<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 Itch and explain in detail? [/INST] Itch (also known as pruritus) is a sensation that causes the desire or reflex to scratch. Itch has resisted many attempts to be classified as any one type of sensory experience. Itch has many similarities to pain, and while both are unpleasant sensory experiences, their behavioral response patterns are different. Pain creates a withdrawal reflex, whereas itch leads to a scratch reflex.Unmyelinated nerve fibers for itch and pain both originate in the skin; however, information for them is conveyed centrally in two distinct systems that both use the same nerve bundle and spinothalamic tract.

Classification
Most commonly, an itch is felt in one place. If it is felt all over the body, then it is called generalized itch or generalized pruritus.If the sensation of itching persists for six weeks or longer, then it is called chronic itch or chronic pruritus. Chronic idiopathic pruritus or essential pruritus is a rare form of itch that persists for longer than six weeks, and for which no clear cause can be identified.

Signs and symptoms
Pain and itch have very different behavioral response patterns. Pain elicits a withdrawal reflex, which leads to retraction and therefore a reaction trying to protect an endangered part of the body. Itch in contrast creates a scratch reflex, which draws one to the affected skin site. Itch generates stimulus of a foreign object underneath or upon the skin and also the urge to remove it. For example, responding to a local itch sensation is an effective way to remove insects from ones skin.
Scratching has traditionally been regarded as a way to relieve oneself by reducing the annoying itch sensation. However, there are hedonic aspects to scratching, as one would find noxious scratching highly pleasurable. This can be problematic with chronic itch patients, such as ones with atopic dermatitis, who may scratch affected spots until they no longer produce a pleasant or painful sensation, instead of when the itch sensation disappears. It has been hypothesized that motivational aspects of scratching include the frontal brain areas of reward and decision making. These aspects might therefore contribute to the compulsive nature of itch and scratching.

Contagious itch
Events of "contagious itch" are very common occurrences. Even a discussion on the topic of itch can give one the desire to scratch. Itch is likely to be more than a localized phenomenon in the place one scratches. Results from a study showed that itching and scratching were induced purely by visual stimuli in a public lecture on itching. The sensation of pain can also be induced in a similar fashion, often by listening to a description of an injury, or viewing an injury itself.
There is little detailed data on central activation for contagious itching, but it is hypothesized that a human mirror neuron system exists in which one imitates certain motor actions when they view others performing the same action. A similar hypothesis has been used to explain the cause of contagious yawning.

Itch inhibition due to pain
Studies done in the last decade have shown that itch can be inhibited by many other forms of painful stimuli, such as noxious heat, physical rubbing/scratching, noxious chemicals, and electric shock.

Causes
Infections
Body louse, found in substandard living conditions
Cutaneous larva migrans, a skin disease
Head lice, if limited to the neck and scalp
Herpes, a viral disease
Insect bites, such as those from mosquitos or chiggers
Pubic lice, if limited to the genital area
Scabies, especially when several other persons in close contact also itch
Shaving, which may irritate the skin
Swimmers itch, a short-term immune reaction
Varicella – i.e. chickenpox, prevalent among young children and highly contagious
Tungiasis, ectoparasite of skin

Environmental and allergic
Allergic reaction to contact with specific chemicals, such as urushiol, derived from poison ivy or poison oak, or Balsam of Peru, found in many foods and fragrances. Certain allergens may be diagnosed in a patch test.
Foreign objects on the skin are the most common cause of non-pathological itching.
Photodermatitis – sunlight reacts with chemicals in the skin, leading to the formation of irritant metabolites.
Urticaria (also called hives) usually causes itching.

Skin disorders
Dandruff; an unusually large amount of flaking is associated with this sensation.
Punctate palmoplantar keratoderma, a group of disorders characterized by abnormal thickening of the palms and soles.
Skin conditions (such as psoriasis, eczema, seborrhoeic dermatitis, sunburn, athletes foot, and hidradenitis suppurativa). Most are of an inflammatory nature.
Scab healing, scar growth, and the development or emergence of moles, pimples, and ingrown hairs from below the epidermis.
Xerosis: dry skin, frequently seen in the winter and also associated with older age, frequent bathing in hot showers or baths, and high-temperature and low-humidity environments.

Other medical disorders
Diabetes mellitus, a group of metabolic diseases in which a person has high blood sugar
Hyperparathyroidism, overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH)
Iron deficiency anemia, a common anemia (low red blood cell or hemoglobin levels)
Cholestasis, where bile acids leaking into the serum activate peripheral opioid receptors, resulting in the characteristic generalized, severe itching
Malignancy or internal cancer, such as lymphoma or Hodgkins disease
Polycythemia, which can cause generalized itching due to increased histamines
Psychiatric disease ("psychogenic itch", as may be seen in delusional parasitosis)
Thyroid illness
Uraemia – the itching sensation this causes is known as uremic pruritus

Medication
Drugs (such as opioids) that activate histamine (H1) receptors or trigger histamine release
Chloroquine, a drug used in the treatment and prevention of malaria
Bile acid congeners such as obeticholic acid

Related to pregnancy
Gestational pemphigoid, a dermatosis of pregnancy
Intrahepatic cholestasis of pregnancy, a medical condition in which cholestasis occurs
Pruritic urticarial papules and plaques of pregnancy (PUPPP), a chronic hives-like rash

Other
Menopause, or changes in hormonal balances associated with aging
Terminal illness

Mechanism
Itch can originate in the peripheral nervous system (dermal or neuropathic) or in the central nervous system (neuropathic, neurogenic, or psychogenic).

Dermal/pruritoceptive
Itch originating in the skin is known as pruritoceptive, and can be induced by a variety of stimuli, including mechanical, chemical, thermal, and electrical stimulation. The primary afferent neurons responsible for histamine-induced itch are unmyelinated C-fibres.Two major classes of human C-fibre nociceptors exist: mechano-responsive nociceptors and mechano-insensitive nociceptors. Mechano-responsive nociceptors have been shown in studies to respond to mostly pain, and mechano-insensitive receptors respond mostly to itch induced by histamine. However, it does not explain mechanically induced itch or itch produced without a flare reaction that involves no histamine. Therefore, it is possible that pruritoceptive nerve fibres have different classes of fibres, which is unclear in current research.Studies have been done to show that itch receptors are found only on the top two skin layers, the epidermis and the epidermal/dermal transition layers. Shelley and Arthur verified the depth by injecting individual itch powder (Mucuna pruriens) spicules and noting that maximal sensitivity occurred at the basal cell layer or the innermost layer of the epidermis. Surgical removal of those skin layers removed the ability for a patient to perceive itch. Itch is never felt in muscle or joints, which strongly suggests that deep tissue probably does not contain itch signaling apparatuses.Itch is often classified as that which is histamine mediated (histaminergic) and nonhistaminergic.
Sensitivity to pruritic stimuli is evenly distributed across the skin and has a clear spot distribution with similar density to that of pain. The different substances that elicit itch upon intracutaneous injection (injection within the skin) elicit only pain when injected subcutaneously (beneath the skin).Itch is readily abolished in skin areas treated with nociceptor excitotoxin capsaicin but remains unchanged in skin areas rendered touch insensitive by pretreatment with anti-inflammatory saponins. Although experimentally induced itch can still be perceived under a complete A-fiber conduction block, it is significantly diminished. Overall, itch sensation is mediated by A-delta and C nociceptors located in the uppermost layer of the skin.

Molecular diversity of itch transmitting primary afferents
Using single-cell mRNA sequencing, sensory-modality specific primary afferent have been molecularly defined into clusters based on gene expression patterns. Here, 11 sub clusters were detected; NF1-3, transmitting innocuous nociceptive information; NF4-5, which transmit proprioceptive information; NP1-3, transmitting itch information; PEP1-2, nociceptive information and TH, which is involved in pleasant touch, The pruriceptive NP1-3 were shown to express genes related to histaminergic and non-histaminergic signaling, where NF1 expresses genes responding to lysophosphatidic acid (Lpar3 and Lpar5), NP2 chloroquine-responsive genes (Mrgpra3 and Mrgprx1), whereas NP3 expresses neuropeptides Nppb and Sst as well as genes involved in inflammatory itch (Il31ra, Osmr and Crystrl2). The histamine receptor gene Hrh1 was found in NP2 and NP3, suggesting that histaminergic itch is transmitted by both these pruriceptive sub clusters.

The spinal itch pathway
After the pruriceptive primary afferent has been activated, the signal is transmitted from the skin into the spinal dorsal horn. In this area, a number of interneurons will either be inhibited or activated to promote activation of projection neurons, mediating the puriceptive signal to the brain. The GRP-GRPR interneuron system has been found to be important for mediating both histaminergic and non-histaminergic itch, where the GRP neurons activate GRPR neurons to promote itch

Neuropathic
Neuropathic itch can originate at any point along the afferent pathway as a result of damage of the nervous system. They could include diseases or disorders in the central nervous system or peripheral nervous system. Examples of neuropathic itch in origin are notalgia paresthetica, brachioradial pruritus, brain tumors, multiple sclerosis, peripheral neuropathy, and nerve irritation.

Neurogenic
Neurogenic itch, which is itch induced centrally but with no neural damage, is mostly associated with increased accumulation of exogenous opioids and possibly synthetic opioids.

Psychogenic
Itch is also associated with some symptoms of psychiatric disorders such as tactile hallucinations, delusions of parasitosis, or obsessive-compulsive disorders (as in OCD-related neurotic scratching).

Peripheral sensitization
Inflammatory mediators—such as bradykinin, serotonin (5-HT) and prostaglandins—released during a painful or pruritic inflammatory condition not only activate pruriceptors but also cause acute sensitization of the nociceptors. In addition, expression of neuro growth factors (NGF) can cause structural changes in nociceptors, such as sprouting. NGF is high in injured or inflamed tissue. Increased NGF is also found in atopic dermatitis, a hereditary and non-contagious skin disease with chronic inflammation. NGF is known to up-regulate neuropeptides, especially substance P. Substance P has been found to have an important role in inducing pain; however, there is no confirmation that substance P directly causes acute sensitization. Instead, substance P may contribute to itch by increasing neuronal sensitization and may affect release of mast cells, which contain many granules rich in histamine, during long-term interaction.

Central sensitization
Noxious input to the spinal cord is known to produce central sensitization, which consists of allodynia, exaggeration of pain, and punctuate hyperalgesia, extreme sensitivity to pain. Two types of mechanical hyperalgesia can occur: 1) touch that is normally painless in the uninjured surroundings of a cut or tear can trigger painful sensations (touch-evoked hyperalgesia), and 2) a slightly painful pin prick stimulation is perceived as more painful around a focused area of inflammation (punctuate hyperalgesia). Touch-evoked hyperalgesia requires continuous firing of primary afferent nociceptors, and punctuate hyperalgesia does not require continuous firing which means it can persist for hours after a trauma and can be stronger than normally experienced. In addition, it was found that patients with neuropathic pain, histamine ionophoresis resulted in a sensation of burning pain rather than itch, which would be induced in normal healthy patients </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 Air embolism and explain in detail? [/INST] An air embolism, also known as a  gas embolism, is a blood vessel blockage caused by one or more bubbles of air or other gas in the circulatory system. Air can be introduced into the circulation during surgical procedures, lung over-expansion injury, decompression, and a few other causes. Air embolisms may also occur in the xylem of vascular plants, especially when suffering from water stress.
Divers can develop arterial gas embolisms as a consequence of lung over-expansion injuries. Breathing gas introduced into the venous system of the lungs  due to pulmonary barotrauma will not be trapped in the alveolar capillaries, and will consequently be circulated to the rest of the body through the systemic arteries, with a high risk of embolism. Inert gas bubbles arising from decompression are generally formed in the venous side of the systemic circulation, where inert gas concentrations are highest, these bubbles are generally trapped in the capillaries of the lungs where they will usually be eliminated without causing symptoms. If they are shunted to the systemic circulation through a patent foramen ovale they can travel to and lodge in the brain where they can cause stroke, the coronary capillaries where they can cause myocardial ischaemia or other tissues, where the consequences are usually less critical. The first aid treatment is to administer oxygen at the highest practicable concentration, treat for shock and transport to a hospital where therapeutic recompression and hyperbaric oxygen therapy are the definitive treatment.

Signs and symptoms
In surgery
Symptoms include:
Hypotension
Shortness of breath

In divers
Symptoms of arterial gas embolism include:
Loss of consciousness
Cessation of breathing
Vertigo
Convulsions
Tremors
Loss of coordination
Loss of control of bodily functions
Numbness
Paralysis
Extreme fatigue
Weakness in the extremities
Areas of abnormal sensation
Visual abnormalities
Hearing abnormalities
Personality changes
Cognitive impairment
Nausea or vomiting
Bloody sputum
Symptoms of other consequences of lung overexpansion such as pneumothorax, subcutaneous or mediastinal emphysema may also be present.

Causes
Interventional procedures
Interventional radiology procedures, cardiac, and neurosurgical procedures can predispose to air embolism. Besides, increasing use of pump injectors for contrast delivery, and percutaneous intervention to the lungs also increases the risk of air embolism.

Decompression illness
Gas embolism is a diving disorder experienced by underwater divers who breathe gases at ambient pressure, and can happen in two distinct ways:

Pulmonary barotrauma:  Air bubbles can enter the bloodstream as a result of gross trauma to the lining of the lung following a rapid ascent while holding the breath; the air held within the lung expands to the point where the tissues tear (pulmonary barotrauma).  This is easy to do as the lungs give little warning through pain until they do burst.  The diver will usually arrive at the surface in pain and distress and may froth or spit blood.  A pulmonary barotrauma is usually obvious and may present quite differently from decompression sickness.
Decompression sickness: Inert gas bubbles form in the bloodstream if the gas dissolved in the blood under pressure during the dive is not allowed sufficient time to be eliminated in solution on ascent. The symptoms may be subtle and not immediately noticeable, and may develop for some time after surfacing.

Ventilator induced pulmonary barotrauma
Trauma to the lung can also cause an air embolism. This may happen after a patient is placed on a ventilator and air is forced into an injured vein or artery, causing sudden death. Breath-holding while ascending from scuba diving may also force lung air into pulmonary arteries or veins in a similar manner, due to the pressure difference.

Direct injection
Air can be injected directly into a vein or artery accidentally during clinical procedures. Misuse of a syringe to meticulously remove air from the vascular tubing of a hemodialysis circuit can allow air into the vascular system. Venous air embolism is a rare complication of diagnostic and therapeutic procedures requiring catheterization of a vein or artery. If a significant embolism occurs, the cardiovascular, pulmonary, or central nervous system may be affected. Interventions to remove or mitigate the embolism may include procedures to reduce bubble size, or withdrawal of air from the right atrium.The lethal dose for humans is considered theoretically between 3 and 5 ml per kg. It is estimated that 300-500 ml of gas introduced at a rate of 100 ml per sec would prove fatal.

Mechanism
Air embolism can occur whenever a blood vessel is open and a pressure gradient exists favoring entry of gas. Because the circulatory pressure in most arteries and veins is greater than atmospheric pressure, an air embolus does not often happen when a blood vessel is injured. In the veins above the heart, such as in the head and neck, the venous pressure may be less than atmospheric and an injury may let air in. This is one reason why surgeons must be particularly careful when operating on the brain, and why the head of the bed is tilted down when inserting or removing a central venous catheter from the jugular or subclavian veins.When air enters the veins, it travels to the right side of the heart, and then to the lungs. This can cause the vessels of the lung to constrict, raising the pressure in the right side of the heart. If the pressure rises high enough in a patient who is one of the 20% to 30% of the population with a patent foramen ovale, the gas bubble can then travel to the left side of the heart, and on to the brain or coronary arteries. Such bubbles are responsible for the most serious of gas embolic symptoms.
Venous or pulmonary air embolism occurs when air enters the systemic veins and is transported to the right side of the heart and from there into the pulmonary arteries, where it may lodge, blocking or reducing blood flow. Gas in the venous circulation can cause cardiac problems by obstructing the pulmonary circulation or forming an air-lock which raises central venous pressure and reduces pulmonary and systemic arterial pressures. Experiments on animals show that the amount of gas necessary for this to happen is quite variable. Human case reports suggest that injecting more than 100 mL of air into the venous system at rates greater than 100 mL/s can be fatal. Very large and symptomatic amounts of venous air emboli may also occur in rapid decompression in severe diving or decompression accidents, where they may interfere with circulation in the lungs and result in respiratory distress and hypoxia.Gas embolism in a systemic artery, termed arterial gas embolism (AGE), is a more serious matter than in a vein, because a gas bubble in an artery may directly stop blood flow to an area fed by the artery. The symptoms of AGE depend on the area of blood flow, and may be those of stroke for a cerebral arterial gas embolism (CAGE) or heart attack if the heart is affected. The amount of arterial gas embolism that causes symptoms depends on location — 2 mL of air in the cerebral circulation can be fatal, while 0.5 mL of air into a coronary artery can cause cardiac arrest.

Prevention and screening
If a patent foramen ovale (PFO) is suspected, an examination by echocardiography may be performed to diagnose the defect. In this test, very fine bubbles are introduced into a patients vein by agitating saline in a syringe to produce the bubbles, then injecting them into an arm vein. A few seconds later, these bubbles may be clearly seen in the ultrasound image, as they travel through the patients right atrium and ventricle. At this time, bubbles may be observed directly crossing a septal defect, or else a patent foramen ovale may be opened temporarily by asking the patient to perform the Valsalva maneuver while the bubbles are crossing through the right heart – an action which will open the foramen flap and show bubbles passing into the left heart. Such bubbles are too small to cause harm in the test, but such a diagnosis may alert the patient to possible problems which may occur from larger bubbles, formed during activities like underwater diving, where bubbles may grow during decompression. A PFO test may be recommended for divers intending to expose themselves to relatively high decompression stress in deep technical diving.

Diagnosis
As a general rule, any diver who has breathed gas under pressure at any depth who surfaces unconscious, loses consciousness soon after surfacing, or displays neurological symptoms within about 10 minutes of surfacing should be assumed to be experiencing arterial gas embolism.Symptoms of arterial gas embolism may be present but masked by environmental effects such as hypothermia, or pain from other obvious causes. Neurological examination is recommended when there is suspicion of lung overexpansion injury. Symptoms of decompression sickness may be very similar to, and confused with, symptoms of arterial gas embolism, however, treatment is basically the same. Discrimination between gas embolism and decompression sickness may be difficult for injured divers, and both may occur simultaneously. Dive history may eliminate decompression sickness in many cases, and the presence of symptoms of other lung overexpansion injury would raise the probability of gas embolism.

Treatment
A large bubble of air in the heart (as can follow certain traumas in which air freely gains access to large veins) will present with a constant "machinery" murmur. It is important to promptly place the patient in Trendelenburg position (head down) and on their left side (left lateral decubitus position). The Trendelendburg position keeps a left-ventricular air bubble away from the coronary artery ostia (which are near the aortic valve) so that air bubbles do not enter and occlude the coronary arteries (which would cause a heart attack). Left lateral decubitus positioning helps to trap air in the non-dependent segment of the right ventricle (where it is more likely to remain instead of progressing into the pulmonary artery and occluding it). The left lateral decubitus position also prevents the air from passing through a potentially patent foramen ovale (present in as many as 30% of adults) and entering the left ventricle, from which it could then embolise to distal arteries (potentially causing occlusive symptoms such as stroke).Administration of high percentage oxygen is recommended for both venous and arterial air embolism. This is intended to counteract ischaemia and accelerate bubble size reduction.For venous air embolism the Trendelenburg or left lateral positioning of a patient with an air-lock obstruction of the right ventricle may move the air bubble in the ventricle and allow blood flow under the bubble.Hyperbaric therapy with 100% oxygen is recommended for patients presenting clinical features of arterial air embolism, as it accelerates removal of nitrogen from the bubbles by solution and improves tissue oxygenation. This is recommended particularly for cases of cardiopulmonary or neurological involvement. Early treatment has greatest benefits, but it can be effective as late as 30 hours after the injury.

Treatment of divers
Oxygen first aid treatment is useful for suspected gas embolism casualties or divers who have made fast ascents or missed decompression stops. Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as an alternative to pure open-circuit oxygen resuscitators. However pure oxygen from an oxygen cylinder through a Non-rebreather mask is the optimal way to deliver oxygen to a decompression illness patient.

Recompression is the most effective, though slow, treatment of gas embolism in divers. Normally this is carried out in a recompression chamber. As pressure increases, the solubility of a gas increases, which reduces bubble size by accelerating absorption of the gas into the surrounding blood and tissues.  Additionally, the volumes of the gas bubbles decrease in inverse proportion to the ambient pressure as described by Boyles law.  In the hyperbaric chamber the patient may breathe 100% oxygen, at ambient pressures up to a depth equivalent of 18 msw.  Under hyperbaric conditions, oxygen diffuses into the bubbles, displacing the nitrogen from the bubble and into solution in the blood.  Oxygen bubbles are more easily tolerated.  Diffusion of oxygen into the blood and tissues under hyperbaric conditions supports areas of the body which are deprived of blood flow when arteries are blocked by gas bubbles.  This helps to reduce ischemic injury </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 X-linked ichthyosis and explain in detail? [/INST] X-linked ichthyosis (abbreviated XLI) is a skin condition caused by the hereditary deficiency of the steroid sulfatase (STS) enzyme that affects 1 in 2000 to 1 in 6000 males.  XLI manifests with dry, scaly skin and is due to deletions or mutations in the STS gene.  XLI can also occur in the context of larger deletions causing contiguous gene syndromes. Treatment is largely aimed at alleviating the skin symptoms. The term is from the Ancient Greek ichthys meaning fish.

Signs and symptoms
The major symptoms of XLI include scaling of the skin, particularly on the neck, trunk, and lower extremities.  The extensor surfaces are typically the most severely affected areas.  The >4 mm diameter scales adhere to the underlying skin and can be dark brown or gray in color.  Symptoms may subside during the summer.

Associated medical conditions
Aside from the skin scaling, XLI is not typically associated with other major medical problems. Atrial fibrillation or atrial flutter may affect up to 1 in 10 males with XLI. Heart rhythm abnormalities in individuals with XLI tend to co-occur with disorders of the gastrointestinal tract, and are likely to result from steroid sulfatase deficiency. Corneal opacities may be present but do not affect vision. Cryptorchidism is reported in some individuals. Individuals with XLI appear at increased risk of developmental disorders such as autism and Attention Deficit Hyperactivity Disorder and some affected individuals exhibit mood problems  Mood problems in XLI appear to be most influenced by stigma or bullying associated with the skin condition, and by difficulties with treating the skin condition. Individuals with XLI can exhibit intellectual disability, although this is thought to be due to deletions encompassing neighboring genes (e.g. VCX) in addition to STS.Female carriers generally do not experience any of these problems but can have difficulty during childbirth, as the STS expressed in the placenta plays a role in normal labor. Female carriers may also be at slightly increased risk of developing mental health problems following childbirth  For these reasons carriers should ensure their obstetrician is aware of the condition.

Genetics
The STS gene is located on the X chromosome at band Xp22.3.  Thus, the syndrome is an X-linked condition, and it affects males and females differently.  The 23rd pair of chromosomes is typically termed the "sex chromosomes".  Females have two X chromosomes and males have one X and one Y chromosome.  Therefore, in normal individuals, males carry a single copy of the STS gene and females carry two copies.  This gene partially escapes X-inactivation and females normally express higher amounts of the STS enzyme than males.XLI can occur through new deletions or mutations of the STS gene but is more commonly inherited from a carrier mother.  A hemizygous deletion or mutation of the STS gene in a male results in complete absence of enzyme activity, while a female carrier of a mutation or deletion is heterozygous and still has a normal copy of the STS gene.  Female carriers of an STS deletion or mutation still express the STS enzyme, although with decreased enzyme activity.For this reason, XLI most commonly affects males, although individuals with numeric abnormalities of the sex chromosomes (45,X and 47,XXY) who also carry STS deletions or mutations would be exceptions to this rule.In addition, a female could be affected if she were the offspring of an affected male and a carrier female and inherited a deletion or mutation of the STS gene on both X chromosomes.

Genetic counseling issues
Since the majority of cases appear to occur through transmission of an STS deletion from a carrier mother, enzyme testing or DNA testing should be performed in the mother of any newly diagnosed simplex case (i.e. the first case in a family).  In the case of an extended family with many affected individuals, carrier status can often be assigned based on pedigree analysis.

Males with XLI will transmit the X chromosome harboring the STS deletion or mutation to each of his female offspring, who will therefore be an obligate carrier.  However, all male offspring will be unaffected, since they receive their fathers Y chromosome.
Female carriers of an STS deletion or mutation have a 50% chance with each pregnancy of transmitting it to an offspring.  Thus, each male offspring has a 50% chance of being affected by XLI, while each female offspring has a 50% chance of being a carrier for this condition.  Any individual that inherits the mothers normal copy of the STS gene will be unaffected and will have an extremely low chance of having a child affected with this condition.Due to random segregation of the chromosomes during gametogenesis, each pregnancy will be subject to the same probabilities, regardless of the number of previously affected or unaffected offspring. The above recurrence risks are based on the assumption that an affected male or carrier female will have children with an unaffected or non-carrier individual.  The risks of having affected offspring would clearly increase in the case of a union between a male with XLI and a carrier female.

Physiology/biochemistry
The STS enzyme (EC 3.1.6.2), also referred to as Arylsulfatase C, is expressed throughout the body, with highest expression in the skin, liver, lymph nodes, and placenta, and lower expression in breast tissue and brain  STS catalyzes the hydrolysis of sulfated steroids, such as estrone sulfate and dehydroepiandrosterone sulfate (DHEAS), to non-sulfated steroids estradiol and androstenediol, respectively.  Prenatally, the enzyme is involved in placental estrogen production.  The enzyme is also involved in adrenal steroid production as well as conversion of sulfated steroids in other tissues.There seems to be a particularly important role for the enzyme in skin.  Deficiency of the enzyme leads to the characteristic dry and scaly skin seen in ichthyosis </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 Electrocution and explain in detail? [/INST] Electrocution is death or severe injury  caused by electric shock from electric current passing through the body. The word is derived from "electro" and "execution", but it is also used for accidental death.The term "electrocution" was coined in 1889 in the US just before the first use of the electric chair and originally referred to only electrical execution and not other electrical deaths. However, since no English word was available for non-judicial deaths due to electric shock, the word "electrocution" eventually took over as a description of all circumstances of electrical death from the new commercial electricity.

Origins
In the Netherlands in 1746 Pieter van Musschenbroeks lab assistant, Andreas Cuneus, received an extreme shock while working with a leyden jar, the first recorded injury from man-made electricity. By the mid-19th century high-voltage electrical systems came into use to power arc lighting for theatrical stage lighting and lighthouses leading to the first recorded accidental death in 1879 when a stage carpenter in Lyon, France, touched a 250-volt wire.The spread of arc light–based street lighting systems (which at the time ran at a voltage above 3,000 volts) after 1880 led to many people dying from coming in contact with these high-voltage lines, a strange new phenomenon which seemed to kill instantaneously without leaving a mark on the victim. This would lead to execution by electricity in the electric chair in the early 1890s as an official method of capital punishment in the U.S. state of New York, thought to be a more humane alternative to hanging. After an 1881 death in Buffalo, New York, caused by a high-voltage arc lighting system, Alfred P. Southwick sought to develop this phenomenon into a way to execute condemned criminals. Southwick, a dentist, based his device on the dental chair.The next nine years saw a promotion by Southwick, the New York state Gerry commission (which included Southwick) recommending execution by electricity, a June 4, 1888 law making it the state form of execution on January 2, 1889, and a further state committee of doctors and lawyers to finalize the details of the method used.The adoption of the electric chair became mixed up in the "war of currents" between Thomas Edisons direct current system and industrialist George Westinghouses alternating current system in 1889 when noted anti-AC activist Harold P. Brown became a consultant to the committee. Brown pushed, with the assistance and sometimes collusion of Edison Electric and Westinghouses chief AC rival, the Thomson-Houston Electric Company, for the successful adoption of alternating current to power the chair, an attempt to portray AC as a public menace and the "executioners current".

Etymology
In May 1889 the state of New York sentenced its first criminal, a street merchant named William Kemmler, to be executed in their new form of capital punishment. Tabloid newspapers, trying to describe this new form of electrical execution, started settling on "electrocution," a portmanteau word derived from "electro" and "execution". It was not the only choice of word people were considering. The New York Times editorial column noted words such as "Westinghoused" (after the Westinghouse Electric alternating current equipment that was to be used), "Gerrycide" (after Elbridge Thomas Gerry, who headed the New York death penalty commission that suggested adopting the electric chair), and "Browned" (after anti-AC activist Harold P. Brown). Thomas Edison preferred the words dynamort, ampermort and electromort. The New York Times hated the word electrocution, describing it as being pushed forward by "pretentious ignoramuses".

Medical aspects
Fish & Geddes state: "Contact with 20 mA of current can be fatal".The health hazard of an electric current flowing through the body depends on the amount of current and the length of time for which it flows, not merely on the voltage. However, a high voltage is required to produce a high current through the body. This is due to the relatively high resistance of skin when dry, requiring a high voltage to pass through </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 Sedative and explain in detail? [/INST] A sedative or tranquilliser is a substance that induces sedation by reducing irritability or excitement. They are CNS depressants and interact with brain activity causing its deceleration. Various kinds of sedatives can be distinguished, but the majority of them affect the neurotransmitter gamma-aminobutyric acid (GABA). In spite of the fact that each sedative acts in its own way, most produce relaxing effects by increasing GABA activity.This group is related to hypnotics. The term sedative describes drugs that serve to calm or relieve anxiety, whereas the term hypnotic describes drugs whose main purpose is to initiate, sustain, or lengthen sleep. Because these two functions frequently overlap, and because drugs in this class generally produce dose-dependent effects (ranging from anxiolysis to loss of consciousness) they are often referred to collectively as sedative-hypnotic drugs.Sedatives can be used to produce an overly-calming effect (alcohol being the most common sedating drug). In the event of an overdose or if combined with another sedative, many of these drugs can cause deep unconsciousness and even death.

Terminology
There is some overlap between the terms "sedative" and "hypnotic".
Advances in pharmacology have permitted more specific targeting of receptors, and greater selectivity of agents, which necessitates greater precision when describing these agents and their effects:

Anxiolytic refers specifically to the effect upon anxiety. (However, some benzodiazepines can be all three: sedatives, hypnotics, and anxiolytics).
Tranquilizer can refer to anxiolytics or antipsychotics.
Soporific and sleeping pill are near-synonyms for hypnotics.

The term "chemical cosh"
The term "chemical cosh" (a club) is sometimes used popularly for a strong sedative, particularly for:

widespread dispensation of antipsychotic drugs in residential care to make people with dementia easier to manage.
use of methylphenidate to calm children with attention deficit hyperactivity disorder, though paradoxically this drug is known to be a stimulant.
See also Antipsychotic controversy

Types of sedatives
Therapeutic use
Doctors and veterinarians often administer sedatives to patients in order to dull the patients anxiety related to painful or anxiety-provoking procedures. Although sedatives do not relieve pain in themselves, they can be a useful adjunct to analgesics in preparing patients for surgery, and are commonly given to patients before they are anaesthetized, or before other highly uncomfortable and  invasive procedures like cardiac catheterization, colonoscopy or MRI.

Risks
Sedative dependence
Some sedatives can cause psychological and physical dependence when taken regularly over a period of time, even at therapeutic doses. Dependent users may get withdrawal symptoms ranging from restlessness and insomnia to convulsions and death. When users become psychologically dependent, they feel as if they need the drug to function, although physical dependence does not necessarily occur, particularly with a short course of use. In both types of dependences, finding and using the sedative becomes the focus in life.  Both physical and psychological dependence can be treated with therapy.

Misuse
Many sedatives can be misused, but barbiturates and benzodiazepines are responsible for most of the problems with sedative use due to their widespread recreational or non-medical use. People who have difficulty dealing with stress, anxiety or sleeplessness may overuse or become dependent on sedatives. Some heroin users may take them either to supplement their drug or to substitute for it. Stimulant users may take sedatives to calm excessive jitteriness. Others take sedatives recreationally to relax and forget their worries. Barbiturate overdose is a factor in nearly one-third of all reported drug-related deaths. These include suicides and accidental drug poisonings. Accidental deaths sometimes occur when a drowsy, confused user repeats doses, or when sedatives are taken with alcohol.
A study from the United States found that in 2011, sedatives and hypnotics were a leading source of adverse drug events (ADEs) seen in the hospital setting: Approximately 2.8% of all ADEs present on admission and 4.4% of ADEs that originated during a hospital stay were caused by a sedative or hypnotic drug.  A second study noted that a total of 70,982 sedative exposures were reported to U.S. poison control centers in 1998, of which 2310 (3.2%) resulted in major toxicity and 89 (0.1%) resulted in death.  About half of all the people admitted to emergency rooms in the U.S. as a result of nonmedical use of sedatives have a legitimate prescription for the drug, but have taken an excessive dose or combined it with alcohol or other drugs.There are also serious paradoxical reactions that may occur in conjunction with the use of sedatives that lead to unexpected results in some individuals.  Malcolm Lader at the Institute of Psychiatry in London estimates the incidence of these adverse reactions at about 5%, even in short-term use of the drugs.   The paradoxical reactions may consist of depression, with or without suicidal tendencies, phobias, aggressiveness, violent behavior and symptoms sometimes misdiagnosed as psychosis.

Dangers of combining sedatives and alcohol
Sedatives and alcohol are sometimes combined recreationally or carelessly. Since alcohol is a strong  depressant that slows brain function and depresses respiration, the two substances compound each others actions and this combination can prove fatal.

Worsening of psychiatric symptoms
The long-term use of benzodiazepines may have a similar effect on the brain as alcohol, and are also implicated in depression, anxiety, posttraumatic stress disorder (PTSD), mania, psychosis, sleep disorders, sexual dysfunction, delirium, and neurocognitive disorders (including benzodiazepine-induced persisting dementia which persists even after the medications are stopped) </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 Parapsoriasis 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 Atrioventricular block and explain in detail? [/INST] Atrioventricular block (AV block) is a type of heart block that occurs when the electrical signal traveling from the atria, or the upper chambers of the heart, to ventricles, or the lower chambers of the heart, is impaired. Normally, the sinoatrial node (SA node) produces an electrical signal to control the heart rate. The signal travels from the SA node to the ventricles through the atrioventricular node (AV node). In an AV block, this electrical signal is either delayed or completely blocked. When the signal is completely blocked, the ventricles produce their own electrical signal to control the heart rate. The heart rate produced by the ventricles is much slower than that produced by the SA node.Some AV blocks are benign, or normal, in certain people, such as in athletes or children. Other blocks are pathologic, or abnormal, and have several causes, including ischemia, infarction, fibrosis, and drugs.

Classification
There are three types, or degrees, of AV block: (1) first-degree, (2) second-degree, and (3) third-degree, with third-degree being the most severe. An ECG is used to differentiate between the different types of AV blocks. However, one important consideration when diagnosing AV blocks from ECGs is the possibility of pseudo- AV blocks which are due to concealed junctional extrasystoles. It is important to diagnose AV-blocks precisely because unnecessary pacemaker placement in patients with pseudo-AV blocks can worsen symptoms and create complications.

First-degree atrioventricular block
First-degree AV block occurs when there is a delay, but not disruption, as the electrical signal moves between the atrium and the ventricles through the AV node.  On ECG, this is defined by a PR interval greater than 200 msec. Additionally, there are no dropped, or skipped, beats.

Second-degree atrioventricular block
Second-degree AV block occurs when the electrical signal between the atria and ventricles is even more impaired than in a first-degree AV block. In a second-degree AV block, the impairment results in a failure to conduct an impulse, which causes a skipped beat.

Mobitz I
Mobitz I is characterized by a progressive yet reversible block of the AV node. On ECG, this is defined by progressive prolongation of the PR interval, with a resulting dropped beat (the PR interval gets longer and longer until a beat is finally dropped, or skipped).Some patients are asymptomatic; those who have symptoms respond to treatment effectively. There is a low risk of a Mobitz I AV block leading to heart attack and complete heart block.

Mobitz II
Mobitz II is caused by a sudden, unexpected failure of the His-Purkinje cells to conduct the electrical impulse. On ECG, the PR interval is unchanged from beat to beat, but there is a sudden failure to conduct the signal to the ventricles, and resulting in random skipped beat.The risks and possible effects of Mobitz II are much more severe than Mobitz I in that it can lead to severe heart attack.

Third-degree atrioventricular block
Third-degree AV block occurs when the signal between the atria and ventricles is completely blocked, and there is no communication between the two. None of the signals from the upper chambers makes it to the lower chambers. On ECG, there is no relationship between P waves and QRS complexes, meaning the P waves and QRS complexes are not in a 1:1 ratio.Third-degree AV block is the most severe of the AV blocks. Persons with third-degree AV block need emergency treatment including but not limited to a pacemaker.

Etiology
There are many causes of AV block, ranging from a normal variant among people to the result of a heart attack.First-degree AV block and Mobitz I second-degree block are often thought to be just normal, benign, conditions in people, and do not often result from a severe underlying condition.Mobitz II second-degree block and third-degree AV block are not normal variants and are associated with an underlying condition. Common causes include ischemia (lack of blood flow and oxygen to the heart muscle) or progressive fibrosis (excessive scaring) of the heart.  It is also possible that a high degree block can result after cardiac surgery during which the surgeon was in close proximity to the electrical conduction system and accidentally injured it. Reversible causes of Mobitz II and third-degree heart block include untreated Lyme disease, hypothyroidism, hyperkalemia (high levels of potassium), and drug toxicity. Drugs that slow the conduction of the electrical signal through AV node, such as beta-blockers, digoxin, calcium channel blockers, and amiodarone, can cause heart block if they are taken in excessive amounts, or the levels in the blood get too high.

Anatomy
The synchronized contraction of the heart occurs through a well-coordinated electrical signal pathway. The initial electrical signal originates from the SA node located in the upper portion of the right atrium. The electrical signal then travels through both the right and left atrium and causes the two atria to contract at the same time. This simultaneous contraction results in the P wave seen in an ECG tracing.The electrical signal then travels to the AV node located on the lower portion of the interatrial septum. At the AV node there is a delay in the electrical signal, which allows the atria to contract and blood to flow from the atria to the ventricles. This delay accounts for the ECG period between the P wave and the QRS complex, and creates the PR interval.
From the AV nodes, the electrical signal travels through Bundle of His and divides into the right bundle and left bundle, which are located within the interventricular septum. Finally, the electrical signal travels into the Purkinje fibers. The division of the signal into a right and left bundle and then into the Purkinje fibers allows for a simultaneous depolarization and contraction of the right and left ventricles. The contraction of the ventricles results in the QRS complex seen on an ECG tracing. After contraction, the ventricles must repolarize, or reset themselves, in order to allow for a second depolarization and contraction. The repolarization creates the T wave in the ECG tracing.

Diagnosis
An electrocardiogram, or ECG, is used to differentiate between the different types of AV block. In AV block, there is a disruption between the signal traveling from the atria to the ventricles </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 Complication 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 Ovarian disease and explain in detail? [/INST] Ovarian diseases refer to diseases or disorders of the ovary.These can be classified as endocrine disorders or as a disorders of the reproductive system.
If the egg fails to release from the follicle in the ovary an ovarian cyst may form. Small ovarian cysts are common in healthy women. Some women have more follicles than usual (polycystic ovary syndrome), which inhibits the follicles to grow normally and this will cause cycle irregularities.
Various types of ovarian diseases exist. Some of the ovarian diseases or disorders include: endometriosis, ovarian cysts, ovarian epithelial cancer, ovarian germ cell tumors, ovarian low malignant potential tumors, and polycystic ovary syndrome (PCOS).

Endometriosis
Endometriosis is a condition in which tissues lining the uterus (endometrial stroma and gland) grows abnormally beyond the uterus that may become quite painful. In simpler terms, it means that the tissue lining the uterus develops in different parts outside of it. It can be either at ovary, fallopian tubes, or peritoneal spaces.There is no single cause of endometriosis.Symptoms:
Menstrual cramps, heavy menstrual bleeding, bowel or urinary problems, nausea, vomiting, blood with stools, painful intercourse, fatigues, spotting or bleeding between periods.Treatment:

Surgery at extreme situations
Hormonal treatments using birth controls.
Healthier lifestyle.

Ovarian cysts
It is common for many women to develop a cyst in their lifetime. At times, these can go unnoticed without pain or visible symptoms. A cyst may develop in either of the ovaries that are responsible for producing hormones and carrying eggs in the bodies of women. Ovarian cysts can be of various types like dermoid cysts, endometrioma cysts and the functional cyst being the most common one [1]
Symptoms:

Abdominal bloating or swelling.
Painful bowel movement.
Pelvic pain before or after the menstrual cycle.
Painful intercourse.
Pain in the lower back or thighs.
Breast tenderness.
Nausea and vomiting.
Fever.
Rapid breathing.
Faintness or dizziness.
Sharp pelvic pain.Treatment:

Taking of oral contraceptives or birth control pills as prescribed by the doctor.
Laparoscopy: Surgery to remove the cyst.
Hysterectomy in case the cyst is cancerous.

Ovarian epithelial cancer
It is one of the common ovarian cancers that affect women worldwide. It develops outside the ovaries and ultimately spreads outside and can affect other organs.
Causes:
It may happen if there is a family medical history of breast cancer, colon cancer, rectal cancer or uterine cancer, or Lynch syndrome </s>