness and total color blindness. Red–green color blindness affects up to 1 in 12 males (8%) and 1 in 200 females (0.5%). The ability to see color also decreases in old age. In certain countries, color blindness may make people ineligible for certain jobs, such as those of aircraft pilots, train drivers, crane operators, and people in the armed forces. The effect of color blindness on artistic ability is controversial, but a number of famous artists are believed to have been color blind.

Signs and symptoms
Color blindness describes both a symptom of reduced color perception, as well as several conditions where colorblindness is the primary – or only – symptom. This section will focus only on color blindness as a symptom.
A colorblind subject will have decreased (or no) color discrimination along the red-green axis, blue-yellow axis, or both, though the vast majority of the colorblind are only affected on their red-green axis.
The first indication of colorblindness generally consists of a person using the wrong color for an object, such as when painting, or calling a color by the wrong name. The colors that are confused are very consistent among people with the same type of color blindness.

Confusion colors
Confusion colors are pairs or groups of colors that will often be mistaken by the colorblind. Confusion colors for red-green color blindness include:

Cyan and Grey
Rose-Pink and Grey
Blue and Purple
Yellow and Neon Green
Red, Green, Orange, BrownConfusion colors for blue-yellow color blindness include:

Yellow and Grey
Blue and Green
Dark Blue/Violet and Black
Violet and Yellow-Green
Red and Rose-PinkThese colors of confusion are defined quantitatively by straight confusion lines plotted in CIEXYZ, usually plotted on the corresponding chromaticity diagram. The lines all intersect at a copunctal point, which varies with the type of color blindness. Chromaticities along a confusion line will appear metameric to dichromats of that type. Anomalous trichromats of that type will see the Chromaticities as metameric if they are close enough, depending on the strength of their CVD. For two colors on a confusion line to be metameric, the Chromaticities first have to be made isoluminant, i.e. to have the same Lightness. Note also that colors that may be isoluminant to the standard observer (typical trichromat) may not be isoluminant to a dichromat.

Color tasks
Cole describes four color tasks, all of which are impeded to some degree by color blindness:

Comparative – When multiple colors must be compared, such as with mixing paint
Connotative – When colors are given an implicit meaning, such as red = stop
Denotative – When identifying colors, for example by name, such as “where is the yellow ball?”
Aesthetic – When colors look nice – or convey an emotional response – but don’t carry explicit meaningColor blindness causes difficulty in all four kinds of color tasks. The following sections will describe specific color tasks that the colorblind typically have difficulty with.

Food
Colorblindness causes difficulty with the connotative color tasks associated with selecting or preparing food, for example:

Selecting food for ripeness can be difficult. The green-yellow transition of bananas is particularly hard to identify.
Detecting bruises, mold or rot on some foods
Determining when meat is done by color
Distinguishing some varietals, such as a Braeburn from a Granny Smith apple
Distinguishing colors associated with artificial flavors (e.g. jelly beans, sports drinks)

Skin color
Changes in skin color due to bruising, sunburn, rashes or even blushing are easily missed by those with red-green colorblindness. These discolorations are often linked to the blood oxygen saturation, which affects skin reflectance.

Traffic lights
The colors of traffic lights can be difficult for the red-green colorblind. This includes distinguishing:

red/amber lights from sodium street lamps;
green lights (closer to cyan) from normal white lights.
Red from amber lights, especially when there are no positional clues available (see image).The main coping mechanism to overcome these challenges is to memorize the position of lights. The order of the common triplet traffic light is standardized as red-amber-green from top to bottom or left to right. Cases that deviate from this standard are rare. One such case is a traffic light in Tipperary Hill in Syracuse, New York, which is upside-down (green-amber-red top to bottom) due to the sentiments of its Irish American community. However, it has been criticized due to the potential hazard it poses for color-blind drivers.

Signal lights
Navigation lights in marine and aviation settings employ red and green lights to signal the relative position of other ships or aircraft. Railway signal lights also rely heavily on red-green-yellow colors. In both cases, these color combinations can be difficult for the red-green colorblind. Lantern Tests are a common means of simulating these light sources to determine not necessarily whether someone is colorblind, but whether they can functionally distinguish these specific signal colors. Those who cannot pass this test are generally completely restricted from working on aircraft, ships or rail.

Fashion
Color analysis is the analysis of color in its use in fashion, to determine personal color combinations that are most aesthetic. Colors to combine can include clothing, accessories, makeup, hair color, skin color, eye color, etc. Color analysis involves many aesthetic and comparative color task that can be difficult for the color blind. Most colorblind individuals conservatively avoid brightly colored clothes to avoid combining colors that may be viewed as unaesthetic by people with normal color vision.

Advantages
People with deuteranomaly are better at distinguishing shades of khaki, which may be advantageous when looking for predators, food, or camouflaged objects hidden among foliage. Dichromats tend to learn to use texture and shape clues and so may be able to penetrate camouflage that has been designed to deceive individuals with normal color vision.In the presence of chromatic noise, the colorblind are more capable of seeing a luminous signal, as long as the chromatic noise appears metameric to them. This is the effect behind most "reverse" Pseudoisochromatic plates (e.g. "hidden digit" Ishihara plates) that are discernible to the colorblind, but unreadable to color normals.

Classification
Much terminology has existed and does exist for the classification of color blindness, but the typical classification for color blindness follows the von Kries classifications, which uses severity and affected cone for naming.

Based on severity
Based on clinical appearance, color blindness may be described as total or partial. Total color blindness (monochromacy) is much less common than partial color blindness.  Partial colorblindness includes dichromacy and anomalous trichromacy, but is often clinically defined as mild, moderate or strong.

Monochromacy
Monochromacy is often called total color blindness since there is no ability to see color. Although the term may refer to acquired disorders such as cerebral achromatopsia, it typically refers to congenital color vision disorders, namely rod monochromacy and blue cone monochromacy).In cerebral achromatopsia, a person cannot perceive colors even though the eyes are capable of distinguishing them. Some sources do not consider these to be true color blindness, because the failure is of perception, not of vision. They are forms of visual agnosia.Monochromacy is the condition of possessing only a single channel for conveying information about color. Monochromats are unable to distinguish any colors and perceive only variations in brightness. Congenital monochromacy occurs in two primary forms:

Rod monochromacy, frequently called complete achromatopsia, where the retina contains no cone cells, so that in addition to the absence of color discrimination, vision in lights of normal intensity is difficult.
Cone monochromacy is the condition of having only a single class of cone. A cone monochromat can have good pattern vision at normal daylight levels, but will not be able to distinguish hues. Cone monochromacy is divided into classes defined by the single remaining cone class. However, red and green cone monochromats have not been definitively described in the literature. Blue cone monochromacy is caused by lack of functionality of L (red) and M (green) cones, and is therefore mediated by the same genes as red–green color blindness (on the X chromosome). Peak spectral sensitivities are in the blue region of the visible spectrum (near 440 nm). People with this condition generally show nystagmus ("jiggling eyes"), photophobia (light sensitivity), reduced visual acuity, and myopia (nearsightedness). Visual acuity usually falls to the 20/50 to 20/400 range.

Dichromacy
Dichromats can match any color they see with some mixture of just two primary colors (in contrast to those with normal sight (trichromats) who can distinguish three primary colors). Dichromats usually know they have a color vision problem, and it can affect their daily lives. Dichromacy in humans includes protanopia, deuteranopia, and tritanopia. Out of the male population, 2% have severe difficulties distinguishing between red, orange, yellow, and green. (Orange and yellow are different combinations of red and green light.) Colors in this range, which appear very different to a normal viewer, appear to a dichromat to be the same or a similar color. The terms protanopia, deuteranopia, and tritanopia come from Greek, and respectively mean "inability to see (anopia) with the first (prot-), second (deuter-), or third (trit-) [cone]".

Anomalous trichromacy
Anomalous trichromacy is the mildest type of color deficiency, but the severity ranges from almost dichromacy (strong) to almost normal trichromacy (mild). In fact, many mild anomalous trichromats have very little difficulty carrying out tasks that require normal color vision and some may not even be aware that they have a color vision deficiency. The types of anomalous trichromacy include protanomaly, deuteranomaly and tritanomaly.  It is approximately three times more common than dichromacy. Anomalous trichromats exhibit trichromacy, but the color matches they make differ from normal trichromats. In order to match a given spectral yellow light, protanomalous observers need more red light in a red/green mixture than a normal observer, and deuteranomalous observers need more green. This difference can be measured by an instrument called an Anomaloscope, where red and green lights are mixed by a subject to match a yellow light.

Based on affected cone
There are two major types of color blindness: difficulty distinguishing between red and green, and difficulty distinguishing between blue and yellow. These definitions are based on the phenotype of the partial colorblindness. Clinically, it is more common to use a genotypical definition, which describes which cone/opsin is affected.

Red–green color blindness
Red-green color blindness includes protan and deutan CVD. Protan CVD is related to the L-cone and includes protanomaly (anomalous trichromacy) and protanopia (dichromacy). Deutan CVD is related to the M-cone and includes deuteranomaly (anomalous trichromacy) and deuteranopia (dichromacy). The phenotype (visual experience) of deutans and protans is quite similar. Common colors of confusion include red/brown/green/yellow as well as blue/purple. Both forms are almost always congenital (genetic) and sex-linked: affecting males much more often than females. This form of colorblindness is sometimes referred to as daltonism after John Dalton, who had red-green dichromacy. In some languages, daltonism is still used to describe red-green color blindness.

Protan (2% of males): Lacking, or possessing anomalous L-opsins for long-wavelength sensitive cone cells. Protans have a neutral point at a cyan-like wavelength around 492 nm (see spectral color for comparison)—that is, they cannot discriminate light of this wavelength from white. For a protanope, the brightness of red, is much reduced compared to normal. This dimming can be so pronounced that reds may be confused with black or dark gray, and red traffic lights may appear to be extinguished. They may learn to distinguish reds from yellows primarily on the basis of their apparent brightness or lightness, not on any perceptible hue difference. Violet, lavender, and purple are indistinguishable from various shades of blue. A very few people have been found who have one normal eye and one protanopic eye. These unilateral dichromats report that with only their protanopic eye open, they see wavelengths shorter than neutral point as blue and those longer than it as yellow.

Deutan (6% of males): Lacking, or possessing anomalous M-opsins for medium-wavelength sensitive cone cells. Their neutral point is at a slightly longer wavelength, 498 nm, a more greenish hue of cyan. Deutans have the same hue discrimination problems as protans, but without the dimming of long wavelengths. Deuteranopic unilateral dichromats report that with only their deuteranopic eye open, they see wavelengths shorter than neutral point as blue and longer than it as yellow.

Blue–yellow color blindness
Blue-yellow color blindness includes tritan CVD. Tritan CVD is related to the S-cone and includes tritanomaly (anomalous trichromacy) and tritanopia (dichromacy). Blue-yellow color blindness is much less common than red-green color blindness, and more often has acquired causes than genetic. Tritans have difficulty discerning between bluish and greenish hues. Tritans have a neutral point at 571 nm (yellowish).

Tritan (<0.01% of individuals): Lacking, or possessing anomalous S-opsins or short-wavelength sensitive cone cells. Tritans see short-wavelength colors (blue, indigo and spectral violet) as greenish and drastically dimmed, some of these colors even as black. Yellow and orange are indistinguishable from white and pink respectively, and purple colors are perceived as various shades of red. Unlike protans and deutans, the mutation for this color blindness is carried on chromosome 7. Therefore, it is not sex-linked (equally prevalent in both males and females). The OMIM gene code for this mutation is 304000 "Colorblindness, Partial Tritanomaly".

Tetartan is the "fourth type" of colorblindness, and a type of blue-yellow color blindness. However, its existence is hypothetical and given the molecular basis of human color vision, it is unlikely this type could exist.

Summary of cone complements
The below table shows the cone complements for different types of human color vision, including those considered color blindness, normal color vision and superior color vision. The cone complement contains the types of cones (or their opsins) expressed by an individual.

Causes
Color vision deficiencies can be classified as inherited or acquired.

Inherited: inherited or congenital/genetic color vision deficiencies are most commonly caused by mutations of the  genes encoding opsin proteins. However, several other genes can also lead to less common and/or more severe forms of color blindness.
Acquired: color blindness that is not present at birth, may be caused by chronic illness, accidents, medication, chemical exposure or simply normal ageing processes.

Genetics
Color blindness is typically an inherited genetic disorder. The most common forms of colorblindness are associated with the Photopsin genes, but the mapping of the human genome has shown there are many causative mutations that dont directly affect the opsins. Mutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man [OMIM]).

Genetics of red–green color blindness
By far the most common form of colorblindness is congenital red–green colorblindness (Daltonism), which includes protanopia/protanomaly and deuteranopia/deuteranomaly. These conditions are mediated by the OPN1LW and OPN1MW genes, respectively, both on the X chromosome. Protanopia and Deuteranopia (Dichromacy) could be caused by either a missing gene, or a mutation that renders the protein fully non-functional. Protanomaly and Deuteranomaly are caused by a mutation of the genes that causes the spectral sensitivity of the associated opsin proteins to shift towards the other. That is, either the spectral sensitivity of the L cone shifts towards the M cone (blue shift), or that of the M cone shifts towards the L cone (red shift). These are then called anomalous cones and denoted by an asterisk (L* or M*).
Since the mutated OPN1LW and OPN1MW genes are on the X chromosome, they are sex-linked, and therefore affected males and females disproportionately. Because the colorblind alleles are recessive, colorblindness follows X-linked recessive inheritance. Males have only one X chromosome (XY), and females have two (XX); Because the male only has one allele of each gene, if it is mutated, the male will be colorblind. Because a female has two alleles of each gene (one on each chromosome), if only one allele is mutated, the dominant normal alleles will "override" the mutated, recessive allele and the female will have normal color vision. However, if the female has two mutated alleles, she will still be colorblind. This is why there is a disproportionate prevalence of colorblindness, with ~8% of males exhibiting colorblindness and ~0.5% of females (0.08² = 0.0064 = 0.64%).
The following table shows the possible allele/chromosome combinations and how their interactions will manifest in an individual. The exact phenotype of some of the combinations depend on whether the mutation yields an anomalous or non-functioning opsin. Blue cone monochromacy also follows these inheritance patterns, since it essentially a superposition of protanopia and deuteranopia.

Y
male-only chromosome, no affect on colorblindness.
X
X chromosome.
M
(as subscript), normal M opsin.
L
(as subscript), normal L opsin.
M*
(as subscript), mutated M opsin.
L*
(as subscript), mutated L opsin.The following table shows the pattern of inheritance for congenital red–green colorblindness (protan/deutan) given affected, unaffected or carrier parents. When daughter 1 and daughter 2 (or son 1 and son 2) differ, this indicates a 50% chance of each outcome. Some conclusions from the table include:

A male cannot inherit colorblindness from his father.
A colorblind female must have a colorblind father.
A female must inherit colorblindness alleles from both parents to be colorblind.
Colorblind females can only produce colorblind males.
Because carrier females often have a colorblind father, colorblind males often will have a colorblind maternal grandfather (or great grandfather). In this way, colorblindness is often said to skip a generation.Note: these conclusions do not apply to other forms of colorblindness (e.g. tritanopia).

Genetics of blue–yellow color blindness
Blue-yellow color blindness is a rarer form of colorblindness including tritanopia/tritanomaly. These conditions are mediated by the OPN1SW gene on Chromosome 7.

Other genetic causes
Several inherited diseases are known to cause color blindness:

achromatopsia(also called rod monochromatism, stationary cone dystrophy or cone dysfunction syndrome)
cone dystrophy
cone-rod dystrophy
Lebers congenital amaurosis
retinitis pigmentosa(initially affects rods but can later progress to cones and therefore color blindness).They can be congenital (from birth) or can commence in childhood or adulthood. They can be stationary, that is, remain the same throughout a persons lifetime, or progressive. As progressive phenotypes involve deterioration of the retina and other parts of the eye, many of the above forms of color blindness can progress to legal blindness, i.e. an acuity of 6/60 (20/200) or worse, and often leave a person with complete blindness.

Non-genetic causes
Physical trauma can cause color blindness, either neurologically – brain trauma which produces swelling of the brain in the occipital lobe – or retinally, either acute (e.g. from laser exposure) or chronic (e.g. from ultraviolet light exposure).
Color blindness may also present itself as a symptom of degenerative diseases of the eye, such as cataract and age-related macular degeneration, and as part of the retinal damage caused by diabetes. Vitamin A deficiency may also cause color blindness.Color blindness may be a side effect of prescription drug use. For example, red–green color blindness can be caused by ethambutol, a drug used in the treatment of tuberculosis. Blue-yellow color blindness can be caused by sildenafil, an active component of Viagra. Hydroxychloroquine can also lead to hydroxychloroquine retinopathy, which includes various color defects. Exposure to chemicals such as styrene or organic solvents can also lead to color vision defects.

Mechanism
Color blindness is any deviation of color vision from normal trichromatic color vision (often as defined by the standard observer) that produces a reduced gamut. Mechanisms for color blindness are related to the functionality of cone cells, and often to the expression of photopsins, the photopigments that catch photons and thereby convert light into chemical signals.
When an individual does not satisfy the requirements for trichromatic vision, they will express dichromacy or monochromacy and be colorblind. The main requirement for trichromacy is three cone cell classes that are each sensitive to different wavelengths of light and therefore have different spectral sensitivities. Dichromats only express two cone classes and cone monochromats express one. For each cone missing, one of the opponent channels (red-green and blue-yellow) that are responsible for color discrimination are disabled. This is the mechanism for protanopia, deuteranopia, blue cone monochromacy and tritanopia.
Even when there is trichromatic color vision and all three opponent channels are active, the size of an individuals color gamut is determined by the dynamic range of the opponent channels, which can be affected by several factors. One of these factors is the peak wavelengths of the spectral sensitivities of the three cones, namely the spectral distance between two cones contributing to an opponent channel. When this distance is smaller, the dynamic range is smaller and the color gamut is smaller, leading to a color vision deficiency. This is the mechanism for congenital protanomaly and deuteranomaly, though not of tritanomaly.
The opponent channels can also be affected by the prevalence of certain cones in the retinal mosaic. The cones are not equally prevalent and not evenly distributed in the retina. When the number of one of these cone types is significantly reduced, this can also lead to or contribute to a color vision deficiency. This is one of the causes of tritanomaly.
Simple colored filters can also create mild color vision deficiencies. John Daltons original hypothesis for his deuteranopia was actually that the vitreous humor of his eye was discolored:

I was led to conjecture that one of the humours of my eye must be a transparent, but coloured, medium, so constituted as to absorb red and green rays principally... I suppose it must be the vitreous humor.
An autopsy of his eye after his death in 1844 showed this to be definitively untrue, though other filters are possible. Actual physiological examples usually affect the blue-yellow opponent channel and are named Cyanopsia and Xanthopsia, and are most typically an effect of yellowing or removal of the lens.

Tetrachromacy in carriers of CVD
Females that are heterozygous for anomalous trichromacy (i.e. carriers) may be tetrachromats. These females have two alleles for either the OPN1MW or OPN1LW gene, and therefore express both the normal and anomalous opsins. Because one X chromosome is inactivated at random in each photoreceptor cell during a females development, those normal and anomalous opsins will be segregated into their own cone cells, and because these cells have different spectral sensitivity, they can functionally operate as different opsins. This theoretical female would therefore have cones with peak sensitivities at 420nm (S cone), 530nm (M cone), 560nm (L cone) and the fourth (anomalous) cone between 530nm and 560nm (either M* or L* cone).If a female is heterozygous for both protanomaly and deuteranomaly, she could be pentachromatic. The degree to which women who are carriers of either protanomaly or deuteranomaly are demonstrably tetrachromatic and require a mixture of four spectral lights to match an arbitrary light is very variable. Jameson et al. have shown that with appropriate and sufficiently sensitive equipment it can be demonstrated that any female carrier of red–green color blindness (i.e. heterozygous protanomaly, or heterozygous deuteranomaly) is a tetrachromat to a greater or lesser extent.
Since the incidence of anomalous trichromacy in males is ~6%, which should equal the incidence of anomalous M opsin or L opsin alleles, it follows that the prevalence of unaffected female carriers of colorblindness (and therefore of potential tetrachromats) is 11.3% (i.e. 94% × 6% × 2), based on the Hardy–Weinberg principle. One such woman has been widely reported to be a true or functional tetrachromat, as she can discriminate colors most other people cant.

Diagnosis
There are several color perception tests, or color vision standards that are capable of diagnosing or screening for color blindness. The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to detect red–green color deficiencies and most often recognized by the public. However, this can be attributed more to its ease of application, and less to do with its precision. In fact, there are several types of common color perception tests. Most clinical tests are designed to be fast, simple, and effective at identifying broad categories of color blindness. In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests to collect precise datasets, identify copunctal points, and measure just noticeable differences.

Pseudoisochromatic plates
A pseudoisochromatic plate (from Greek pseudo, meaning "false", iso, meaning "same" and chromo, meaning "color") is the type of test exemplified by the Ishihara test, where a figure (usually one or more numerals) is embedded in the plate as a number of spots surrounded by spots of a slightly different color. The figure can be seen with normal color vision, but not with a particular color defect. The figure and background colors must be carefully chosen to appear isochromatic to a color deficient individual, but not an individual with normal color vision.
Pseudoisochromatic Plates are used as screening tools because they are cheap, fast and simple, but they do not provide precise diagnosis of CVD, and are often followed with another test if a user fails the Ishihara test.The basic Ishihara test may not be useful in diagnosing young, preliterate children, who cant read the numerals, but larger editions contain plates that showcase a simple path to be traced with a finger, rather than numerals.One of the most common alternative color vision tests based on pseudoisochromatic plates is the HRR color test (developed by Hardy, Rand, and Rittler), which solves many of the criticisms of the Ishihara test. For example, it detects blue-yellow color blindness, is less susceptible to memorization and uses shapes, so it is accessible to the illiterate and young children.

Lantern
Instead of the Ishihara test, the US Navy and US Army also allow testing with the a lantern, such as the Farnsworth Lantern Test. Lanterns project small colored lights to a subject, who is required to identify the color of the lights. The colors are those of typical signal lights, i.e. red, green and yellow, which also happen to be colors of confusion of red-green CVD. Lanterns do not diagnose colorblind, but they are occupational screening tests to ensure an applicant has sufficient color discrimination to be able to perform a job. This test allows 30% of color deficient individuals, generally with mild CVD, to pass.

Arrangement tests
Arrangement tests can be used as screening or diagnostic tools. The Farnsworth–Munsell 100 hue test is sensitive enough that it not only can detect color blindness, but also evaluate the color vision of color normals, ranking them as low, average or superior. The Farnsworth D-15 is simpler and is used for screening for CVD. In either case, the subject is asked to arrange a set of colored caps or chips to form a gradual transition of color between two anchor caps.

Anomaloscope
An instrument called an anomaloscope can also be used for diagnosis. These instruments are very expensive and require expertise to administer, so are generally only used in academic settings. However, they are very precise, being able to diagnose the type and severity of color blindness with high confidence. An anomaloscope designed to detect red-green color blindnesses is based on the Rayleigh match, which compares a mixture of red and green light in variable proportions to a fixed spectral yellow of variable luminosity. The subject must change the two variables until the colors appear to match. The values of the variables at match (and the deviation from the variables of a color normal subject) are used to diagnose the type and severity of colorblindness. For example, deutans will put too much green in the mixture and protans will put too much red in the mixture.

Genetic testing
Most tests evaluate the phenotype of the subject, i.e. the functionality of their color vision, but the genotype can also be directly evaluated. This is especially useful for progressive forms that do not have a strongly deviant phenotype at a young age. However, it can also be used to sequence the L and M opsins on the X Chromosome. The most common anomalous alleles of these two genes are known and have even been related to exact spectral sensitivities and peak wavelengths. A subjects anomalous alleles can therefore be classified through genetic testing.

Management
Despite much recent improvement in Gene therapy for color blindness, there is currently no FDA approved treatment for any form of CVD, and otherwise no cure for CVD currently exists. Management of the condition by using lenses to alleviate symptoms or smartphone apps to aid with daily tasks is possible.

Lenses
There are several kinds of lenses that an individual can wear that can increase their accuracy in some color related tasks. However, none of these will "fix" color blindness or grant the wearer normal color vision. There are three kinds of lenses:

A red-tint contact lens worn over the non-dominant eye, will leverage binocular disparity to improve discrimination of some colors. However, it can make other colors more difficult to distinguish. A 1981 review of various studies to evaluate the effect of the X-chrom (one brand) contact lens concluded that, while the lens may allow the wearer to achieve a better score on certain color vision tests, it did not correct color vision in the natural environment. A case history using the X-Chrom lens for a rod monochromat is reported and an X-Chrom manual is online.
Tinted glasses (e.g. Pilestone/Colorlite glasses) apply a tint (e.g. magenta) to incoming light that can distort colors in a way that makes some color tasks easier to complete. These glasses can circumvent many colorblind tests, though this is typically not allowed.
Glasses with a notch filter (e.g. EnChroma glasses) filter a narrow band of light that excites both the L and M cones (yellow-green wavelengths). When combined with an additional stopband in the short wavelength (blue) region, these lenses may constitute a neutral-density filter (have no color tint). They improve on the other lens types by causing less distortion of colors and will essentially increase the saturation of some colors. They will only work on trichromats (anomalous or normal), and unlike the other types, do not have a significant effect on Dichromats. The glasses do not significantly increase ones ability on colorblind tests.

Apps
Many mobile and computer applications have been developed to aid color blind individuals in completing color tasks:

Some applications can identify a color - by name or RGB code - of a color on screen or the color of an object by using the devices camera.
Some applications will make images easier to interpret by the colorblind by enhancing color contrast in natural images and/or information graphics. These methods are generally called daltonization algorithms.
Some applications can simulate color blindness by applying a filter to an image or screen that reduces the gamut of an image to that of a specific type of color blindness. While they dont directly help colorblind people, they allow those with normal color vision to understand how people with color blindness see the world. Their use can help improve inclusive design by allowing designers to simulate their own images to ensure they are accessible to the colorblind.

Epidemiology
Color blindness affects a large number of individuals, with protans and deutans being the most common types. In individuals with Northern European ancestry, as many as 8 percent of men and 0.4 percent of women experience congenital color deficiency. Interestingly, even Daltons very first paper already arrived upon this 8% number:
...it is remarkable that, out of 25 pupils I once had, to whom I explained this subject, 2 were found to agree with me...
However, despite his accuracy, the number varies among groups. Isolated communities with a restricted gene pool sometimes produce high proportions of color blindness, including the less usual types. Examples include rural Finland, Hungary, and some of the Scottish islands. In the United States, about 7 percent of the male population—or about 10.5 million men—and 0.4 percent of the female population either cannot distinguish red from green, or see red and green differently from how others do (Howard Hughes Medical Institute, 2006). More than 95 percent of all variations in human color vision involve the red and green receptors in male eyes. It is very rare for males or females to be "blind" to the blue end of the spectrum.

History
During the 17th and 18th century, several philosophers hypothesized that not all individuals perceived colors in the same way:
...there is no reason to suppose a perfect resemblance in the disposition of the Optic Nerve in all Men, since there is an infinite variety in every thing in Nature, and chiefly in those that are Material, tis therefore very probable that all Men see not the same Colours in the same Objects.
In the power of conceiving colors, too, there are striking differences among individuals: and, indeed, I am inclined to suspect, that, in the greater number of instances, the supposed defects of sight in this respect ought to be ascribed rather to a defect in the power of conception.
The phenomenon only came to be scientifically studied in 1794, when English chemist John Dalton gave the first account of colour blindness in a paper to the Manchester Literary and Philosophical Society, which was published in 1798 as Extraordinary Facts relating to the Vision of Colours: With Observations. Genetic analysis of Daltons preserved eyeball confirmed him as having deuteranopia in 1995, some 150 years after his death.Influenced by Dalton, German writer J. W. von Goethe studied color vision abnormalities in 1798 by asking two young subjects to match pairs of colors.In 1875, the Lagerlunda train crash in Sweden brought color blindness to the forefront. Following the crash, Professor Alarik Frithiof Holmgren, a physiologist, investigated and concluded that the color blindness of the engineer (who had died) had caused the crash. Professor Holmgren then created the first test for color vision using multicolored skeins of wool to detect color blindness and thereby exclude the colorblind from jobs in the transportation industry requiring color vision to interpret safety signals. However, there is a claim that there is no firm evidence that color deficiency did cause the collision, or that it might have not been the sole cause.In 1920, Frederick William Edridge-Green devised an alternative theory of color vision and color blindness based on Newtons classification of 7 fundamental colors (ROYGBIV). Edridge-Green classified color vision based on how many distinct colors a subject could see in the spectrum. Normal subjects were termed hexachromic as they could not discern Indigo. Subjects with superior color vision, who could discern indigo, where heptachromic. The colorblind were therefore dichromic (equivalent to dichromacy) or tri-, tetra- or pentachromic (anomalous trichromacy).

Society and culture
Design implications
Color codes are useful tools for designers to convey information. The interpretation of this information requires users to perform a variety of Color Tasks, usually comparative but also sometimes connotative or denotative. However, these tasks are often problematic for the colorblind when design of the color code has not followed best practices for accessibility. For example, one of the most ubiquitous connotative color codes is the "red means bad and green means good" or similar systems, based on the classic signal light colors. However, this color coding will almost always be undifferentiable to either (Deutans or Protans) and therefore should be avoided or supplemented with a parallel connotative system (symbols, smileys, etc.).
Good practices to ensure design is accessible to the colorblind, include:

When possible (e.g. in simple video games or apps), allowing the user to choose their own colors is the most inclusive design practice.
Using other signals that are parallel to the color coding, such as patterns, shapes, size or order. This not only helps color blind people, but also aids understanding by normally sighted people by providing them with multiple reinforcing cues.
Using brightness contrast (different shades) in addition to color contrast (different hues)
To achieve good contrast, conventional wisdom suggests converting a (digital) design to grayscale to ensure there is sufficient brightness contrast between colors. However, this does not account for the different perceptions of brightness to different varieties of colorblindness, especially Protans, Tritans and Monochromats.
Viewing the design through a CVD Simulator to ensure the information carried by color is still sufficiently conveyed. At a minimum, the design should be visible for Deutans, the most common kind of colorblindness.
Maximizing the area of colors (e.g. increase size, thickness or boldness of colored element) makes the color easier to identify. Color contrast improves as the angle the color subtends on the retina increases. This applies to all types of color vision.
Maximizing brightness (value) and saturation (chroma) of the colors to maximize color contrast.
Converting connotative tasks to comparative tasks by including a legend, even when the meaning is considered obvious (e.g. red means danger).
Avoiding denotative color tasks (color naming) when possible. Some denotative tasks can be converted to comparative tasks by depicting the actual color whenever the color name is mentioned; for example, colored typography in "purple", or "purple (█)".
For denotative tasks (color naming), using the most common shades of colors. For example, green and yellow are colors of confusion in red-green CVD, but it is very common to mix forest green (█) with bright yellow (█). Mistakes by the colorblind increase drastically when uncommon shades are used, e.g. neon green (█) with dark yellow (█).
For denotative tasks, using colors that are classically associated with a color name. For example, dont use burgundy (█) to represent "red".

Unordered Information
A common task for designers is to select a subset of colors (qualitative colormap) that are as mutually differentiable as possible (salient). For example, player pieces in a board game should be as different as possible.
Classic advice suggests using Brewer palettes, but several of these are not actually colorblind-accessible. A recent, free, powerful tool that checks color contrast of a group of colors is Adobes Color Blind Safe Tool.
Unfortunately, the colors with the greatest contrast to the red-green colorblind tend to be colors of confusion to the blue-yellow colorblind, and vice versa. However, since red-green is much more prevalent than blue-yellow CVD, design should generally prioritize those users (Deutans, then Protans).

Ordered Information
A common task for data visualization is to represent a color scale, or sequential colormap, often in the form of a heat map or choropleth. Several scales are designed with special consideration for the colorblind and are widespread in academia, including Cividis, Viridis and Parula (Matlab). These comprise a light-to-dark scale superimposed on a yellow-to-blue scale, making them monotonic and perceptually uniform to all forms of color vision.

Occupations
Color blindness may make it difficult or impossible for a person to engage in certain occupations. Persons with color blindness may be legally or practically barred from occupations in which color perception is an essential part of the job (e.g., mixing paint colors), or in which color perception is important for safety (e.g., operating vehicles in response to color-coded signals). This occupational safety principle originates from the aftermath of the 1875 Lagerlunda train crash, which Alarik Frithiof Holmgren blamed on the color blindness of the engineer and created the first occupational screening test against the colorblind.
...I consider that to [Holmgren] above all others do we owe the present and future control of color-blindness on land and sea, by which life and property are safer, and the risks of travelling less.
Color vision is important for occupations using telephone or computer networking cabling, as the individual wires inside the cables are color-coded using green, orange, brown, blue and white colors. Electronic wiring, transformers, resistors, and capacitors are color-coded as well, using black, brown, red, orange, yellow, green, blue, violet, gray, white, silver, gold.

Driving
Red-green colorblindness can make it difficult to drive, primarily due to the inability to differentiate red-amber-green traffic lights. Protans are further disadvantaged due to the darkened perception of reds, which can make it more difficult to quickly recognize brake lights. In response, some countries have refused to grant drivers licenses to individuals with color blindness:

In April 2003, Romania removed color blindness from its list of disqualifying conditions for learner drivers licenses. It is now qualified as a condition that could potentially compromise driver safety, therefore a driver may have to be evaluated by an authorized ophthalmologist to determine if they can drive safely. As of May 2008, there is an ongoing campaign to remove the legal restrictions that prohibit colorblind citizens from getting drivers licenses.
In June 2020, India relaxed its ban on drivers licenses for the colorblind to now only apply to those with strong CVD. While previously restricted, those who test as mild or moderate can now pass the medical requirements.
Australia instituted a tiered ban on the colorblind from obtaining commercial drivers licenses in 1994. This included a ban for all protans, and a stipulation that deutans must pass the Farnsworth Lantern. The stipulation on deutans was revoked in 1997 citing a lack of available test facilities, and the ban on protans was revoked in 2003.
All colorblind individuals are banned from obtaining a drivers license in China and since 2016 in Russia (2012 for dichromats).
There are several features available that help the colorblind compensate for their color vision deficiency:

British Rail signals use more easily identifiable colors: the red is blood red, the amber is yellow and the green is a bluish color.
The relative position of traffic lights is fixed internationally as red, amber, green from top to bottom. Horizontal lights will differ depending on the country, but right hand traffic typically follows a "red light always on the left" pattern.
Most British road traffic lights are mounted vertically on a black rectangle with a white border (forming a "sighting board") so drivers can more easily look for the position of the light.
In the eastern provinces of Canada traffic lights are sometimes differentiated by shape in addition to color: square for red, diamond for yellow, and circle for green (see included image of horizontal traffic light from Nova Scotia).

Piloting aircraft
Although many aspects of aviation depend on color coding, only a few of them are critical enough to be interfered with by some milder types of color blindness. Some examples include color-gun signaling of aircraft that have lost radio communication, color-coded glide-path indications on runways, and the like. Some jurisdictions restrict the issuance of pilot credentials to persons with color blindness for this reason. Restrictions may be partial, allowing color-blind persons to obtain certification but with restrictions, or total, in which case color-blind persons are not permitted to obtain piloting credentials at all.In the United States, the Federal Aviation Administration requires that pilots be tested for normal color vision as part of their medical clearance in order to obtain the required medical certificate, a prerequisite to obtaining a pilots certification. If testing reveals color blindness, the applicant may be issued a license with restrictions, such as no night flying and no flying by color signals—such a restriction effectively prevents a pilot from holding certain flying occupations, such as that of an airline pilot, although commercial pilot certification is still possible, and there are a few flying occupations that do not require night flight and thus are still available to those with restrictions due to color blindness (e.g., agricultural aviation). The government allows several types of tests, including medical standard tests (e.g., the Ishihara, Dvorine, and others) and specialized tests oriented specifically to the needs of aviation. If an applicant fails the standard tests, they will receive a restriction on their medical certificate that states: "Not valid for night flying or by color signal control". They may apply to the FAA to take a specialized test, administered by the FAA. Typically, this test is the "color vision light gun test". For this test an FAA inspector will meet the pilot at an airport with an operating control tower. The color signal light gun will be shone at the pilot from the tower, and they must identify the color. If they pass they may be issued a waiver, which states that the color vision test is no longer required during medical examinations. They will then receive a new medical certificate with the restriction removed </s>


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


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


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


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Gunshot wound and explain in detail? [/INST] A gunshot wound (GSW) is a penetrating injury caused by a projectile (e.g. a bullet) from a gun (typically firearm or air gun). Damages may include bleeding, bone fractures, organ damage, wound infection, loss of the ability to move part of the body and, in more severe cases, death. Damage depends on the part of the body hit, the path the bullet follows through the body, and the type and speed of the bullet. Long-term complications can include lead poisoning and post-traumatic stress disorder (PTSD).Factors that determine rates of gun violence vary by country. These factors may include the illegal drug trade, easy access to firearms, substance misuse including alcohol, mental health problems, firearm laws, social attitudes, economic differences and occupations such as being a police officer. Where guns are more common, altercations more often end in death.Before management begins it should be verified the area is safe. This is followed by stopping major bleeding, then assessing and supporting the airway, breathing, and circulation. Firearm laws, particularly background checks and permit to purchase, decrease the risk of death from firearms. Safer firearm storage may decrease the risk of firearm-related deaths in children.In 2015, about a million gunshot wounds occurred from interpersonal violence. In 2016, firearms resulted in 251,000 deaths globally, up from 209,000 in 1990. Of these deaths 161,000 (64%) were the result of assault, 67,500 (27%) were the result of suicide, and 23,000 (9%) were accidents. In the United States, guns resulted in about 40,000 deaths in 2017. Firearm-related deaths are most common in males between the ages of 20 to 24 years. Economic costs due to gunshot wounds have been estimated at US$140 billion a year in the United States.

Signs and symptoms
Trauma from a gunshot wound varies widely based on the bullet, velocity, mass, entry point, trajectory, affected anatomy, and exit point. Gunshot wounds can be particularly devastating compared to other penetrating injuries because the trajectory and fragmentation of bullets can be unpredictable after entry. Moreover, gunshot wounds typically involve a large degree of nearby tissue disruption and destruction caused by the physical effects of the projectile correlated with the bullet velocity classification.The immediate damaging effect of a gunshot wound is typically severe bleeding with the potential for hypovolemic shock, a condition characterized by inadequate delivery of oxygen to vital organs. In the case of traumatic hypovolemic shock, this failure of adequate oxygen delivery is due to blood loss, as blood is the means of delivering oxygen to the bodys constituent parts. Devastating effects can result when a bullet strikes a vital organ such as the heart, lungs or liver, or damages a component of the central nervous system such as the spinal cord or brain.Common causes of death following gunshot injury include bleeding, low oxygen caused by pneumothorax, catastrophic injury to the heart and major blood vessels, and damage to the brain or central nervous system. Non-fatal gunshot wounds frequently have mild to severe long-lasting effects, typically some form of major disfigurement such as amputation because of a severe bone fracture and may cause permanent disability. A sudden blood gush may take effect immediately from a gunshot wound if a bullet directly damages larger blood vessels, especially arteries.

Pathophysiology
The degree of tissue disruption caused by a projectile is related to the cavitation the projectile creates as it passes through tissue. A bullet with sufficient energy will have a cavitation effect in addition to the penetrating track injury. As the bullet passes through the tissue, initially crushing then lacerating, the space left forms a cavity; this is called the permanent cavity. Higher-velocity bullets create a pressure wave that forces the tissues away, creating not only a permanent cavity the size of the caliber of the bullet but a temporary cavity or secondary cavity, which is often many times larger than the bullet itself. The temporary cavity is the radial stretching of tissue around the bullets wound track, which momentarily leaves an empty space caused by high pressures surrounding the projectile that accelerate material away from its path. The extent of cavitation, in turn, is related to the following characteristics of the projectile:

Kinetic energy: KE = 1/2mv2 (where m is mass and v is velocity). This helps to explain why wounds produced by projectiles of higher mass and/or higher velocity produce greater tissue disruption than projectiles of lower mass and velocity. The velocity of the bullet is a more important determinant of tissue injury. Although both mass and velocity contribute to the overall energy of the projectile, the energy is proportional to the mass while proportional to the square of its velocity. As a result, for constant velocity, if the mass is doubled, the energy is doubled; however, if the velocity of the bullet is doubled, the energy increases four times. The initial velocity of a bullet is largely dependent on the firearm. The US military commonly uses 5.56-mm bullets, which have a relatively low mass as compared with other bullets; however, the speed of these bullets is relatively fast. As a result, they produce a larger amount of kinetic energy, which is transmitted to the tissues of the target. The size of the temporary cavity is approximately proportional to the kinetic energy of the bullet and depends on the resistance of the tissue to stress. Muzzle energy, which is based on muzzle velocity, is often used for ease of comparison.
Yaw: Handgun bullets will generally travel in a relatively straight line or make one turn if a bone is hit. Upon travel through deeper tissue, high-energy rounds may become unstable as they decelerate, and may tumble (pitch and yaw) as the energy of the projectile is absorbed, causing stretching and tearing of the surrounding tissue.
Fragmentation: Most commonly, bullets do not fragment, and secondary damage from fragments of shattered bone is a more common complication than bullet fragments.

Diagnosis
Classification
Gunshot wounds are classified according to the speed of the projectile using the Gustilo open fracture classification:

Low-velocity: Less than 1,100 ft/s (340 m/s)Low velocity wounds are typical of small caliber handguns and display wound patterns like Gustilo Anderson Type 1 or 2 wounds

Medium-velocity: Between 1,200 ft/s (340 m/s) and 2,000 ft/s (610 m/s)These are more typical of shotgun blasts or higher caliber handguns like magnums. The risk of infection from these types of wounds can vary depending on the type and pattern of bullets fired as well as the distance from the firearm.

High-velocity: Between 2,000 ft/s (610 m/s) and 3,500 ft/s (1,100 m/s)Usually caused by powerful assault or hunting rifles and usually display wound pattern similar to Gustilo Anderson Type 3 wounds. The risk of infection is especially high due to the large area of injury and destroyed tissue.Bullets from handguns are sometimes less than 1,000 ft/s (300 m/s) but with modern pistol loads, they usually are slightly above 1,000 ft/s (300 m/s), while bullets from most modern rifles exceed 2,500 ft/s (760 m/s). One recently developed class of firearm projectiles is the hyper-velocity bullet, such cartridges are usually either wildcats made for achieving such high speed or purpose-built factory ammunition with the same goal in mind. Examples of hyper velocity cartridges include the .220 Swift, .17 Remington and .17 Mach IV cartridges. The US military commonly uses 5.56mm bullets, which have a relatively low mass as compared with other bullets (40-62 grains); however, the speed of these bullets is relatively fast (Approximately 2,800 ft/s (850 m/s), placing them in the high velocity category). As a result, they produce a larger amount of kinetic energy, which is transmitted to the tissues of the target. However, one must remember that high kinetic energy does not necessarily equate to high stopping power, as incapacitation usually results from remote wounding effects such as bleeding, rather than raw energy transfer. High energy does indeed result in more tissue disruption, which plays a role in incapacitation, but other factors such as wound size and shot placement play as big of, if not a bigger role in stopping power and thus, effectiveness. Muzzle velocity does not consider the effect of aerodynamic drag on the flight of the bullet for the sake of ease of comparison.

Prevention
Medical organizations in the United States recommend a criminal background check being held before a person buys a gun and that a person who has convictions for crimes of violence should not be permitted to buy a gun. Safe storage of firearms is recommended, as well as better mental health care and removal of guns from those at risk of suicide. In an effort to prevent mass shootings greater regulations on guns that can rapidly fire many bullets is recommended.

Management
Initial assessment for a gunshot wound is approached in the same way as other acute trauma using the advanced trauma life support (ATLS) protocol. These include:

A) Airway - Assess and protect airway and potentially the cervical spine
B) Breathing - Maintain adequate ventilation and oxygenation
C) Circulation - Assess for and control bleeding to maintain organ perfusion including focused assessment with sonography for trauma (FAST)
D) Disability - Perform basic neurological exam including Glasgow Coma Scale (GCS)
E) Exposure - Expose entire body and search for any missed injuries, entry points, and exit points while maintaining body temperatureDepending on the extent of injury, management can range from urgent surgical intervention to observation. As such, any history from the scene such as gun type, shots fired, shot direction and distance, blood loss on scene, and pre-hospital vitals signs can be very helpful in directing management. Unstable people with signs of bleeding that cannot be controlled during the initial evaluation require immediate surgical exploration in the operating room. Otherwise, management protocols are generally dictated by anatomic entry point and anticipated trajectory.

Neck
A gunshot wound to the neck can be particularly dangerous because of the high number of vital anatomical structures contained within a small space. The neck contains the larynx, trachea, pharynx, esophagus, vasculature (carotid, subclavian, and vertebral arteries; jugular, brachiocephalic, and vertebral veins; thyroid vessels), and nervous system anatomy (spinal cord, cranial nerves, peripheral nerves, sympathetic chain, brachial plexus). Gunshots to the neck can thus cause severe bleeding, airway compromise, and nervous system injury.Initial assessment of a gunshot wound to the neck involves non-probing inspection of whether the injury is a penetrating neck injury (PNI), classified by violation of the platysma muscle. If the platysma is intact, the wound is considered superficial and only requires local wound care. If the injury is a PNI, surgery should be consulted immediately while the case is being managed. Of note, wounds should not be explored on the field or in the emergency department given the risk of exacerbating the wound.
Due to the advances in diagnostic imaging, management of PNI has been shifting from a "zone-based" approach, which uses anatomical site of injury to guide decisions, to a "no-zone" approach which uses a symptom-based algorithm. The no-zone approach uses a hard signs and imaging system to guide next steps. Hard signs include airway compromise, unresponsive shock, diminished pulses, uncontrolled bleeding, expanding hematoma, bruits/thrill, air bubbling from wound or extensive subcutaneous air, stridor/hoarseness, neurological deficits. If any hard signs are present, immediate surgical exploration and repair is pursued alongside airway and bleeding control. If there are no hard signs, the person receives a multi-detector CT angiography for better diagnosis. A directed angiography or endoscopy may be warranted in a high-risk trajectory for the gunshot. A positive finding on CT leads to operative exploration. If negative, the person may be observed with local wound care.

Chest
Important anatomy in the chest includes the chest wall, ribs, spine, spinal cord, intercostal neurovascular bundles, lungs, bronchi, heart, aorta, major vessels, esophagus, thoracic duct, and diaphragm. Gunshots to the chest can thus cause severe bleeding (hemothorax), respiratory compromise (pneumothorax, hemothorax, pulmonary contusion, tracheobronchial injury), cardiac injury (pericardial tamponade), esophageal injury, and nervous system injury.Initial workup as outlined in the Workup section is particularly important with gunshot wounds to the chest because of the high risk for direct injury to the lungs, heart, and major vessels. Important notes for the initial workup specific for chest injuries are as follows. In people with pericardial tamponade or tension pneumothorax, the chest should be evacuated or decompressed if possible prior to attempting tracheal intubation because the positive pressure ventilation can cause hypotention or cardiovascular collapse. Those with signs of a tension pneumothorax (asymmetric breathing, unstable blood flow, respiratory distress) should immediately receive a chest tube (> French 36) or needle decompression if chest tube placement is delayed. FAST exam should include extended views into the chest to evaluate for hemopericardium, pneumothorax, hemothorax, and peritoneal fluid.Those with cardiac tamponade, uncontrolled bleeding, or a persistent air leak from a chest tube all require surgery. Cardiac tamponade can be identified on FAST exam. Blood loss warranting surgery is 1–1.5 L of immediate chest tube drainage or ongoing bleeding of 200-300 mL/hr. Persistent air leak is suggestive of tracheobronchial injury which will not heal without surgical intervention. Depending on the severity of the persons condition and if cardiac arrest is recent or imminent, the person may require surgical intervention in the emergency department, otherwise known as an emergency department thoracotomy (EDT).However, not all gunshot to the chest require surgery. Asymptomatic people with a normal chest X-ray can be observed with a repeat exam and imaging after 6 hours to ensure no delayed development of pneumothorax or hemothorax. If a person only has a pneumothorax or hemothorax, a chest tube is usually sufficient for management unless there is large volume bleeding or persistent air leak as noted above. Additional imaging after initial chest X-ray and ultrasound can be useful in guiding next steps for stable people. Common imaging modalities include chest CT, formal echocardiography, angiography, esophagoscopy, esophagography, and bronchoscopy depending on the signs and symptoms.

Abdomen
Important anatomy in the abdomen includes the stomach, small bowel, colon, liver, spleen, pancreas, kidneys, spine, diaphragm, descending aorta, and other abdominal vessels and nerves. Gunshots to the abdomen can thus cause severe bleeding, release of bowel contents, peritonitis, organ rupture, respiratory compromise, and neurological deficits.
The most important initial evaluation of a gunshot wound to the abdomen is whether there is uncontrolled bleeding, inflammation of the peritoneum, or spillage of bowel contents. If any of these are present, the person should be transferred immediately to the operating room for laparotomy. If it is difficult to evaluate for those indications because the person is unresponsive or incomprehensible, it is up to the surgeons discretion whether to pursue laparotomy, exploratory laparoscopy, or alternative investigative tools.
Although all people with abdominal gunshot wounds were taken to the operating room in the past, practice has shifted in recent years with the advances in imaging to non-operative approaches in more stable people. If the persons vital signs are stable without indication for immediate surgery, imaging is done to determine the extent of injury. Ultrasound (FAST) and help identify intra-abdominal bleeding and X-rays can help determine bullet trajectory and fragmentation. However, the best and preferred mode of imaging is high-resolution multi-detector CT (MDCT) with IV, oral, and sometimes rectal contrast. Severity of injury found on imaging will determine whether the surgeon takes an operative or close observational approach.
Diagnostic peritoneal lavage (DPL) has become largely obsolete with the advances in MDCT, with use limited to centers without access to CT to guide requirement for urgent transfer for operation.

Extremities
The four main components of extremities are bones, vessels, nerves, and soft tissues. Gunshot wounds can thus cause severe bleeding, fractures, nerve deficits, and soft tissue damage. The Mangled Extremity Severity Score (MESS) is used to classify the severity of injury and evaluates for severity of skeletal and/or soft tissue injury, limb ischemia, shock, and age. Depending on the extent of injury, management can range from superficial wound care to limb amputation.
Vital sign stability and vascular assessment are the most important determinants of management in extremity injuries. As with other traumatic cases, those with uncontrolled bleeding require immediate surgical intervention. If surgical intervention is not readily available and direct pressure is insufficient to control bleeding, tourniquets or direct clamping of visible vessels may be used temporarily to slow active bleeding. People with hard signs of vascular injury also require immediate surgical intervention. Hard signs include active bleeding, expanding or pulsatile hematoma, bruit/thrill, absent distal pulses and signs of extremity ischemia.For stable people without hard signs of vascular injury, an injured extremity index (IEI) should be calculated by comparing the blood pressure in the injured limb compared to an uninjured limb in order to further evaluate for potential vascular injury. If the IEI or clinical signs are suggestive of vascular injury, the person may undergo surgery or receive further imaging including CT angiography or conventional arteriography.
In addition to vascular management, people must be evaluated for bone, soft tissue, and nerve injury. Plain films can be used for fractures alongside CTs for soft tissue assessment. Fractures must be debrided and stabilized, nerves repaired when possible, and soft tissue debrided and covered. This process can often require multiple procedures over time depending on the severity of injury.

Epidemiology
In 2015, about a million gunshot wounds occurred from interpersonal violence. Firearms, globally in 2016, resulted in 251,000 deaths up from 209,000 in 1990. Of these deaths 161,000 (64%) were the result of assault, 67,500 (27%) were the result of suicide, and 23,000 were accidents. Firearm related deaths are most common in males between the ages of 20 to 24 years.The countries with the greatest number of deaths from firearms are Brazil, United States, Mexico, Colombia, Venezuela, Guatemala and South Africa which make up just over half the total. In the United States in 2015 about half of the 44,000 people who died by suicide did so with a gun.As of 2016, the countries with the highest rates of gun violence per capita were El Salvador, Venezuela, and Guatemala with 40.3, 34.8, and 26.8 violent gun deaths per 100,000 people respectively. The countries with the lowest rates of were Singapore, Japan, and South Korea with 0.03, 0.04, and 0.05 violent gun deaths per 100,000 people respectively.

Canada
In 2016, about 893 people died due to gunshot wounds in Canada (2.1 per 100,000). About 80% were suicides, 12% were assaults, and 4% percent were an accident.

United States
In 2017, there were 39,773 deaths in the United States as a result gunshot wounds. Of these 60% were suicides, 37% were homicides, 1.4% were by law enforcement, 1.2% were accidents, and 0.9% were from an unknown cause. This is up from 37,200 deaths in 2016 due to a gunshot wound (10.6 per 100,000). With respect to those that pertain to interpersonal violence, it had the 31st highest rate in the world with 3.85 deaths per 100,000 people in 2016. The majority of all homicides and suicides are firearm-related, and the majority of firearm-related deaths are the result of murder and suicide. When sorted by GDP, however, the United States has a much higher violent gun death rate compared to other developed countries, with over 10 times the number of firearms assault deaths than the next four highest GDP countries combined. Gunshot violence is the third most costly cause of injury and the fourth most expensive form of hospitalization in the United States.

History
Until the 1880s, the standard practice for treating a gunshot wound called for physicians to insert their unsterilized fingers into the wound to probe and locate the path of the bullet. Standard surgical theory such as opening abdominal cavities to repair gunshot wounds, germ theory, and Joseph Listers technique for antiseptic surgery using diluted carbolic acid, had not yet been accepted as standard practice. For example, sixteen doctors attended to President James A </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Radiation burn and explain in detail? [/INST] A radiation burn is a damage to the skin or other biological tissue and organs as an effect of radiation. The radiation types of greatest concern are thermal radiation, radio frequency energy, ultraviolet light and ionizing radiation.
The most common type of radiation burn is a sunburn caused by UV radiation. High exposure to X-rays during diagnostic medical imaging or radiotherapy can also result in radiation burns. As the ionizing radiation interacts with cells within the body—damaging them—the body responds to this damage, typically resulting in erythema—that is, redness around the damaged area. Radiation burns are often discussed in the same context as radiation-induced cancer due to the ability of ionizing radiation to interact with and damage DNA, occasionally inducing a cell to become cancerous. Cavity magnetrons can be improperly used to create surface and internal burning. Depending on the photon energy, gamma radiation can cause deep gamma burns, with 60Co internal burns common. Beta burns tend to be shallow as beta particles are not able to penetrate deeply into a body; these burns can be similar to sunburn. Alpha particles can cause internal alpha burns if inhaled, with external damage (if any) being limited to minor erythema.
Radiation burns can also occur with high power radio transmitters at any frequency where the body absorbs radio frequency energy and converts it to heat. The U.S. Federal Communications Commission (FCC) considers 50 watts to be the lowest power above which radio stations must evaluate emission safety. Frequencies considered especially dangerous occur where the human body can become resonant, at 35 MHz, 70 MHz, 80-100 MHz, 400 MHz, and 1 GHz. Exposure to microwaves of too high intensity can cause microwave burns.

Types
Radiation dermatitis (also known as radiodermatitis) is a skin disease associated with prolonged exposure to ionizing radiation.: 131–2  Radiation dermatitis occurs to some degree in most patients receiving radiation therapy, with or without chemotherapy.There are three specific types of radiodermatitis: acute radiodermatitis, chronic radiodermatitis, and eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy.: 39–40  Radiation therapy can also cause radiation cancer.: 40 With interventional fluoroscopy, because of the high skin doses that can be generated in the course of the intervention, some procedures have resulted in early (less than two months after exposure) and/or late (two months or more after exposure) skin reactions, including necrosis in some cases.: 773 Radiation dermatitis, in the form of intense erythema and vesiculation of the skin, may be observed in radiation ports.: 131 As many as 95% of patients treated with radiation therapy for cancer will experience a skin reaction. Some reactions are immediate, while others may be later (e.g., months after treatment).

Acute
Acute radiodermatitis occurs when an "erythema dose" of ionizing radiation is given to the skin, after which visible erythema appears up to 24 hours after.: 39   Radiation dermatitis generally manifests within a few weeks after the start of radiotherapy.: 143   Acute radiodermatitis, while presenting as red patches, may sometimes also present with desquamation or blistering.  Erythema may occur at a dose of 2 Gy radiation or greater.

Chronic
Chronic radiodermatitis occurs with chronic exposure to "sub-erythema" doses of ionizing radiation over a prolonged period, producing varying degrees of damage to the skin and its underlying parts after a variable latent period of several months to several decades.: 40   In the distant past this type of radiation reaction occurred most frequently in radiologists and radiographers who were constantly exposed to ionizing radiation, especially before the use of X-ray filters.: 40   Chronic radiodermatitis, squamous and
basal cell carcinomas may develop months to years after radiation exposure.: 130   Chronic radiodermatitis presents as atrophic indurated plaques, often whitish or yellowish, with telangiectasia, sometimes with hyperkeratosis.: 130

Other
Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy is a skin condition that occurs most often in women receiving cobalt radiotherapy for internal cancer.: 39–40 Radiation-induced erythema multiforme may occur when phenytoin is given prophylactically to neurosurgical patients who are receiving whole-brain therapy and systemic steroids.: 130

Delayed effects
Radiation acne is a cutaneous condition characterized by comedo-like papules occurring at sites of previous exposure to therapeutic ionizing radiation, skin lesions that begin to appear as the acute phase of radiation dermatitis begins to resolve.: 501 Radiation recall reactions occur months to years after radiation treatment, a reaction that follows recent administration of a chemotherapeutic agent and occurs with the prior radiation port, characterized by features of radiation dermatitis.  Restated, radiation recall dermatitis is an inflammatory skin reaction that occurs in a previously irradiated body part following drug administration.  There does not appear to be a minimum dose, nor an established radiotherapy dose relationship.

Alpha burns
"Alpha burns" are caused by alpha particles, which can cause extensive tissue damage if inhaled. Due to the keratin in the epidermal layer of the skin, external alpha burns are limited to only mild reddening of the outermost layer of skin.

Beta burns
"Beta burns"—caused by beta particles—are shallow surface burns, usually of skin and less often of lungs or gastrointestinal tract, caused by beta particles, typically from hot particles or dissolved radionuclides that came to direct contact with or close proximity to the body. They can appear similar to sunburn. Unlike gamma rays, beta emissions are stopped much more effectively by materials and therefore deposit all their energy in only a shallow layer of tissue, causing more intense but more localized damage. On cellular level, the changes in skin are similar to radiodermatitis.
High doses of radiation can cause rapid browning of skin, known as "nuclear tan".The dose is influenced by relatively low penetration of beta emissions through materials. The cornified keratine layer of epidermis has enough stopping power to absorb beta radiation with energies lower than 70 keV. Further protection is provided by clothing, especially shoes. The dose is further reduced by limited retention of radioactive particles on skin; a 1 millimeter particle is typically released in 2 hours, while a 50 micrometer particle usually does not adhere for more than 7 hours. Beta emissions are also severely attenuated by air; their range generally does not exceed 6 feet (1.8 m) and intensity rapidly diminishes with distance.The eye lens seems to be the most sensitive organ to beta radiation, even in doses far below maximum permissible dose. Safety goggles are recommended to attenuate strong beta.Beta burns can occur also to plants. An example of such damage is the Red Forest, a victim of the Chernobyl accident.
Careful washing of exposed body surface, removing the radioactive particles, may provide significant dose reduction. Exchanging or at least brushing off clothes also provides a degree of protection.
If the exposure to beta radiation is intense, the beta burns may first manifest in 24–48 hours by itching and/or burning sensation that last for one or two days, sometimes accompanied by hyperaemia. After 1–3 weeks burn symptoms appear; erythema, increased skin pigmentation (dark colored patches and raised areas), followed by epilation and skin lesions. Erythema occurs after 5–15 Gy, dry desquamation after 17 Gy, and bullous epidermitis after 72 Gy. Chronic radiation keratosis may develop after higher doses. Primary erythema lasting more than 72 hours is an indication of injury severe enough to cause chronic radiation dermatitis. Edema of dermal papillae, if present within 48 hours since the exposition, is followed by transepidermal necrosis. After higher doses, the malpighian layer cells die within 24 hours; lower doses may take 10–14 days to show dead cells. Inhalation of beta radioactive isotopes may cause beta burns of lungs and nasopharyngeal region, ingestion may lead to burns of gastrointestinal tract; the latter being a risk especially for grazing animals.

In first degree beta burns the damage is largely limited to epidermis. Dry or wet desquamation occurs; dry scabs are formed, then heal rapidly, leaving a depigmented area surrounded with irregular area of increased pigmentation. The skin pigmentation returns to normal within several weeks.
Second degree beta burns lead to formation of blisters.
Third and fourth degree beta burns result in deeper, wet ulcerated lesions, which heal with routine medical care after covering themselves with dry scab. In case of heavy tissue damage, ulcerated necrotic dermatitis may occur. Pigmentation may return to normal within several months after wound healing.Lost hair begins regrowing in nine weeks and is completely restored in about half a year.The acute dose-dependent effects of beta radiation on skin are as follows:
According to other source:
As shown, the dose thresholds for symptoms vary by source and even individually. In practice, determining the exact dose tends to be difficult.
Similar effects apply to animals, with fur acting as additional factor for both increased particle retention and partial skin shielding. Unshorn thickly wooled sheep are well protected; while the epilation threshold for sheared sheep is between 23 and 47 Gy (2500–5000 rep) and the threshold for normally wooled face is 47–93 Gy (5000–10000 rep), for thickly wooled (33 mm hair length) sheep it is 93–140 Gy (10000–15000 rep). To produce skin lesions comparable with contagious pustular dermatitis, the estimated dose is between 465 and 1395 Gy.

Energy vs penetration depth
The effects depend on both the intensity and the energy of the radiation. Low-energy beta (sulfur-35, 170 keV) produces shallow ulcers with little damage to dermis, while cobalt-60 (310 keV), caesium-137 (550 keV), phosphorus-32 (1.71 MeV), strontium-90 (650 keV) and its daughter product yttrium-90 (2.3 MeV) damage deeper levels of the dermis and can result in chronic radiation dermatitis. Very high energies from electron beams from particle accelerators, reaching tens of megaelectronvolts, can be deeply penetrating. Conversely, megavolt-scale beams can deposit their energy deeper with less damage to the dermis; modern radiotherapy electron beam accelerators take advantage of this. At yet higher energies, above 16 MeV, the effect does not show significantly anymore, limiting the usefulness of higher energies for radiotherapy. As a convention, surface is defined as the topmost 0.5 mm of skin. High-energy beta emissions should be shielded with plastic instead of lead, as high-Z elements generate deeply penetrating gamma bremsstrahlung.
The electron energies from beta decay are not discrete but form a continuous spectrum with a cutoff at maximum energy. The rest of the energy of each decay is carried off by an antineutrino which does not significantly interact and therefore does not contribute to the dose. Most energies of beta emissions are at about a third of the maximum energy. Beta emissions have much lower energies than what is achievable from particle accelerators, no more than few megaelectronvolts.
The energy-depth-dose profile is a curve starting with a surface dose, ascending to the maximum dose in a certain depth dm (usually normalized as 100% dose), then descends slowly through depths of 90% dose (d90) and 80% dose (d80), then falls off linearly and relatively sharply though depth of 50% dose (d50). The extrapolation of this linear part of the curve to zero defines the maximum electron range, Rp. In practice, there is a long tail of weaker but deep dose, called "bremsstrahlung tail", attributable to bremsstrahlung. The penetration depth depends also on beam shape, narrower beam tend to have less penetration. In water, broad electron beams, as is the case in homogeneous surface contamination of skin, have d80 about E/3 cm and Rp about E/2 cm, where E is the beta particle energy in MeV.The penetration depth of lower-energy beta in water (and soft tissues) is about 2 mm/MeV. For a 2.3 MeV beta the maximum depth in water is 11 mm, for 1.1 MeV it is 4.6 mm. The depth where maximum of the energy is deposited is significantly lower.The energy and penetration depth of several isotopes is as follows:
For a wide beam, the depth-energy relation for dose ranges is as follows, for energies in megaelectronvolts and depths in millimeters. The dependence of surface dose and penetration depth on beam energy is clearly visible.

Causes
Radiation burns are caused by exposure to high levels of radiation. Levels high enough to cause burn are generally lethal if received as a whole-body dose, whereas they may be treatable if received as a shallow or local dose.

Medical imaging
Fluoroscopy may cause burns if performed repeatedly or for too long.Similarly, X-ray computed tomography and traditional projectional radiography have the potential to cause radiation burns if the exposure factors and exposure time are not appropriately controlled by the operator.
A study of radiation-induced skin injuries has been performed by the Food and Drug Administration (FDA) based on results from 1994, followed by an advisory to minimize further fluoroscopy-induced injuries. The problem of radiation injuries due to fluoroscopy has been further investigated in review articles in 2000, 2001, 2009 and 2010.

Radioactive fallout
Beta burns are frequently the result of exposure to radioactive fallout after nuclear explosions or nuclear accidents. Shortly after the explosion, the fission products have very high beta activity, with about two beta emissions per each gamma photon.
After the Trinity test, the fallout caused localized burns on the backs of cattle in the area downwind. The fallout had the appearance of small flaky dust particles. The cattle showed temporary burns, bleeding, and loss of hair. Dogs were also affected; in addition to localized burns on their backs, they also had burned paws, likely from the particles lodged between their toes as hoofed animals did not show problems with feet. About 350–600 cattle were affected by superficial burns and localized temporary loss of dorsal hair; the army later bought 75 most affected cows as the discolored regrown hair lowered their market value. The cows were shipped to Los Alamos and Oak Ridge, where they were observed. They healed, now sporting large patches of white fur; some looked as if they had been scalded.The fallout produced by the Castle Bravo test was unexpectedly strong. A white snow-like dust, nicknamed by the scientists "Bikini snow" and consisting of contaminated crushed calcined coral, fell for about 12 hours upon the Rongelap Atoll, depositing a layer of up to 2 cm. Residents developed beta burns, mostly on the backs of their necks and on their feet, and were resettled after three days. After 24–48 hours their skin was itching and burning; in a day or two the sensations subsided, to be followed after 2–3 weeks by epilation and ulcers. Darker-colored patches and raised areas appeared on their skin, blistering was uncommon. Ulcers formed dry scabs and healed. Deeper lesions, painful, weeping and ulcerated, formed on more contaminated residents; the majority healed with simple treatment. In general, the beta burns healed with some cutaneous scarring and depigmentation. Individuals who bathed and washed the fallout particles from their skin did not develop skin lesions. The fishing ship Daigo Fukuryu Maru was affected by the fallout as well; the crew suffered skin doses between 1.7 and 6.0 Gy, with beta burns manifesting as severe skin lesions, erythema, erosions, sometimes necrosis, and skin atrophy. Twenty-three U.S. radar servicemen of the 28-member weather station on Rongerik were affected, experiencing discrete 1–4 mm skin lesions which healed quickly, and ridging of fingernails several months later. Sixteen crew members of the aircraft carrier USS Bairoko received beta burns, and there was an increased cancer rate.During the Zebra test of the Operation Sandstone in 1948, three men had beta burns on their hands when removing sample collection filters from drones flying through the mushroom cloud; their estimated skin surface dose was 28 to 149 Gy, and their disfigured hands required skin grafts. A fourth man showed weaker burns after the earlier Yoke test.The Upshot–Knothole Harry test at the Frenchman Flat site released a large amount of fallout. A significant number of sheep died after grazing on contaminated areas. The AEC however had a policy to compensate farmers only for animals showing external beta burns, so many claims were denied. Other tests on the Nevada Test Site also caused fallout and corresponding beta burns to sheep, horses and cattle. During the Operation Upshot–Knothole, sheep as far as 50 miles (80 km) from the test site developed beta burns to their backs and nostrils.During underground nuclear testing in Nevada, several workers developed burns and skin ulcers, in part attributed to exposure to tritium.

Nuclear accidents
Beta burns were a serious medical issue for some victims of the Chernobyl disaster; from 115 patients treated in Moscow, 30% had burns covering 10–50% of body surface, 11% were affected on 50–100% of skin; the massive exposure was often caused by clothes drenched with radioactive water. Some firefighters developed beta burns of lungs and nasopharyngeal region after inhalation of massive amounts of radioactive smoke. Out of 28 deaths, 16 had skin injuries listed among the causes. The beta activity was extremely high, with beta/gamma ratio reaching 10–30 and beta energy high enough to damage basal layer of the skin, resulting in large area portals for infections, exacerbated by damage to bone marrow and weakened immune system. Some patients received skin dose of 400–500 Gy. The infections caused more than half of the acute deaths. Several died of fourth degree beta burns between 9–28 days after dose of 6–16 Gy </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Pinguecula and explain in detail? [/INST] A pinguecula is a common type of conjunctival stromal degeneration in the eye. It appears as an elevated yellow-white plaque in the bulbar conjunctiva near the limbus. Calcification may also seen occasionally.

Etiology
The exact etiology is unknown, but it may be associated with aging and excessive exposure to UV light.

Signs and symptoms
It is seen as a yellow-white deposit on the conjunctiva adjacent to the limbus (the junction between the cornea and sclera). (It is to be distinguished clinically from a pterygium, which is a wedge shaped area of fibrosis that may grow onto the cornea.) A pinguecula usually does not cause any symptoms. It is most common in tropical climates and there is a direct correlation with UV exposure.
Histologically, there is degeneration of the collagen fibers of the conjunctival stroma with thinning of the overlying epithelium and occasionally calcification. Actinic exposure of the thin conjunctival tissue is thought to cause fibroblasts to produce more elastin fibers, which are more twisted than normal elastin fibers and may lead to the degradation of the collagen fibers. Alternatively, it has been postulated that the sub-epithelial collagen fibers undergo degradation and assume the qualities of elastic tissue while fragmenting and twisting in a different configuration from their normal state.It is thought that the high reflectivity of the solid white scleral tissue underlying the conjunctival tissue may result in additional UV exposure to the back side of the tissue. The side of the nose also reflects sunlight on to the conjunctiva. As a result, pingueculae tend to occur more often on the nasal side of the eye.  While most pingueculae are found in people over the age of 40, they are not uncommon in 20- and 30-year-old adults who spend significant time in the sun.
The surface of the conjunctival tissue overlying a pinguecula interferes with the normal spreading of the tear film. The tear ferning test reveals abnormalities of the mucous component of the tear film, making it useful as a predictor of a persons tolerance of hydrophilic soft contact lenses </s>