<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Earthquake and can you explain it in depth? [/INST] An earthquake (also known as a quake, tremor or temblor) is the shaking of the surface of the Earth resulting from a sudden release of energy in the Earths lithosphere that creates seismic waves. Earthquakes can range in intensity, from those that are so weak that they cannot be felt, to those violent enough to propel objects and people into the air, damage critical infrastructure, and wreak destruction across entire cities. The seismic activity of an area is the frequency, type, and size of earthquakes experienced over a particular time period. The seismicity at a particular location in the Earth is the average rate of seismic energy release per unit volume.  The word tremor is also used for non-earthquake seismic rumbling.
At the Earths surface, earthquakes manifest themselves by shaking and displacing or disrupting the ground. When the epicenter of a large earthquake is located offshore, the seabed may be displaced sufficiently to cause a tsunami. Earthquakes can also trigger landslides.
In its most general sense, the word earthquake is used to describe any seismic event—whether natural or caused by humans—that generates seismic waves. Earthquakes are caused mostly by rupture of geological faults but also by other events such as volcanic activity, landslides, mine blasts, and nuclear tests. An earthquakes point of initial rupture is called its hypocenter or focus. The epicenter is the point at ground level directly above the hypocenter.

Naturally occurring earthquakes
Tectonic earthquakes occur anywhere in the earth where there is sufficient stored elastic strain energy to drive fracture propagation along a fault plane. The sides of a fault move past each other smoothly and aseismically only if there are no irregularities or asperities along the fault surface that increase the frictional resistance. Most fault surfaces do have such asperities, which leads to a form of stick-slip behavior. Once the fault has locked, continued relative motion between the plates leads to increasing stress and, therefore, stored strain energy in the volume around the fault surface. This continues until the stress has risen sufficiently to break through the asperity, suddenly allowing sliding over the locked portion of the fault, releasing the stored energy. This energy is released as a combination of radiated elastic strain seismic waves, frictional heating of the fault surface, and cracking of the rock, thus causing an earthquake. This process of gradual build-up of strain and stress punctuated by occasional sudden earthquake failure is referred to as the elastic-rebound theory. It is estimated that only 10 percent or less of an earthquakes total energy is radiated as seismic energy. Most of the earthquakes energy is used to power the earthquake fracture growth or is converted into heat generated by friction. Therefore, earthquakes lower the Earths available elastic potential energy and raise its temperature, though these changes are negligible compared to the conductive and convective flow of heat out from the Earths deep interior.

Earthquake fault types
There are three main types of fault, all of which may cause an interplate earthquake: normal, reverse (thrust), and strike-slip. Normal and reverse faulting are examples of dip-slip, where the displacement along the fault is in the direction of dip and where movement on them involves a vertical component. Many earthquakes are caused by movement on faults that have components of both dip-slip and strike-slip; this is known as oblique slip. The topmost, brittle part of the Earths crust, and the cool slabs of the tectonic plates that are descending into the hot mantle, are the only parts of our planet that can store elastic energy and release it in fault ruptures. Rocks hotter than about 300 °C (572 °F) flow in response to stress; they do not rupture in earthquakes. The maximum observed lengths of ruptures and mapped faults (which may break in a single rupture) are approximately 1,000 km (620 mi). Examples are the earthquakes in Alaska (1957), Chile (1960), and Sumatra (2004), all in subduction zones. The longest earthquake ruptures on strike-slip faults, like the San Andreas Fault (1857, 1906), the North Anatolian Fault in Turkey (1939), and the Denali Fault in Alaska (2002), are about half to one third as long as the lengths along subducting plate margins, and those along normal faults are even shorter.

Normal faults
Normal faults occur mainly in areas where the crust is being extended such as a divergent boundary. Earthquakes associated with normal faults are generally less than magnitude 7. Maximum magnitudes along many normal faults are even more limited because many of them are located along spreading centers, as in Iceland, where the thickness of the brittle layer is only about six kilometres (3.7 mi).

Reverse faults
Reverse faults occur in areas where the crust is being shortened such as at a convergent boundary. Reverse faults, particularly those along convergent plate boundaries, are associated with the most powerful earthquakes, megathrust earthquakes, including almost all of those of magnitude 8 or more. Megathrust earthquakes are responsible for about 90% of the total seismic moment released worldwide.

Strike-slip faults
Strike-slip faults are steep structures where the two sides of the fault slip horizontally past each other; transform boundaries are a particular type of strike-slip fault. Strike-slip faults, particularly continental transforms, can produce major earthquakes up to about magnitude 8. Strike-slip faults tend to be oriented near vertically, resulting in an approximate width of 10 km (6.2 mi) within the brittle crust. Thus, earthquakes with magnitudes much larger than 8 are not possible.

In addition, there exists a hierarchy of stress levels in the three fault types. Thrust faults are generated by the highest, strike-slip by intermediate, and normal faults by the lowest stress levels. This can easily be understood by considering the direction of the greatest principal stress, the direction of the force that "pushes" the rock mass during the faulting. In the case of normal faults, the rock mass is pushed down in a vertical direction, thus the pushing force (greatest principal stress) equals the weight of the rock mass itself. In the case of thrusting, the rock mass "escapes" in the direction of the least principal stress, namely upward, lifting the rock mass, and thus, the overburden equals the least principal stress. Strike-slip faulting is intermediate between the other two types described above. This difference in stress regime in the three faulting environments can contribute to differences in stress drop during faulting, which contributes to differences in the radiated energy, regardless of fault dimensions.

Energy released
For every unit increase in magnitude, there is a roughly thirtyfold increase in the energy released. For instance, an earthquake of magnitude 6.0 releases approximately 32 times more energy than a 5.0 magnitude earthquake and a 7.0 magnitude earthquake releases 1,000 times more energy than a 5.0 magnitude earthquake. An 8.6 magnitude earthquake releases the same amount of energy as 10,000 atomic bombs of the size used in World War II.This is so because the energy released in an earthquake, and thus its magnitude, is proportional to the area of the fault that ruptures and the stress drop. Therefore, the longer the length and the wider the width of the faulted area, the larger the resulting magnitude.  The most important parameter controlling the maximum earthquake magnitude on a fault, however, is not the maximum available length, but the available width because the latter varies by a factor of 20. Along converging plate margins, the dip angle of the rupture plane is very shallow, typically about 10 degrees. Thus, the width of the plane within the top brittle crust of the Earth can become 50–100 km (31–62 mi) (Japan, 2011; Alaska, 1964), making the most powerful earthquakes possible.

Shallow-focus and deep-focus earthquakes
The majority of tectonic earthquakes originate in the ring of fire at depths not exceeding tens of kilometers. Earthquakes occurring at a depth of less than 70 km (43 mi) are classified as "shallow-focus" earthquakes, while those with a focal-depth between 70 and 300 km (43 and 186 mi) are commonly termed "mid-focus" or "intermediate-depth" earthquakes. In subduction zones, where older and colder oceanic crust descends beneath another tectonic plate, deep-focus earthquakes may occur at much greater depths (ranging from 300 to 700 km (190 to 430 mi)). These seismically active areas of subduction are known as Wadati–Benioff zones. Deep-focus earthquakes occur at a depth where the subducted lithosphere should no longer be brittle, due to the high temperature and pressure. A possible mechanism for the generation of deep-focus earthquakes is faulting caused by olivine undergoing a phase transition into a spinel structure.

Earthquakes and volcanic activity
Earthquakes often occur in volcanic regions and are caused there, both by tectonic faults and the movement of magma in volcanoes. Such earthquakes can serve as an early warning of volcanic eruptions, as during the 1980 eruption of Mount St. Helens. Earthquake swarms can serve as markers for the location of the flowing magma throughout the volcanoes. These swarms can be recorded by seismometers and tiltmeters (a device that measures ground slope) and used as sensors to predict imminent or upcoming eruptions.

Rupture dynamics
A tectonic earthquake begins as an area of initial slip on the fault surface that forms the focus. Once the rupture has initiated, it begins to propagate away from the focus, spreading out along the fault surface. Lateral propagation will continue until either the rupture reaches a barrier, such as the end of a fault segment, or a region on the fault where there is insufficient stress to allow continued rupture. For larger earthquakes, the depth extent of rupture will be constrained downwards by the brittle-ductile transition zone and upwards by the ground surface. The mechanics of this process are poorly understood, because it is difficult either to recreate such rapid movements in a laboratory or to record seismic waves close to a nucleation zone due to strong ground motion.In most cases the rupture speed approaches, but does not exceed, the shear wave (S-wave) velocity of the surrounding rock. There are a few exceptions to this:

Supershear earthquakes
Supershear earthquake ruptures are known to have propagated at speeds greater than the S-wave velocity. These have so far all been observed during large strike-slip events. The unusually wide zone of damage caused by the 2001 Kunlun earthquake has been attributed to the effects of the sonic boom developed in such earthquakes.

Slow earthquakes
Slow earthquake ruptures travel at unusually low velocities. A particularly dangerous form of slow earthquake is the tsunami earthquake, observed where the relatively low felt intensities, caused by the slow propagation speed of some great earthquakes, fail to alert the population of the neighboring coast, as in the 1896 Sanriku earthquake.

Co-seismic overpressuring and effect of pore pressure
During an earthquake, high temperatures can develop at the fault plane so increasing pore pressure consequently to vaporization of the ground water already contained within rock.
In the coseismic phase, such increase can significantly affect slip evolution and speed and, furthermore, in the post-seismic phase it can control the Aftershock sequence  because, after the main event, pore pressure increase slowly propagates into the surrounding fracture network.
From the point of view of the Mohr-Coulomb strength theory, an increase in fluid pressure reduces the normal stress acting on the fault plane that holds it in place, and fluids can exert a lubricating effect.
As thermal overpressurization may provide positive feedback between slip and strength fall at the fault plane, a common opinion is that it may enhance the faulting process instability. After the mainshock, the pressure gradient between the fault plane and the neighboring rock causes a fluid flow which increases pore pressure in the surrounding fracture networks; such increase may trigger new faulting processes by reactivating adjacent faults, giving rise to aftershocks. Analogously, artificial pore pressure increase, by fluid injection in Earths crust, may induce seismicity.

Tidal forces
Tides may induce some seismicity.

Earthquake clusters
Most earthquakes form part of a sequence, related to each other in terms of location and time. Most earthquake clusters consist of small tremors that cause little to no damage, but there is a theory that earthquakes can recur in a regular pattern. Earthquake clustering has been observed, for example, in Parkfield, California where a long term research study is being conducted around the Parkfield earthquake cluster.

Aftershocks
An aftershock is an earthquake that occurs after a previous earthquake, the mainshock. Rapid changes of stress between rocks, and the stress from the original earthquake are the main causes of these aftershocks, along with the crust around the ruptured fault plane as it adjusts to the effects of the mainshock. An aftershock is in the same region of the main shock but always of a smaller magnitude, however they can still be powerful enough to cause even more damage to buildings that were already previously damaged from the mainshock. If an aftershock is larger than the mainshock, the aftershock is redesignated as the mainshock and the originalmain shock is redesignated as a foreshock. Aftershocks are formed as the crust around the displaced fault plane adjusts to the effects of the mainshock.

Earthquake swarms
Earthquake swarms are sequences of earthquakes striking in a specific area within a short period. They are different from earthquakes followed by a series of aftershocks by the fact that no single earthquake in the sequence is obviously the main shock, so none has a notable higher magnitude than another. An example of an earthquake swarm is the 2004 activity at Yellowstone National Park. In August 2012, a swarm of earthquakes shook Southern Californias Imperial Valley, showing the most recorded activity in the area since the 1970s.Sometimes a series of earthquakes occur in what has been called an earthquake storm, where the earthquakes strike a fault in clusters, each triggered by the shaking or stress redistribution of the previous earthquakes. Similar to aftershocks but on adjacent segments of fault, these storms occur over the course of years, and with some of the later earthquakes as damaging as the early ones. Such a pattern was observed in the sequence of about a dozen earthquakes that struck the North Anatolian Fault in Turkey in the 20th century and has been inferred for older anomalous clusters of large earthquakes in the Middle East.

Intensity and magnitude of earthquakes
Shaking of the earth is a common phenomenon that has been experienced by humans from the earliest of times. Before the development of strong-motion accelerometers, the intensity of a seismic event was estimated based on the observed effects. Magnitude and intensity are not directly related and calculated using different methods. The magnitude of an earthquake is a single value that describes the size of the earthquake at its source. Intensity is the measure of shaking at different locations around the earthquake. Intensity values vary from place to place, depending on distance from the earthquake and underlying rock or soil makeup.The first scale for measuring earthquake magnitudes was developed by Charles F. Richter in 1935. Subsequent scales (see seismic magnitude scales) have retained a key feature, where each unit represents a ten-fold difference in the amplitude of the ground shaking and a 32-fold difference in energy. Subsequent scales are also adjusted to have approximately the same numeric value within the limits of the scale.Although the mass media commonly reports earthquake magnitudes as "Richter magnitude" or "Richter scale", standard practice by most seismological authorities is to express an earthquakes strength on the moment magnitude scale, which is based on the actual energy released by an earthquake.

Frequency of occurrence
It is estimated that around 500,000 earthquakes occur each year, detectable with current instrumentation. About 100,000 of these can be felt. Minor earthquakes occur nearly constantly around the world in places like California and Alaska in the U.S., as well as in El Salvador, Mexico, Guatemala, Chile, Peru, Indonesia, the Philippines, Iran, Pakistan, the Azores in Portugal, Turkey, New Zealand, Greece, Italy, India, Nepal and Japan. Larger earthquakes occur less frequently, the relationship being exponential; for example, roughly ten times as many earthquakes larger than magnitude 4 occur in a particular time period than earthquakes larger than magnitude 5. In the (low seismicity) United Kingdom, for example, it has been calculated that the average recurrences are:
an earthquake of 3.7–4.6 every year, an earthquake of 4.7–5.5 every 10 years, and an earthquake of 5.6 or larger every 100 years. This is an example of the Gutenberg–Richter law.
The number of seismic stations has increased from about 350 in 1931 to many thousands today. As a result, many more earthquakes are reported than in the past, but this is because of the vast improvement in instrumentation, rather than an increase in the number of earthquakes. The United States Geological Survey (USGS) estimates that, since 1900, there have been an average of 18 major earthquakes (magnitude 7.0–7.9) and one great earthquake (magnitude 8.0 or greater) per year, and that this average has been relatively stable. In recent years, the number of major earthquakes per year has decreased, though this is probably a statistical fluctuation rather than a systematic trend. More detailed statistics on the size and frequency of earthquakes is available from the United States Geological Survey.
A recent increase in the number of major earthquakes has been noted, which could be explained by a cyclical pattern of periods of intense tectonic activity, interspersed with longer periods of low intensity. However, accurate recordings of earthquakes only began in the early 1900s, so it is too early to categorically state that this is the case.Most of the worlds earthquakes (90%, and 81% of the largest) take place in the 40,000-kilometre-long (25,000 mi), horseshoe-shaped zone called the circum-Pacific seismic belt, known as the Pacific Ring of Fire, which for the most part bounds the Pacific Plate. Massive earthquakes tend to occur along other plate boundaries too, such as along the Himalayan Mountains.With the rapid growth of mega-cities such as Mexico City, Tokyo and Tehran in areas of high seismic risk, some seismologists are warning that a single earthquake may claim the lives of up to three million people.

Induced seismicity
While most earthquakes are caused by movement of the Earths tectonic plates, human activity can also produce earthquakes. Activities both above ground and below may change the stresses and strains on the crust, including building reservoirs, extracting resources such as coal or oil, and injecting fluids underground for waste disposal or fracking. Most of these earthquakes have small magnitudes. The 5.7 magnitude 2011 Oklahoma earthquake is thought to have been caused by disposing wastewater from oil production into injection wells, and studies point to the states oil industry as the cause of other earthquakes in the past century. A Columbia University paper suggested that the 8.0 magnitude 2008 Sichuan earthquake was induced by loading from the Zipingpu Dam, though the link has not been conclusively proved.

Measuring and locating earthquakes
The instrumental scales used to describe the size of an earthquake began with the Richter magnitude scale in the 1930s. It is a relatively simple measurement of an events amplitude, and its use has become minimal in the 21st century. Seismic waves travel through the Earths interior and can be recorded by seismometers at great distances. The surface wave magnitude was developed in the 1950s as a means to measure remote earthquakes and to improve the accuracy for larger events. The moment magnitude scale not only measures the amplitude of the shock but also takes into account the seismic moment (total rupture area, average slip of the fault, and rigidity of the rock). The Japan Meteorological Agency seismic intensity scale, the Medvedev–Sponheuer–Karnik scale, and the Mercalli intensity scale are based on the observed effects and are related to the intensity of shaking.

Seismic waves
Every earthquake produces different types of seismic waves, which travel through rock with different velocities:

Longitudinal P-waves (shock- or pressure waves)
Transverse S-waves (both body waves)
Surface waves – (Rayleigh and Love waves)

Speed of seismic waves
Propagation velocity of the seismic waves through solid rock ranges from approx. 3 km/s (1.9 mi/s) up to 13 km/s (8.1 mi/s), depending on the density and elasticity of the medium. In the Earths interior, the shock- or P-waves travel much faster than the S-waves (approx. relation 1.7:1). The differences in travel time from the epicenter to the observatory are a measure of the distance and can be used to image both sources of earthquakes and structures within the Earth. Also, the depth of the hypocenter can be computed roughly.

P-wave speed
Upper crust soils and unconsolidated sediments: 2–3 km (1.2–1.9 mi) per second
Upper crust solid rock: 3–6 km (1.9–3.7 mi) per second
Lower crust: 6–7 km (3.7–4.3 mi) per second
Deep mantle: 13 km (8.1 mi) per second.

S-waves speed
Light sediments: 2–3 km (1.2–1.9 mi) per second in
Earths crust:4–5 km (2.5–3.1 mi) per second
Deep mantle: 7 km (4.3 mi) per second

Seismic wave arrival
As a consequence, the first waves of a distant earthquake arrive at an observatory via the Earths mantle.
On average, the kilometer distance to the earthquake is the number of seconds between the P- and S-wave times 8. Slight deviations are caused by inhomogeneities of subsurface structure. By such analysis of seismograms, the Earths core was located in 1913 by Beno Gutenberg.
S-waves and later arriving surface waves do most of the damage compared to P-waves. P-waves squeeze and expand the material in the same direction they are traveling, whereas S-waves shake the ground up and down and back and forth.

Earthquake location and reporting
Earthquakes are not only categorized by their magnitude but also by the place where they occur. The world is divided into 754 Flinn–Engdahl regions (F-E regions), which are based on political and geographical boundaries as well as seismic activity. More active zones are divided into smaller F-E regions whereas less active zones belong to larger F-E regions.
Standard reporting of earthquakes includes its magnitude, date and time of occurrence, geographic coordinates of its epicenter, depth of the epicenter, geographical region, distances to population centers, location uncertainty, several parameters that are included in USGS earthquake reports (number of stations reporting, number of observations, etc.), and a unique event ID.Although relatively slow seismic waves have traditionally been used to detect earthquakes, scientists realized in 2016 that gravitational measurements could provide instantaneous detection of earthquakes, and confirmed this by analyzing gravitational records associated with the 2011 Tohoku-Oki ("Fukushima") earthquake.

Effects of earthquakes
The effects of earthquakes include, but are not limited to, the following:

Shaking and ground rupture
Shaking and ground rupture are the main effects created by earthquakes, principally resulting in more or less severe damage to buildings and other rigid structures. The severity of the local effects depends on the complex combination of the earthquake magnitude, the distance from the epicenter, and the local geological and geomorphological conditions, which may amplify or reduce wave propagation. The ground-shaking is measured by ground acceleration.
Specific local geological, geomorphological, and geostructural features can induce high levels of shaking on the ground surface even from low-intensity earthquakes. This effect is called site or local amplification. It is principally due to the transfer of the seismic motion from hard deep soils to soft superficial soils and the effects of seismic energy focalization owing to the typical geometrical setting of such deposits.
Ground rupture is a visible breaking and displacement of the Earths surface along the trace of the fault, which may be of the order of several meters in the case of major earthquakes. Ground rupture is a major risk for large engineering structures such as dams, bridges, and nuclear power stations and requires careful mapping of existing faults to identify any that are likely to break the ground surface within the life of the structure.

Soil liquefaction
Soil liquefaction occurs when, because of the shaking, water-saturated granular material (such as sand) temporarily loses its strength and transforms from a solid to a liquid. Soil liquefaction may cause rigid structures, like buildings and bridges, to tilt or sink into the liquefied deposits. For example, in the 1964 Alaska earthquake, soil liquefaction caused many buildings to sink into the ground, eventually collapsing upon themselves.

Human impacts
Physical damage from an earthquake will vary depending on the intensity of shaking in a given area and they type of population.  Undeserved and developing communities frequently experience more severe impacts (and longer lasting) from a seismic event compared to well developed communities. Impacts may include:

Injuries and loss of life
Damage to critical infrastructure (short and long term)
Roads, bridges and public transportation networks
Water, power, swear and gas interruption
Communication systems
Loss of critical community services including hospitals, police and fire
General property damage
Collapse or destabilization (potentially leading to future collapse) of buildingsWith these impacts and others, the aftermath may bring disease, lack of basic necessities, mental consequences such as panic attacks, depression to survivors, and higher insurance premiums. Recovery times will vary based off the level of damage along with the socioeconomic status of the impacted community.

Landslides
Earthquakes can produce slope instability leading to landslides, a major geological hazard. Landslide danger may persist while emergency personnel are attempting rescue work.

Fires
Earthquakes can cause fires by damaging electrical power or gas lines. In the event of water mains rupturing and a loss of pressure, it may also become difficult to stop the spread of a fire once it has started. For example, more deaths in the 1906 San Francisco earthquake were caused by fire than by the earthquake itself.

Tsunami
Tsunamis are long-wavelength, long-period sea waves produced by the sudden or abrupt movement of large volumes of water—including when an earthquake occurs at sea. In the open ocean, the distance between wave crests can surpass 100 kilometres (62 mi), and the wave periods can vary from five minutes to one hour. Such tsunamis travel 600–800 kilometers per hour (373–497 miles per hour), depending on water depth. Large waves produced by an earthquake or a submarine landslide can overrun nearby coastal areas in a matter of minutes. Tsunamis can also travel thousands of kilometers across open ocean and wreak destruction on far shores hours after the earthquake that generated them.Ordinarily, subduction earthquakes under magnitude 7.5 do not cause tsunamis, although some instances of this have been recorded. Most destructive tsunamis are caused by earthquakes of magnitude 7.5 or more.

Floods
Floods may be secondary effects of earthquakes, if dams are damaged. Earthquakes may cause landslips to dam rivers, which collapse and cause floods.The terrain below the Sarez Lake in Tajikistan is in danger of catastrophic flooding if the landslide dam formed by the earthquake, known as the Usoi Dam, were to fail during a future earthquake. Impact projections suggest the flood could affect roughly 5 million people.

Major earthquakes
One of the most devastating earthquakes in recorded history was the 1556 Shaanxi earthquake, which occurred on 23 January 1556 in Shaanxi, China. More than 830,000 people died. Most houses in the area were yaodongs—dwellings carved out of loess hillsides—and many victims were killed when these structures collapsed. The 1976 Tangshan earthquake, which killed between 240,000 and 655,000 people, was the deadliest of the 20th century.The 1960 Chilean earthquake is the largest earthquake that has been measured on a seismograph, reaching 9.5 magnitude on 22 May 1960. Its epicenter was near Cañete, Chile. The energy released was approximately twice that of the next most powerful earthquake, the Good Friday earthquake (27 March 1964), which was centered in Prince William Sound, Alaska. The ten largest recorded earthquakes have all been megathrust earthquakes; however, of these ten, only the 2004 Indian Ocean earthquake is simultaneously one of the deadliest earthquakes in history.
Earthquakes that caused the greatest loss of life, while powerful, were deadly because of their proximity to either heavily populated areas or the ocean, where earthquakes often create tsunamis that can devastate communities thousands of kilometers away. Regions most at risk for great loss of life include those where earthquakes are relatively rare but powerful, and poor regions with lax, unenforced, or nonexistent seismic building codes.

Prediction
Earthquake prediction is a branch of the science of seismology concerned with the specification of the time, location, and magnitude of future earthquakes within stated limits. Many methods have been developed for predicting the time and place in which earthquakes will occur. Despite considerable research efforts by seismologists, scientifically reproducible predictions cannot yet be made to a specific day or month.

Forecasting
While forecasting is usually considered to be a type of prediction, earthquake forecasting is often differentiated from earthquake prediction. Earthquake forecasting is concerned with the probabilistic assessment of general earthquake hazard, including the frequency and magnitude of damaging earthquakes in a given area over years or decades. For well-understood faults the probability that a segment may rupture during the next few decades can be estimated.Earthquake warning systems have been developed that can provide regional notification of an earthquake in progress, but before the ground surface has begun to move, potentially allowing people within the systems range to seek shelter before the earthquakes impact is felt.

Preparedness
The objective of earthquake engineering is to foresee the impact of earthquakes on buildings and other structures and to design such structures to minimize the risk of damage. Existing structures can be modified by seismic retrofitting to improve their resistance to earthquakes. Earthquake insurance can provide building owners with financial protection against losses resulting from earthquakes. Emergency management strategies can be employed by a government or organization to mitigate risks and prepare for consequences.
Artificial intelligence may help to assess buildings and plan precautionary operations: the Igor expert system is part of a mobile laboratory that supports the procedures leading to the seismic assessment of masonry buildings and the planning of retrofitting operations on them. It has been successfully applied to assess buildings in Lisbon, Rhodes, Naples.Individuals can also take preparedness steps like securing water heaters and heavy items that could injure someone, locating shutoffs for utilities, and being educated about what to do when the shaking starts. For areas near large bodies of water, earthquake preparedness encompasses the possibility of a tsunami caused by a large earthquake.

Historical views
From the lifetime of the Greek philosopher Anaxagoras in the 5th century BCE to the 14th century CE, earthquakes were usually attributed to "air (vapors) in the cavities of the Earth." Thales of Miletus (625–547 BCE) was the only documented person who believed that earthquakes were caused by tension between the earth and water. Other theories existed, including the Greek philosopher Anaxamines (585–526 BCE) beliefs that short incline episodes of dryness and wetness caused seismic activity. The Greek philosopher Democritus (460–371 BCE) blamed water in general for earthquakes. Pliny the Elder called earthquakes "underground thunderstorms".

In culture
Mythology and religion
In Norse mythology, earthquakes were explained as the violent struggling of the god Loki. When Loki, god of mischief and strife, murdered Baldr, god of beauty and light, he was punished by being bound in a cave with a poisonous serpent placed above his head dripping venom. Lokis wife Sigyn stood by him with a bowl to catch the poison, but whenever she had to empty the bowl the poison dripped on Lokis face, forcing him to jerk his head away and thrash against his bonds, which caused the earth to tremble.In Greek mythology, Poseidon was the cause and god of earthquakes. When he was in a bad mood, he struck the ground with a trident, causing earthquakes and other calamities. He also used earthquakes to punish and inflict fear upon people as revenge.In Japanese mythology, Namazu (鯰) is a giant catfish who causes earthquakes. Namazu lives in the mud beneath the earth and is guarded by the god Kashima who restrains the fish with a stone. When Kashima lets his guard fall, Namazu thrashes about, causing violent earthquakes.

In popular culture
In modern popular culture, the portrayal of earthquakes is shaped by the memory of great cities laid waste, such as Kobe in 1995 or San Francisco in 1906. Fictional earthquakes tend to strike suddenly and without warning. For this reason, stories about earthquakes generally begin with the disaster and focus on its immediate aftermath, as in Short Walk to Daylight (1972), The Ragged Edge (1968) or Aftershock: Earthquake in New York (1999). A notable example is Heinrich von Kleists classic novella, The Earthquake in Chile, which describes the destruction of Santiago in 1647. Haruki Murakamis short fiction collection After the Quake depicts the consequences of the Kobe earthquake of 1995.
The most popular single earthquake in fiction is the hypothetical "Big One" expected of Californias San Andreas Fault someday, as depicted in the novels Richter 10 (1996), Goodbye California (1977), 2012 (2009) and San Andreas (2015) among other works. Jacob M. Appels widely anthologized short story, A Comparative Seismology, features a con artist who convinces an elderly woman that an apocalyptic earthquake is imminent.Contemporary depictions of earthquakes in film are variable in the manner in which they reflect human psychological reactions to the actual trauma that can be caused to directly afflicted families and their loved ones. Disaster mental health response research emphasizes the need to be aware of the different roles of loss of family and key community members, loss of home and familiar surroundings, loss of essential supplies and services to maintain survival. Particularly for children, the clear availability of caregiving adults who are able to protect, nourish, and clothe them in the aftermath of the earthquake, and to help them make sense of what has befallen them has been shown even more important to their emotional and physical health than the simple giving of provisions. As was observed after other disasters involving destruction and loss of life and their media depictions, recently observed in the 2010 Haiti earthquake, it is also important not to pathologize the reactions to loss and displacement or disruption of governmental administration and services, but rather to validate these reactions, to support constructive problem-solving and reflection as to how one might improve the conditions of those affected.

See also
Earth sciences portal
United States Geological Survey
Asteroseismology – Study of oscillations in stars
Helioseismology – Sunquake
European-Mediterranean Seismological Centre
Injection-induced earthquakes
IRIS Consortium
Lists of earthquakes – Lists of earthquakes
Marsquake
Quake (natural phenomenon) – Surface shaking on interstellar bodies in general
Seismite – Sediment/structure shaken seismically
Seismological Society of America
Seismotectonics
Types of earthquake
Vertical displacement

References
Sources
Further reading
Hyndman, Donald; Hyndman, David (2009). "Chapter 3: Earthquakes and their causes". Natural Hazards and Disasters (2nd ed.). Brooks/Cole: Cengage Learning. ISBN 978-0-495-31667-1.
Liu, ChiChing; Linde, Alan T.; Sacks, I </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Japanese encephalitis and can you explain it in depth? [/INST] Japanese encephalitis (JE) is an infection of the brain caused by the Japanese encephalitis virus (JEV). While most infections result in little or no symptoms, occasional inflammation of the brain occurs. In these cases, symptoms may include headache, vomiting, fever, confusion and seizures. This occurs about 5 to 15 days after infection.JEV is generally spread by mosquitoes, specifically those of the Culex type. Pigs and wild birds serve as a reservoir for the virus. The disease occurs mostly outside of cities. Diagnosis is based on blood or cerebrospinal fluid testing.Prevention is generally with the Japanese encephalitis vaccine, which is both safe and effective. Other measures include avoiding mosquito bites. Once infected, there is no specific treatment, with care being supportive. This is generally carried out in a hospital. Permanent problems occur in up to half of people who recover from JE.The disease primarily occurs in East and Southeast Asia as well as the Western Pacific. About 3 billion people live in areas where the disease occurs. About 68,000 symptomatic cases occur a year, with about 17,000 deaths. Often, cases occur in outbreaks. The disease was first described in Japan in 1871.

Signs and symptoms
The Japanese encephalitis virus (JEV) has an incubation period of 2 to 26 days. The vast majority of infections are asymptomatic: only 1 in 250 infections develop into encephalitis.Severe rigors may mark the onset of this disease in humans. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between 38–41 °C (100.4–105.8 °F). The mortality rate of the disease is around 25% and is generally higher in children under five, the immuno-suppressed and the elderly. Transplacental spread has been noted. Neurological disorders develop in 40% of those who survive with lifelong neurological defects such as deafness, emotional lability and hemiparesis occurring in those who had central nervous system involvement.

Increased microglial activation following Japanese encephalitis infection has been found to influence the outcome of viral pathogenesis. Microglia are the resident immune cells of the central nervous system (CNS) and have a critical role in host defense against invading microorganisms. Activated microglia secrete cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α), which can cause toxic effects in the brain. Additionally, other soluble factors such as neurotoxins, excitatory neurotransmitters, prostaglandin, reactive oxygen, and nitrogen species are secreted by activated microglia.In a murine model of JE, it was found that in the hippocampus and the striatum, the number of activated microglia was more than anywhere else in the brain, closely followed by that in the thalamus. In the cortex, the number of activated microglia was significantly less when compared to other regions of the mouse brain. An overall induction of differential expression of proinflammatory cytokines and chemokines from different brain regions during a progressive Japanese encephalitis infection was also observed.Although the net effect of the proinflammatory mediators is to kill infectious organisms and infected cells as well as to stimulate the production of molecules that amplify the mounting response to damage, it is also evident that in a nonregenerating organ such as the brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial activation that possibly leads to bystander neuronal damage. In animals, key signs include infertility and abortion in pigs, neurological disease in horses, and systemic signs including fever, lethargy and anorexia.

Cause
It is a disease caused by the mosquito-borne Japanese encephalitis virus (JEV).

Virology
JEV is a virus from the family Flaviviridae, part of the Japanese encephalitis serocomplex of 9 genetically and antigenically related viruses, some which are particularly severe in horses, and four known to infect humans including West Nile virus. The enveloped virus is closely related to the West Nile virus and the St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also. NS3 is a putative helicase, and NS5 is the viral polymerase. It has been noted that Japanese encephalitis infects the lumen of the endoplasmic reticulum (ER) and rapidly accumulates substantial amounts of viral proteins.
Based on the envelope gene, there are five genotypes (I–V). The Muar strain, isolated from a patient in Malaya in 1952, is the prototype strain of genotype V. Genotype IV appears to be the ancestral strain, and the virus may have evolved in the Malay Archipelago. The first clinical reports date from 1870, but the virus appears to have evolved in the mid-16th century. Over sixty complete genomes of this virus had been sequenced by 2010.

Diagnosis
Japanese encephalitis is diagnosed by commercially available tests detecting JE virus-specific IgM antibodies in serum and/or cerebrospinal fluid, for example by IgM capture ELISA.JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed.
Confirmatory testing in the US is available only at the CDC and a few specialized reference laboratories. In fatal cases, nucleic acid amplification and virus culture of autopsy tissues can be useful. Viral antigen can be shown in tissues by indirect fluorescent antibody staining.

Prevention
Infection with Japanese encephalitis confers lifelong immunity. There are currently three vaccines available: SA14-14-2, IXIARO (IC51, also marketed in Australia, New Zealand as JESPECT and India as JEEV) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus.A formalin-inactivated mouse-brain-derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s.  The widespread use of vaccine and urbanization has led to control of the disease in Japan and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program.The most common adverse effects are redness and pain at the injection site.  Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there are few adverse effects compared to placebo, the main side effects being headache and myalgia.The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer.  The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there are no data available regarding the interchangeability of other JE vaccines and IXIARO.

Treatment
There is no specific treatment for Japanese encephalitis and treatment is supportive, with assistance given for feeding, breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol.  There is no transmission from person to person and therefore patients do not need to be isolated.A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapies for Japanese encephalitis.The effectiveness of intravenous immunoglobulin for the management of encephalitis is unclear due to a lack of evidence. Intravenous immunoglobulin for Japanese encephalitis appeared to have no benefit.

Epidemiology
Japanese encephalitis (JE) is the leading cause of viral encephalitis in Asia, with up to 70,000 cases reported annually. Case-fatality rates range from 0.3% to 60% and depend on the population and age. Rare outbreaks in U.S. territories in the Western Pacific have also occurred. Residents of rural areas in endemic locations are at highest risk; Japanese encephalitis does not usually occur in urban areas.Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination, include China, South Korea, Singapore, Japan, Taiwan and Thailand. Other countries that still have periodic epidemics include Vietnam, Cambodia, Myanmar, India, Nepal, and Malaysia. Japanese encephalitis has been reported in the Torres Strait Islands, and two fatal cases were reported in mainland northern Australia in 1998. There were reported cases in Kachin State, Myanmar in 2013. There were 116 deaths reported in Odishas Malkangiri district of India in 2016.In 2022, the notable increase in distribution of the virus in Australia due to climate change became a concern to health officials as the population has limited immunity to the disease and the presence of large numbers of farmed and feral pigs could act as reservoirs for the virus. In February 2022, Japanese encephalitis was detected and confirmed in piggeries in Victoria, Queensland and New South Wales. On 4 March, cases were detected in South Australia. By October 2022, the outbreak in eastern mainland Australia had caused 42 symptomatic human cases of the disease, resulting in seven deaths.Human, cattle, and horses are dead-end hosts as the disease manifests as fatal encephalitis.  Pigs act as an amplifying host and have a very important role in the epidemiology of the disease </s>


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


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bradycardia and can you explain it in depth? [/INST] Bradycardia (also sinus bradycardia) is a slow resting heart rate, commonly under 60 beats per minute (BPM) as determined by an electrocardiogram. It is considered to be a normal heart rate during sleep, in young and healthy or elderly adults, and in athletes.In some people, bradycardia below 60 BPM may be associated with fatigue, weakness, dizziness, sweating, and fainting. The term "relative bradycardia" is used to refer to a heart rate slower than an individuals typical resting heart rate. Athletes may have athletic heart syndrome, which includes bradycardia as part of the cardiovascular adaptations to training and participation.The word "bradycardia" is from the Greek βραδύς bradys "slow", and καρδία kardia "heart".

Classification
Sinus
Atrial bradycardias are divided into three types. The first, respiratory sinus arrhythmia, is usually found in young and healthy adults. Heart rate increases during inhalation and decreases during exhalation.  This is thought to be caused by changes in the vagal tone during respiration.Sinus bradycardia is a sinus rhythm of less than 60 BPM. It is a common condition found in both healthy individuals and those considered well-conditioned athletes. Studies have found that 50–85% of conditioned athletes have benign sinus bradycardia, as compared to 23% of the general population studied. The heart muscle of athletes has a higher stroke volume, so requires fewer contractions to circulate the same volume of blood.The third, sick sinus syndrome, covers conditions that include severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardia-tachycardia syndrome (atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia).

Atrioventricular junction
An AV-junctional rhythm, or atrioventricular nodal bradycardia, is usually caused by the absence of the electrical impulse from the sinus node. This usually appears on an electrocardiogram (ECG) with a normal QRS complex accompanied with an inverted P wave either before, during, or after the QRS complex.An AV-junctional escape beat is a delayed heartbeat originating from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the SA node falls below the rate of the AV node. This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block. This is a protective mechanism for the heart, to compensate for an SA node that is no longer handling the pacemaking activity and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so. This would present with a longer PR interval. An AV-junctional escape complex is a normal response that may result from excessive vagal tone on the SA node. Pathological causes include sinus bradycardia, sinus arrest, sinus exit block, or AV block.

Ventricular
Idioventricular rhythm, also known as atrioventricular bradycardia or ventricular escape rhythm, is a heart rate of less than 50 BPM. This is a safety mechanism when a lack of electrical impulse or stimuli from the atrium occurs. Impulses originating within or below the bundle of His in the AV node will produce a wide QRS complex with heart rates between 20 and 40 BPM. Those above the bundle of His, also known as junctional, will typically range between 40 and 60 BPM with a narrow QRS complex. In a third-degree heart block, about 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the bundle of His. AV block may be ruled out with an ECG indicating "a 1:1 relationship between P waves and QRS complexes." Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block. Treatment often consists of the administration of atropine and cardiac pacing.

Infantile
For infants, bradycardia is defined as a heart rate less than 100 BPM (normal is around 120–160 BPM). Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood. The spells may be related to centers inside the brain that regulate breathing which may not be fully developed. Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate. Medications (theophylline or caffeine) can be used to treat these spells in babies if necessary. Neonatal intensive-care unit (NICU) standard practice is to electronically monitor the heart and lungs for this reason.

Causes
Bradycardia arrhythmia may have many causes, both cardiac and non-cardiac.
Non-cardiac causes are usually secondary, and can involve recreational drug use or abuse, metabolic or endocrine issues, especially hypothyroidism, an electrolyte imbalance, neurological factors, autonomic reflexes, situational factors, such as prolonged bed rest, and autoimmunity.Cardiac causes include acute or chronic ischemic heart disease, vascular heart disease, valvular heart disease, or degenerative primary electrical disease. Ultimately, the causes act by three mechanisms: depressed automaticity of the heart, conduction block, or escape pacemakers and rhythms.In general, two types of problems result in bradycardias: disorders of the SA node, and disorders of the AV node.With SA node dysfunction (sometimes called sick sinus syndrome), there may be disordered automaticity or impaired conduction of the impulse from the SA node into the surrounding atrial tissue (an "exit block"). Second-degree sinoatrial blocks can be detected only by use of a 12-lead ECG </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Chronic kidney disease and can you explain it in depth? [/INST] Chronic kidney disease (CKD) is a type of kidney disease  in which a gradual loss of kidney function occurs over a period of months to years. Initially generally no symptoms are seen, but later symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications can relate to hormonal dysfunction of the kidneys and include (in chronological order) high blood pressure (often related to activation of the renin–angiotensin system system), bone disease, and anemia. Additionally CKD patients have markedly increased cardiovascular complications with increased risks of death and hospitalization.Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk factors include a family history of chronic kidney disease. Diagnosis is by blood tests to measure the estimated glomerular filtration rate (eGFR), and a urine test to measure albumin. Ultrasound or kidney biopsy may be performed to determine the underlying cause. Several severity-based staging systems are in use.Screening at-risk people is recommended. Initial treatments may include medications to lower blood pressure, blood sugar, and cholesterol. Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are generally first-line agents for blood pressure control, as they slow progression of the kidney disease and the risk of heart disease. Loop diuretics may be used to control edema and, if needed, to further lower blood pressure. NSAIDs should be avoided. Other recommended measures include staying active, and certain dietary changes such as a low-salt diet and the right amount of protein. Treatments for anemia and bone disease may also be required. Severe disease requires hemodialysis, peritoneal dialysis, or a kidney transplant for survival.Chronic kidney disease affected 753 million people globally in 2016 - 417 million females and 336 million males. In 2015, it caused 1.2 million deaths, up from 409,000 in 1990. The causes that contribute to the greatest number of deaths are high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000.

Signs and symptoms
CKD is initially without symptoms, and is usually detected on routine screening blood work by either an increase in serum creatinine, or protein in the urine. As the kidney function decreases, more unpleasant symptoms may emerge:
Blood pressure is increased due to fluid overload and production of vasoactive hormones created by the kidney via the renin–angiotensin system, increasing the risk of developing hypertension and heart failure. People with CKD are more likely than the general population to develop atherosclerosis with consequent cardiovascular disease, an effect that may be at least partly mediated by uremic toxins. People with both CKD and cardiovascular disease have significantly worse prognoses than those with only  cardiovascular disease.
Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to its high systemic concentration, urea is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates ("uremic frost").
Potassium accumulates in the blood (hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20–25 mL/min/1.73 m2, when the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin.
Fluid overload symptoms may range from mild edema to life-threatening pulmonary edema.
Hyperphosphatemia results from poor phosphate elimination in the kidney, and contributes to increased cardiovascular risk by causing vascular calcification. Circulating concentrations of fibroblast growth factor-23 (FGF-23) increase progressively as the kidney capacity for phosphate excretion declines, which may contribute to left ventricular hypertrophy and increased mortality in people with CKD .
Hypocalcemia results from 1,25 dihydroxyvitamin D3 deficiency (caused by high FGF-23 and reduced kidney mass) and resistance to the action of parathyroid hormone. Osteocytes are responsible for the increased production of FGF-23, which is a potent inhibitor of the enzyme 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol into 1,25 dihydroxyvitamin D3). Later, this progresses to secondary hyperparathyroidism, kidney osteodystrophy, and vascular calcification that further impairs cardiac function. An extreme consequence is the occurrence of the rare condition named calciphylaxis.
Changes in mineral and bone metabolism that may cause 1) abnormalities of calcium, phosphorus (phosphate), parathyroid hormone, or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (kidney osteodystrophy); and 3) vascular or other soft-tissue calcification. CKD-mineral and bone disorders have been associated with poor outcomes.
Metabolic acidosis may result from decreased capacity to generate enough ammonia from the cells of the proximal tubule. Acidemia affects the function of enzymes and increases excitability of cardiac and neuronal membranes by the promotion of hyperkalemia.
Anemia is common and is especially prevalent in those requiring haemodialysis. It is multifactorial in cause, but includes increased inflammation, reduction in erythropoietin, and hyperuricemia leading to bone-marrow suppression. Hypoproliferative anemia occurs due to inadequate production of erythropoietin by the kidneys.
In later stages, cachexia may develop, leading to unintentional weight loss, muscle wasting, weakness, and anorexia.
Sexual dysfunction is very common in both men and women with CKD.  A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age.  Most women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.

Causes
The three most common causes of CKD in order of frequency as of 2015 are diabetes mellitus, hypertension, and glomerulonephritis. About one of five adults with hypertension and one of three adults with diabetes have CKD.
If the cause is unknown, it is called idiopathic.

By anatomical location
Vascular disease includes large-vessel disease such as bilateral kidney artery stenosis and small-vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome, and vasculitis.
Glomerular disease comprises a diverse group and is classified into:Primary glomerular disease such as focal segmental glomerulosclerosis and IgA nephropathy (or nephritis)
Secondary glomerular disease such as diabetic nephropathy and lupus nephritis
Tubulointerstitial disease includes drug- and toxin-induced chronic tubulointerstitial nephritis, and reflux nephropathy
Obstructive nephropathy, as exemplified by bilateral kidney stones and benign prostatic hyperplasia of the prostate gland; rarely, pinworms infecting the kidney can cause obstructive nephropathy.

Other
Genetic congenital disease such as polycystic kidney disease or 17q12 microdeletion syndrome.
Mesoamerican nephropathy, is "a new form of kidney disease that could be called agricultural nephropathy". A high and so-far unexplained number of new cases of CKD, referred to as the Mesoamerican nephropathy, has been noted among male workers in Central America, mainly in sugarcane fields in the lowlands of El Salvador and Nicaragua. Heat stress from long hours of piece-rate work at high average temperatures of about 36 °C (96 °F) is suspected, as are agricultural chemicals

Diagnosis
Diagnosis of CKD is largely based on history, examination, and urine dipstick combined with the measurement of the serum creatinine level (see above). Differentiating CKD from acute kidney injury (AKI) is important because AKI can be reversible. One diagnostic clue that helps differentiate CKD from AKI is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). In many people with CKD, previous kidney disease or other underlying diseases are already known. A significant number present with CKD of unknown cause.

Screening
Screening those who have neither symptoms nor risk factors for CKD is not recommended. Those who should be screened include: those with hypertension or history of cardiovascular disease, those with diabetes or marked obesity, those aged > 60 years, subjects with African American ancestry, those with a history of kidney disease in the past, and subjects who have relatives who had kidney disease requiring dialysis.Screening should include calculation of the estimated GFR (eGFR) from the serum creatinine level, and measurement of urine albumin-to-creatinine ratio (ACR) in a first-morning urine specimen (this reflects the amount of a protein called albumin in the urine), as well as a urine dipstick screen for hematuria.The GFRis derived from the serum creatinine and is proportional to 1/creatinine, i.e. it is a reciprocal relationship; the higher the creatinine, the lower the GFR. It reflects one aspect of kidney function, how efficiently the glomeruli - the filtering units - work. Normal GFR is 90-120 ml/min. The units of creatinine vary from country to country, but since the glomeruli make up <5% of the mass of the kidney, the GFR does not indicate all aspects of kidney health and function. This can be done by combining the GFR level with the clinical assessment of the person, including fluid status, and measuring the levels of hemoglobin, potassium, phosphate, and parathyroid hormone.

Ultrasound
Kidney ultrasonography is useful for diagnostic and prognostic purposes in chronic kidney disease. Whether the underlying pathologic change is glomerular sclerosis, tubular atrophy, interstitial fibrosis, or inflammation, the result is often increased echogenicity of the cortex. The echogenicity of the kidney should be related to the echogenicity of either the liver or the spleen (Figure 22 and Figure 23). Moreover, decreased kidney size and cortical thinning are also often seen and especially when disease progresses (Figure 24 and Figure 25). However, kidney size correlates to height, and short persons tend to have small kidneys; thus, kidney size as the only parameter is not reliable.

Additional imaging
Additional tests may include nuclear medicine MAG3 scan to confirm blood flow and establish the differential function between the two kidneys. Dimercaptosuccinic acid (DMSA) scans are also used in kidney imaging; with both MAG3 and DMSA being used chelated with the radioactive element technetium-99.

Stages
A glomerular filtration rate (GFR) ≥ 60 mL/min/1.73 m2 is considered normal without chronic kidney disease if there is no kidney damage present.
Kidney damage is defined signs of damage seen in blood, urine, or imaging studies which includes lab albumin/creatinine ratio (ACR) ≥ 30. All people with a GFR <60 mL/min/1.73 m2 for 3 months are defined as having chronic kidney disease.Protein in the urine is regarded as an independent marker for worsening of kidney function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if protein loss is significant.
Stage 1: Slightly diminished function; kidney damage with normal or relatively high GFR (≥90 mL/min/1.73 m2) and persistent albuminuria. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.
Stage 2: Mild reduction in GFR (60–89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.
Stage 3: Moderate reduction in GFR (30–59 mL/min/1.73 m2):. British guidelines distinguish between stage 3A (GFR 45–59) and stage 3B (GFR 30–44) for purposes of screening and referral.
Stage 4: Severe reduction in GFR (15–29 mL/min/1.73 m2) Preparation for kidney replacement therapy.
Stage 5: Established kidney failure (GFR <15 mL/min/1.73 m2), permanent kidney replacement therapy, or end-stage kidney disease.The term "non-dialysis-dependent chronic kidney disease" (NDD-CKD) is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for kidney failure known as kidney replacement therapy (RRT, including maintenance dialysis or kidney transplantation).  The condition of individuals with CKD, who require either of the two types of kidney replacement therapy (dialysis or transplant), is referred to as the end-stage kidney disease (ESKD). Hence, the start of the ESKD is practically the irreversible conclusion of the NDD-CKD. Even though the NDD-CKD status refers to the status of persons with earlier stages of CKD (stages 1 to 4), people with advanced stage of CKD (stage 5), who have not yet started kidney replacement therapy, are also referred to as NDD-CKD.

Management
Apart from controlling other risk factors, the goal of therapy is to slow down or halt the progression of CKD. Control of blood pressure and treatment of the original disease are the broad principles of management.

Blood pressure
Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are recommended as first-line agents since they have been found to slow the decline of kidney function, relative to a more rapid decline in those not on one of these agents. They have also been found to reduce the risk of major cardiovascular events such as myocardial infarction, stroke, heart failure, and death from cardiovascular disease when compared to placebo in individuals with CKD. ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD. Aggressive blood pressure lowering decreases peoples risk of death.

Other measures
Aggressive treatment of high blood lipids is recommended.
A low-protein, low-salt diet may result in slower progression of CKD and reduction in proteinuria as well as controlling symptoms of advanced CKD to delay dialysis start. A tailored low-protein diet, designed for low acidity, may help prevent damage to kidneys for people with CKD. Additionally, controlling salt ingestion helps to decrease the incidence of coronary heart disease, lowering blood pressure and reducing albuminuria.
Anemia - A target hemoglobin level of 9–12 g/dL is recommended; raising hemoglobin levels to the normal range has not been found to be of benefit.Guidelines recommend treatment with parenteral iron prior to treatment with erythropoietin.
Replacement of erythropoietin is often necessary in people with advanced disease.
It is unclear if androgens improve anemia.
Calcitriol is recommended for vitamin D deficiency and control of metabolic bone disease.
Phosphate binders are used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease.
Phosphodiesterase-5 inhibitors and zinc may improve sexual dysfunction in men.

Lifestyle Interventions
Obesity may have a negative impact in CKD, increasing the risk of disease progression to ESKD or kidney failure compared to controls with healthy weight, and when in advanced stages also may hinder peoples eligibility to kidney transplantation.  For example, the consumption of high calorie and high fructose beverages can make an individual "60% more likely to develop CKD". Weight management interventions in overweight and obese adults with CKD (of various stages) have been studied to assess its safety and efficacy. A recent systematic review collected evidence from 17 studies which evaluated lifestyle (including dietary, physical activity/exercise, or behavioural strategies used in isolation or in combination), pharmacological (used to reduce absorption or suppress appetite) and surgical interventions. The review concluded that lifestyle interventions may provide some health benefits, namely improving body weight, low density lipoprotein (LDL) cholesterol and diastolic blood pressure (DBP), when compared to usual care or controls. Whether these benefits extend to help reducing cardiovascular events, kidney function and risk of death is uncertain. These conclusions were based on very low quality of evidence, so future robust studies are needed. Thus, it is recommended that weight management interventions should be individualised, according to a thorough patients assessment regarding clinical condition, motivations and preferences.

Sleep
People with CKD experience sleep disorders, thus not being able to get quality sleep. There are several strategies that could help, such as relaxation techniques, exercise, acupressure and medication:
Exercise: weak evidence demonstrates that exercise may be helpful with sleep regulation. Nevertheless, exercise possibly decreases fatigue and depression in people with CKD.
Acupressure: evidence suggests that this technique may have slight effects on latency and sleep duration, as well as on fatigue reduction, although these results are not reliable due to the diversity of conclusions in several articles.Despite all the available options studied so far, evidence shows that none of them is effective in the treatment of sleep disorders. This means that we are not able to conclude which is the best guidance to improve sleep quality in this type of population.

eHealth interventions
There is currently limited evidence suggesting that eHealth interventions may improve dietary sodium intake and fluid management for people with chronic kidney disease (CKD). The findings are based on low certainty evidence of 43 studies. So, more large and higher quality research studies are needed to understand the impact of eHealth on the health of people with CKD.

Referral to a nephrologist
Guidelines for referral to a nephrologist vary between countries.  Most agree that nephrology referral is required by Stage 4 CKD (when eGFR/1.73m2 is less than 30 mL/min; or decreasing by more than 3 mL/min/year).It may also be useful at an earlier stage (e.g. CKD3) when urine albumin-to-creatinine ratio is more than 30 mg/mmol, when blood pressure is difficult to control, or when hematuria or other findings suggest either a primarily glomerular disorder or secondary disease amenable to specific treatment.  Other benefits of early nephrology referral include proper education regarding options for kidney replacement therapy as well as pre-emptive transplantation, and timely workup and placement of an arteriovenous fistula in those people with chronic kidney disease opting for future hemodialysis.

Renal replacement therapy
At stage 5 CKD, kidney replacement therapy is usually required, in the form of either dialysis or a kidney transplant.
In CKD numerous uremic toxins accumulate in the blood. Even when ESKD (largely synonymous with CKD5) is treated with dialysis, the toxin levels do not go back to normal as dialysis is not that efficient. Similarly, after a kidney transplant, the levels may not go back to normal as the transplanted kidney may not work 100%. If it does, the creatinine level is often normal. The toxins show various cytotoxic activities in the serum and have different molecular weights, and some of them are bound to other proteins, primarily to albumin. Uremic toxins are classified into three groups as small water-soluble solutes, middle molecular-weight solutes, and protein-bound solutes. Hemodialysis with high-flux dialysis membrane, long or frequent treatment, and increased blood/dialysate flow has improved removal of water-soluble small molecular weight uremic toxins. Middle molecular weight molecules are removed more effectively with hemodialysis using a high-flux membrane, hemodiafiltration and hemofiltration. However, conventional dialysis treatment is limited in its ability to remove protein-bound uremic toxins.

Prognosis
CKD increases the risk of cardiovascular disease, and people with CKD often have other risk factors for heart disease, such as high blood lipids. The most common cause of death in people with CKD is cardiovascular disease rather than kidney failure.
Chronic kidney disease results in worse all-cause mortality (the overall death rate) which increases as kidney function decreases.  The leading cause of death in chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.While kidney replacement therapies can maintain people indefinitely and prolong life, the quality of life is negatively affected. Kidney transplantation increases the survival of people with stage 5 CKD when compared to other options; however, it is associated with an increased short-term mortality due to complications of the surgery. Transplantation aside, high-intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three-times-a-week hemodialysis and peritoneal dialysis.People with ESKD are at increased overall risk for cancer. This risk is particularly high in younger people and gradually diminishes with age. Medical specialty professional organizations recommend that physicians do not perform routine cancer screening in people with limited life expectancies due to ESKD because evidence does not show that such tests lead to improved outcomes.In children, growth failure is a common complication from CKD. Children with CKD will be shorter than 97% of children the same age and sex. This can be treated with additional nutritional support, or medication such as Growth hormone

Epidemiology
About one in ten people have chronic kidney disease. In Canada 1.9 to 2.3 million people were estimated to have CKD in 2008. CKD affected an estimated 16.8% of U.S. adults aged 20 years and older in the period from 1999 to 2004. In 2007 8.8% of the population of Great Britain and Northern Ireland had symptomatic CKD.Chronic kidney disease was the cause of 956,000 deaths globally in 2013, up from 409,000 deaths in 1990.

Chronic kidney disease of unknown aetiology
The cause of chronic kidney disease is in some cases not known; it is referred to as chronic kidney disease of unknown aetiology (CKDu). As of 2020 a rapidly progressive chronic kidney disease, unexplained by diabetes and hypertension, had increased dramatically in prevalence over a few decades in several regions in Central America and Mexico, a CKDu referred to as the Mesoamerican nephropathy (MeN). It was estimated in 2013 that at least 20,000 men had died prematurely, some in their 20s and 30s; a figure of 40,000 per year was estimated in 2020. In some affected areas CKD mortality was five times the national rate. MeN primarily affects men working as sugarcane labourers. The cause is unknown, but in 2020 the science found a clearer connection between heavy labour in high temperatures and incidence of CKDu; improvements such as regular access to water, rest and shade, can significantly decrease the potential CKDu incidence. CKDu also affects people in Sri Lanka where it is the eighth largest cause of in-hospital mortality.Although CKDu was first documented among sugar cane workers in Costa Rica in the 1970s, it may well have affected plantation labourers since the introduction of sugar cane farming to the Caribbean in the 1600s. In colonial times the death records of slaves on sugar plantations was much higher than for slaves forced into other labour.

Race
African, Hispanics, and South Asians, particularly those from Pakistan, Sri Lanka, Bangladesh, and India, are at high risk of developing CKD </s>