<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 Psychasthenia and can you explain it in depth? [/INST] Psychasthenia was a psychological disorder characterized by phobias, obsessions, compulsions, or excessive anxiety. The term is no longer in psychiatric diagnostic use, although it still forms one of the ten clinical subscales of the popular self-report personality inventories MMPI and MMPI-2.

Signs and symptoms
The MMPI subscale 7 describes psychasthenia as akin to obsessive-compulsive disorder, and as characterised by excessive doubts, compulsions, obsessions, and unreasonable fears.  The psychasthenic has an inability to resist specific actions or thoughts, regardless of their maladaptive nature.  In addition to obsessive-compulsive features, the scale taps abnormal fears, self-criticism, difficulties in concentration, and guilt feelings </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 Developmental dysfluency and can you explain it in depth? [/INST] Developmental dysfluency, or "normal dysfluency", is a lack of language fluency that occurs during early childhood development. It is commonly observed in children ages 2 to 4 years old. This typically occurs as they begin to learn language and communication skills. Developmental dysfluency refers to speech that is continually interrupted rather than flowing naturally. Developmental dysfluency is most commonly expressed through inconsistencies in speech such as stuttering, repetition, lengthening of sounds and syllables, mistiming, and poor inflection.Speech is a complicated skill involving a series of cognitive and linguistic processes that are both sensorimotor and auditory. As children grow, their language and vocabulary grow exponentially. Dysfluencies in early speech are typical as their speech skills develop. The most common form of dysfluency in children younger than three years is the repetition of one-syllable words or parts of words. Words or syllables are often repeated in the beginning of their sentences as they try to process how to form the rest of the sentence.
Language dysfluency may be common in children as they learn basic language skills throughout the crucial development stages in early childhood. Developmental dysfluency is normal in children as they work to acquire language skills and semantic/syntactic processing. About twenty-five percent of children experience some loss in fluency in their linguistic abilities. Some children between the ages of 2 and 6 encounter some obstacles in the path to fluent speech. Fluency in a normal child will typically improve around the age of 4. When attempting to master spoken language, children gradually develop fluent speech. Children go through the same learning patterns while developing their first language as adults do when learning languages other than their native language.Although many adults display types of dysfluency, it is usually in relation to comprehending or expressing different materials under stress. Developmental dysfluency is a normal part of the acquisition of language. An individual may not be fluent in language due to frequent stuttering or as a result of neurogenic dysfunction.
The origin of stuttering is not yet fully understood but parents/adults can mitigate the risk of developmental dysfluency by reducing the conversational demands on their child. Modeling slow, smooth speech and acknowledging the demanding and complex nature of learning language can help.

Symptoms
Symptoms of developmental dysfluency include the repetition of sounds or pauses between words. These symptoms have generally been noted within children from 18 months to 5 years of age. This may persist for weeks or months but eventually disappears due to the maturation of the childs nervous system. Children with a family history of stuttering are more likely to develop the disorder than those without.ex.: "Mommy, I am, I am, um, I am..."
Usually, this language dysfluency is a transitional stage that most children will leave behind as they master oral communications. At this point, there is little to no need for any therapeutic intervention. The typical occurrence lies between the ages of 18 months and 7 years as children pass through stages of speech dysfluency as they learn how to talk. Those with these types of dysfluencies will exhibit the afore mentioned repetitions about once every 10 sentencesMistiming and stuttering are common ways that developmental dysfluency manifests itself. When a child mistimes, they prolong a certain letter/syllable in the word they are saying, thereby taking much longer for their sentence to be said. Pauses or blocking are another side effect relating to developmental dysfluency. This is when one inserts a silent interval within the word. Revision is similar to this but is the halting completely, mid-flow of a sentence and taking the thought in a different direction. There is evidence to show that this may not only be an issue of speech motor areas but also the auditory cortex. In a MEG study by Beal et al. they found that adults with "persistent developmental stuttering" or PDS, had slower cortical timing than those who spoke completely fluent. This shows us something is wrong in their auditory motor integration. As far as the underlying ailments behind stuttering, It is not well known whether this side effect has to do with "errors in linguistic planning" or issues with "access or retrieval of linguistic elements" and it could very well involve both issues.On occasion, children will go beyond the normal dysfluency patterns. Instances like the previously mentioned example indicate that the child is learning to use language. In contrast, children with stuttering disorder, will likely repeat sounds or one-syllable words three or more times. They may also prolong sounds for two or more seconds. In comparison, stuttering can be seen as a process where a word appears to become "stuck," and the person may grimace, jerk the head or neck as he struggles to overcome the stutter.

Characteristics
Characteristics of developmental dysfluency include:
Repeating phrases (e.g. "he ate-he ate my cookie)
Use of filler words (um, uh, like, ah, etc)
No tension of physical inability and struggle to speak
Lack of problematic behaviors when speaking
No negative reaction or frustration
Appearance of dysfluencies only last less than 6 monthsChildren with normal dysfluency tend to have stuttering difficulties that come and go. Generally this is during preschool years and the problem normally ceases altogether by the time a child starts school. Everyone experiences periods of dysfluency - normal speech patterns include about 2-4% interruptions in flow or fluency. Revisions, word and phrase repetitions and interjections are all common in children speech (see typical dysfluencies below) whereas; sound and syllable repetition, sound prolongation and broken words are much more atypical.

Typical Dysfluency Examples
The term dysfluency is used to describe normal irregularities that occur during speech. As children begin to learn how to communicate with language some will experience issues between the ages of 2-6. These can include:
Phrase revisions or abandoned utterances ("Im want. Can I have...")
Hesitations between words ("Can you give me ... blocks")
Multisyllabic word repetitions ("Gimme, Wanna ... etc)
Phrase repetitions ("I need I need I need ... a hug")
Interjections/Interruptions in sentence structure ("Youre ummm, really funny")Children are learning language and linguistics among many other things. It is speculated that children will experience developmental linguistic delays at some point due to their muscle and motor plans not working as quickly as their brains. While they are learning speech, they are also developmentally mastering other skills (walking, potty training, motor skills, etc.)
The origin of stuttering is not yet fully understood but parents/adults can mitigate the risk of developmental dysfluency by reducing the conversational demands on their child. Modeling slow, smooth speech and acknowledging the demanding and complex nature of learning language can help.

Background
Speech is a complicated achievement that involves a series of cognitive, linguistic, sensorimotor and auditory processes that generate an in-depth understanding of language and speech. As children grow up their language and vocabulary grows with them. However, as this happens it is possible that the child might begin to demonstrate forms of disfluencies in their speech as they struggle to get words out when they are engaged in conversation or speaking in general.
Preschool children usually go through a period of dysfluency as they attempt to learn linguistic and speech skills. About 10% of these children will experience a speech or language delay that is serious enough to benefit from early referral and assessment by a speech language pathologist. Normal disfluency begins during a childs intensive language learning years and resolves on its own as the child undergoes growth and development. This is considered the normal phase of language development.
Most children will outgrow the period of dysfluency but those who do not will require speech therapy.Therefore, it is necessary that there is a distinction between childhood dysfluency, that will likely correct itself and other disorders, such as stuttering. The most common form of dysfluency in children younger than 3 years of age is the repetition of one syllable words or parts of words, especially at the beginning of their sentences as they try to form the sentence correctly ("I-I-I want my toy).
Language learning in some children may be more problematic than that of others. As a child grows, their language and vocabulary will grow with them. Due to the large input they are receiving throughout their development it is inevitable that some forms of dysfluencies will be present in their communication efforts. These occurrences, however, are normal. When attempting to master our complex spoken language, childrens fluency will increase as their proficiency in the language increases. In a similar way to if an adult learns a second language, children may go through the same learning patterns as they learn their first language. Research specifically in computational linguistics has shown that there is a correlation that exists between native language and patterns of dysfluencies that can occur beyond developmental stages. If a child is bilingual, meaning they are learning two languages at once, they are more likely to experience prolonged periods of dysfluency as they try to work out the differences between the two language inputs they have been receiving.

The brain and language development
As a child attempts to develop their language acquisition as one of the most fundamental human traits it is the brain that undergoes the developmental changes. During the phases of language acquisition the brain both stores linguistic information and adapts to the grammatical regularities and irregularities of language. Recent advances in Functional neuroimaging (fMRI) have contributed to the system leave analysis of the brain in relation to linguistic processing.
In order for language to be obtained, there needs to be brain stimulation and memory processes at work in order to form the correct brain pathways. When synapses are stimulated repeatedly that pattern of neural connections is then written into the brain and it becomes a more efficient permanent pathway that allows signals to be quickly transmitted. In terms of language, these pathways need to be created in order to remember and understand the language and communicate with it.
During specific periods in a childs development the brain is active in forming connections for different abilities, one of which being language. Infants start out able to distinguish sound and process different auditory stimuli but after six months they are only able to do so in their native language. As infants hear sounds repeated a different cluster of neurons in the auditory cortex of the brain that responds to sound. During preschool years, the development of syntax and grammar takes place. It is during this period that children begin to exhibit symptoms of developmental dysfluency if they have it. At this point, because they are learning language and other motor activities, their brain take in an overload of information and often will backtrack in language development as they try to pair linguistics to sound and syntax.

Prevalence and prognosis
Preschool children usually go through a period of dysfluency as they attempt to learn linguistic and speech skills. About 10% of these children will experience a speech or language delay that is serious enough for them to benefit from early referral and assessment by a speech language pathologist. Normal dysfluency begins during a childs intensive language years and dissipates as the child continues to grow and develop. These dysfluencies are considered a normal phase of language development.Additionally, 85% of children, before preschool age will experience developmental dysfluency. These children wont require intervention because their dysfluency is a normal part of their development. 1 in 12 children, ages 3–17, will experience issues with their speech that is not considered within the normal realm of developmental dysfluency. However, only half of those individuals will receive intervention and speech therapy.Children who do not require speech therapy will often outgrow the period of dysfluency. Experts find that there is a distinction between childhood dysfluency that will likely correct itself and other disorders such as stuttering.

Dysfluency disorders
The following disorders can be diagnosed following the years in which speech pattern disruptions could be the result of developmental dysfluency that is common within the age range of 2–6 years old. There are types of dysfluencies that are normal developmental processes and others that are more abnormal and atypical.

Stuttering
Stuttering is the most common dysfluency disorder. it is an interruption in the flow of speaking characterized by repetitions, sound prolongations, and blocks that change the rhythm of sleep. A disturbance in the normal fluency and time patterning of speech that is inappropriate for the age of the person. Stuttering typically has its origins in childhood. Most who stutter will begin to do so around 2.5 years of age. Approximately 95% of children who stutter will start to do so before the age of 5.
Stuttering symptoms may include dysfluencies such as hesitations, word fillers, nonword fillers, silent pauses, and interjections. All very similar to developmental dysfluency symptoms. Less typical stuttering will include sound/syllable repetitions, prolongations, and blocks. Stuttering can also occur with other speech and sound disorders, and intellectual language disabilities.
Stuttering can greatly interfere with school, work or social interactions. Children who stutter may also experience fear or anxiety about social settings or public speaking. Speech patterns and behaviors that might signal that a child is potentially going to develop a stuttering disorder can include within-word or part0word repetitions prolonged sounds, avoiding speaking situations, looking frustrated or upset and tense appearance in neck muscles.If stuttering is familial there is likely a genetic mutation that causes the disorder. Unlike the aforementioned typical dysfluencies, stuttering can be a result of genetics. Mutations on the GNPTAB, GNPTG, and NAGPA have been found to disrupt the signal that directs enzymes to target locations in the brain and cause stuttering in vocal and linguistic processes.

Cluttering
Cluttering (Tachyphemia) is a fluency disorder that can co-occur with stuttering but may also occur individually. When someone is experiencing cluttering disorder their conversation segments may be perceived as too fast, too irregular or both. Other symptoms may include stuttering, language or phonological errors, and attention deficits. It may result from disorganized speech planning or being unsure of what to say.
Both cluttering and stuttering are forms of fluency disorders that develop beyond the key years of about ages 2–6. During these ages, dysfluency is mainly just considered to be developmental dysfluency. Cluttering, unlike stuttering, can be distinguished by little to no physical structure, little to no secondary behaviors, decreased awareness of speech problems and the aforementioned typical dysfluencies such as revisions and interjections.
Both stuttering and cluttering both have a genetic component. About 1/3 of those who stutter will also clutter which can prove even more difficult to overcome with Speech therapy. A consequence of cluttering is individuals may not be willing to attempt to repair breakdowns in communication which may result in less effective social integration and interactions that can lead to a sense of isolation, anxiety, and depression.

Differences between disorders and developmental dysfluency
There are several warning signs of speech delays that are not considered developmentally normal.
Babies that dont "coo" or babble
Babies that dont respond to noise or speech around them
Their first words have not been spoken by 15 months
They have a 50-word vocabulary, or less, by two years old
Others struggle to understand what the child is saying at 3 years or older
Other adults should be able to understand at least 75% of what child says.
Struggles to follow simple instructions at 2 years old and beyond
Has speech sound error after five years old
"t", "d" and "n" should be pronounced correctly by age 3Experts recommend an initial evaluation by a pediatrician, who might also recommend an evaluation by a speech-language pathologist.

Indications for referral to a speech language pathologist
Indications include:
Doubt as to the nature of the childs speech changes
Exhibit of reactions of avoidance or escape (pauses, interjections, eye blinks and head nods)
Three or more stuttering dysfluencies (e.g. b-but, a-and, thi-this) per 100 syllables uttered.Children may feel a demand to start speaking at a higher level and can have difficulties with speech that exhibits the following patterns:
Fast-paced speech rate with few pauses
The use of several questions in a sentence
Interruption
Lack of learning time
If their teacher/parent does not listen to themWhen those around a child speak too quickly or input several questions within one sentence, the child must engage several cortices as well as comprehension skills in order to verbally respond to the person they are talking to. If the child lacks learning time as they develop, they will be unable to process harder words and hit a stalling point in sentence comprehension. Normal children may be dysfluent at any time butter likely to increase their dysfluencies when they are tired, excited, upset or being rushed to speak. The dysfluencies may appear in a cycle meaning that they may increase in frequency for several days or weeks and then be hardly noticeable again for weeks or months and could return again following this until the behavior is outgrown.
Usually, children with normal dysfluencies such as these appear to be unaware that they are occurring and show no signs of surprise or frustration. It is evident that the child is not struggling to speak but rather taking more time to complete a thought or sentence.

See also
ADHD
Aphasia
Articulation disorder
Child development
Language disorder
Learning disability

References
Sources
Trubo, Richard (2001). "Stuttering". The New Book Of Knowledge - Health and Medicine: 112–123. United States of America: Grolier Incorporated. ISBN 0-7172-0608-4 </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 Lepidopterism and can you explain it in depth? [/INST] Lepidopterism is an irritant contact dermatitis caused by irritating caterpillar or moth hairs coming into contact with the skin or mucosa. When referring to the cause, moth dermatitis and caterpillar dermatitis are commonly used; Caripito itch (known as papillonite in French) is an older name referring to the moth dermatitis caused by some Hylesia species.

See also
Millipede burn
List of cutaneous conditions

References
Further reading
Hossler EW (2009). "Caterpillars and moths". Dermatol Ther. 22 (4): 353–66. doi:10.1111/j.1529-8019.2009.01247.x. PMID 19580579. S2CID 31799282.
Hossler EW (January 2010). "Caterpillars and moths: Part II. Dermatologic manifestations of encounters with Lepidoptera". J. Am. Acad. Dermatol. 62 (1): 13–28, quiz 29–30. doi:10.1016/j.jaad.2009.08.061. PMID 20082887.
Hossler EW (January 2010). "Caterpillars and moths: Part I. Dermatologic manifestations of encounters with Lepidoptera". J. Am. Acad. Dermatol. 62 (1): 1–10, quiz 11–2. doi:10.1016/j.jaad.2009.08.060. PMID 20082886.
Katzenellenbogen, I. (1955) </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 Mediastinal lymphadenopathy 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 Hypospadias and can you explain it in depth? [/INST] Hypospadias is a common variation in fetal development of the penis in which the urethra does not open from its usual location in the head of the penis. It is the second-most common birth abnormality of the male reproductive system, affecting about one of every 250 males at birth. Roughly 90% of cases are the less serious distal hypospadias, in which the urethral opening (the meatus) is on or near the head of the penis (glans). The remainder have proximal hypospadias, in which the meatus is all the way back on the shaft of the penis, near or within the scrotum. Shiny tissue that should have made the urethra extends from the meatus to the tip of the glans; this tissue is called the urethral plate.
In most cases, the foreskin is less developed and does not wrap completely around the penis, leaving the underside of the glans uncovered. Also, a downward bending of the penis, commonly referred to as chordee, may occur. Chordee is found in 10% of distal hypospadias and 50% of proximal hypospadias cases at the time of surgery. Also, the scrotum may be higher than usual on either side of the penis (called penoscrotal transposition).
The cause of hypospadias is unknown. It most often occurs by itself, without other variations, although in about 10% of cases it may be part of an intersex condition or a medical syndrome with multiple abnormalities.The most common associated difference is an undescended testicle, which has been reported in around 3% of infants with distal hypospadias and 10% with proximal hypospadias. The combination of hypospadias and an undescended testicle sometimes indicates a child has an intersex condition, so additional testing may be recommended to make sure the child does not have congenital adrenal hyperplasia with salt wasting or a similar condition where immediate medical intervention is needed. Otherwise no blood tests or X-rays are routinely needed in newborns with hypospadias.Hypospadias can be a symptom or indication of a difference in sex development or an intersex condition, but some consider that the presence of hypospadias alone is not enough to classify someone as a person with a difference/variation in sex development or as intersex. In most cases, hypospadias is not associated with any other condition. Hypospadias is however itself recognized as an intersex condition by several intersex rights activist groups, who consider the repositioning of a working urethra on a child too young to consent to be a human rights violation.

Presentation
Complications
There is noted to be an increase in erectile problems in people with hypospadias, particularly when associated with a chordee (down curving of the shaft). There is usually minimal interaction with ability to ejaculate in hypospadias providing the meatus remains distal. This can also be affected by the coexistence of posterior urethral valves. There is an increase in difficulties associated with ejaculation however including increased rate of pain on ejaculation and weak/dribbling ejaculation. The rates of these problems are the same regardless of whether or not the hypospadias is surgically corrected.

Diagnosis
A penis with hypospadias usually has a characteristic appearance. Not only is the meatus (urinary opening) lower than usual, but the foreskin is also often only partially developed, lacking the usual amount that would cover the glans on the underside, causing the glans to have a hooded appearance. However, newborns with partial foreskin development do not necessarily have hypospadias, as some have a meatus in the usual place with a hooded foreskin, called "chordee without hypospadias".In other cases, the foreskin (prepuce) is typical and the hypospadias is concealed. This is called "megameatus with intact prepuce". The condition is discovered during newborn circumcision or later in childhood when the foreskin begins to retract. A newborn with typical-appearing foreskin and a straight penis who is discovered to have hypospadias after the start of circumcision can have circumcision completed without concern for jeopardizing hypospadias repair.

Treatment
Where hypospadias is seen as a genital ambiguity in a child, the World Health Organization standard of care is to delay surgery until the child is old enough to participate in informed consent, unless emergency surgery is needed because the child lacks a urinary opening. Hypospadias is not a serious medical condition. A urinary opening that is not surrounded by glans tissue is more likely to "spray" the urine, which can cause a man to sit to urinate because he cannot reliably stand and hit the toilet. Chordee is a separate condition, but where it occurs, the downward curvature of the penis may be enough to make sexual penetration more difficult. For these reasons or others, people with hypospadias may choose to seek urethroplasty, a surgical extension of the urethra using a skin graft.Surgery can extend the urinary channel to the end of the penis, straighten bending, and/or change the foreskin (by either circumcision or by altering its appearance to look more typical ("preputioplasty"), depending on the desire of the patient. Urethroplasty failure rates vary enormously, from around 5% for the simplest repairs to damage in a normal urethra by an experienced surgeon, to 15-20% when a buccal graft from the inside of the mouth can be used to extend a urethra, to close to 50% when graft urethral tubes are constructed from other skin.When the hypospadias is extensive–third degree/penoscrotal–or has associated differences in sex development such as chordee or cryptorchidism, the best management can be a more complicated decision. The world standard (UN and WHO) forbids nonessential surgery to produce a "normal" appearance without the informed consent of the patient, and the American Academy of Pediatrics currently recommends but does not require the same standard. The AAP Textbook of Pediatric Care states "Gender assignment in patients with genital ambiguity should be made only after careful investigation by a multidisciplinary team; increasingly, surgical decisions are delayed until the child is able to participate in the decision-making process." A karyotype and endocrine evaluation should be performed to detect intersex conditions or hormone deficiencies that have major health risks (i.e. salt-wasting). If the penis is small, testosterone or human chorionic gonadotropin (hCG) injections may be given with consent to enlarge it before surgery if this will increase the chance of a successful urethral repair.Surgical repair of severe hypospadias may require multiple procedures and mucosal grafting. Preputial skin is often used for grafting and circumcision should be avoided before repair. In patients with severe hypospadias, surgery often produces unsatisfactory results, such as scarring, curvature, or formation of urethral fistulas, diverticula, or strictures. A fistula is an unwanted opening through the skin along the course of the urethra, and can result in urinary leakage or an abnormal stream. A diverticulum is an "outpocketing" of the lining of the urethra which interferes with urinary flow and may result in posturination leakage. A stricture is a narrowing of the urethra severe enough to obstruct flow. Reduced complication rates even for third-degree repair (e.g., fistula rates below 5%) have been reported in recent years from centers with the most experience. However, typical complications in urethroplasty for severe hypospadias can lead to long surgical cycles of failure and repair, and side effects may include loss of sexual or urinary function. Research suggests failure rates are higher when urethroplasty corrects a born condition rather than disease or injury so patients and families considering surgery for hypospadias should have realistic expectations about the risks and benefits.

Age at surgery
The results of surgery are probably not influenced by the age at which repair is done. Teens and adults typically spend one night in the hospital after surgery.

Preoperative hormones
Hormones potentially increase the size of the penis, and have been used in children with proximal hypospadias who have a smaller penis. Numerous articles report testosterone injections or topical creams increase the length and circumference of the penis. However, few studies discuss the impact of this treatment on the success of corrective surgery, with conflicting results.

Surgery
Hypospadias repair is done under general anesthesia, most often supplemented by a nerve block to the penis or a caudal block to reduce the general anesthesia needed, and to minimize discomfort after surgery.Many techniques have been used during the past 100 years to extend the urinary channel to the desired location. Today, the most common operation, known as the tubularized incised plate or "TIP" repair, rolls the urethral plate from the low meatus to the end of the glans.  TIP repair, also called the Snodgrass Repair (after the creator of the method, Dr. Warren Snodgrass), is the most widely used procedure and surgical method for hypospadias repair worldwide. This procedure can be used for all distal hypospadias repairs, with complications afterwards expected in less than 10% of cases.Less consensus exists regarding proximal hypospadias repair. TIP repair can be used when the penis is straight or has mild downward curvature, with success in 85%. Alternatively, the urinary channel can be reconstructed using the foreskin, with reported success in from 55% to 75%.Most distal and many proximal hypospadias are corrected in a single operation. However, those with the most severe condition having a urinary opening in the scrotum and downward bending of the penis are often corrected in a two-stage operation. During the first operation the curvature is straightened. At the second, the urinary channel is completed. Any complications may require additional interventions for repair.

Outcomes
Problems that can arise include a small hole in the urinary channel below the meatus, called a fistula. The head of the penis, which is open at birth in children with hypospadias and is closed around the urinary channel at surgery, sometimes reopens, known as glans dehiscence. The new urinary opening can scar, resulting in meatal stenosis, or internal scarring can create a stricture, either of which cause partial blockage to urinating. If the new urinary channel balloons when urinating a child is diagnosed with a diverticulum.Most complications are discovered within six months after surgery, although they occasionally are not found for many years </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 Vasa praevia and can you explain it in depth? [/INST] Vasa praevia is a condition in which fetal blood vessels cross or run near the internal opening of the uterus. These vessels are at risk of rupture when the supporting membranes rupture, as they are unsupported by the umbilical cord or placental tissue.
Risk factors include low-lying placenta, in vitro fertilization.Vasa praevia occurs in about 0.6 per 1000 pregnancies. The term "vasa previa" is derived from the Latin; "vasa" means vessels and "previa" comes from "pre" meaning "before" and "via" meaning "way". In other words, vessels lie before the fetus in the birth canal and in the way.

Cause
Vasa previa is present when unprotected fetal vessels traverse the fetal membranes over the internal cervical os. These vessels may be from either a velamentous insertion of the umbilical cord or may be joining an accessory (succenturiate) placental lobe to the main disk of the placenta. If these fetal vessels rupture the bleeding is from the fetoplacental circulation, and fetal exsanguination will rapidly occur, leading to fetal death. It is thought that vasa previa arises from an early placenta previa. As the pregnancy progresses, the placenta tissue surrounding the vessels over the cervix undergoes atrophy, and the placenta grows preferentially toward the upper portion of the uterus. This leaves unprotected vessels running over the cervix and in the lower uterine segment. This has been demonstrated using serial ultrasound. Oyelese et al. found that 2/3 of patient with vasa previa at delivery had a low-lying placenta or placenta previa that resolved prior to the time of delivery.
There are three types of vasa previa. Types 1 and 2 were described by Catanzarite et al. In Type 1, there is a velamentous insertion with vessels running over the cervix. In Type 2, unprotected vessels run between lobes of a bilobed or succenturiate lobed placenta. In Type 3, a portion of the placenta overlying the cervix undergoes atrophy. In this type, there is a normal placental cord insertion and the placenta has only one lobe. However, vessels at a margin of the placenta are exposed.

Risk factors
Vasa previa is seen more commonly with velamentous insertion of the umbilical cord, accessory placental lobes (succenturiate or bilobate placenta), multiple gestation, and in vitro fertilisation pregnancy. In IVF pregnancies, incidence as high as one in 300 has been reported. The reasons for this association are not clear, but disturbed orientation of the blastocyst at implantation, vanishing embryos and the increased frequency of placental morphological variations in IVF pregnancies have all been postulated.

Diagnosis
The classic triad of the vasa praevia is: membrane rupture, painless vaginal bleeding and fetal bradycardia or fetal death.
Prior to the advent of ultrasound, this diagnosis was most often made after a stillbirth or neonatal death in which the mother had ruptured her membranes, had some bleeding, and delivered an exsanguinated baby. In these cases, examination of the placenta and membranes after delivery would show evidence of a velamentous cord insertion with rupture of the vessels. However, with almost universal use of ultrasound in the developed world, many cases are now detected during pregnancy, giving the opportunity to deliver the baby before this catastrophic rupture of the membranes occurs.  Vasa previa is diagnosed with ultrasound when echolucent linear or tubular structures are found overlying the cervix or in close proximity to it. Transvaginal ultrasound is the preferred modality </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 Tyzzers disease and can you explain it in depth? [/INST] Tyzzers disease is an acute epizootic bacterial disease found in rodents, rabbits, dogs, cats, birds, pandas, deer, foals, cattle, and other mammals including gerbils  and spinifex hopping-mice (Notomys alexis) . It is caused by the spore-forming bacterium Clostridium piliforme, formerly known as Bacillus piliformis. It is an infectious disease characterized by necrotic lesions on the liver, is usually fatal, and is present worldwide. Animals with the disease become infected through oral ingestion of the bacterial spores and usually die within a matter of days. Animals most commonly affected include young, stressed animals in laboratory environments, such as immature rodents and rabbits. Most commonly affected wild animals include muskrats (Ondatra zibethicus) and occasionally cottontail rabbits (Sylvilagus spp.). Even today, much remains unknown about Tyzzers disease, including how and why it occurs.

Distribution
Although Tyzzers disease is commonly found in laboratory animals worldwide, infected wild animal populations have been identified in North America and Australia. Specific locations where the disease has been reported in the United States include Connecticut, Idaho, Iowa, Maryland, Michigan, Montana, Ohio, Wisconsin, and Wyoming. In Canada, it has been reported in British Columbia, Manitoba, Ontario, and Saskatchewan. Outbreaks in these locations are primarily attributed to muskrat populations; however infected cottontail rabbits  have been discovered in Maryland.

Transmission
Tyzzers disease is transmitted horizontally through the fecal-oral route. Bacterial spores within infected fecal matter can contaminate soil or feed and become orally ingested by a viable host. Success of the disease is determined by the amount and virulence of the bacteria and the resistance of the host. Laboratory animals are more susceptible to this disease, as bacteria spores from infected feces can survive in bedding at room temperature for over one year. Animals do occasionally transfer the disease asymptomatically, acting as carriers. Infected animals are more likely to develop the disease when subjected to stressful conditions.

Clinical Signs
Common clinical signs of Tyzzers Disease include watery diarrhea, depression, emaciation, and a ruffled coat. Other observed clinical signs include melena, depression, lethargy, and decreased temperature. In muskrats, this disease is characterized by extensive hemorrhaging within the lower intestine and abdomen.  Due to the fast-acting nature of this disease, infected individuals often do not live long enough to exhibit symptoms. It is not uncommon for an infected animal to die within 1–10 days of disease contraction.During necropsy, inflammation of the ileum, cecum, and colon are commonly present.  Perhaps the most distinctive trait of this disease, however, is the grayish yellow necrotic lesions found on the liver of diseased animals. The number of these spots present can range from one to countless. Occasionally, lesions are discovered in the lower intestinal tract and heart as well.  Even with physical signs and symptoms present, a conclusive diagnosis is dependent upon the presence of C. piliforme within the liver of the infected animal.

Prevention
In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

Treatment and Control
Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.

History
Tyzzers disease was first discovered by parasitologist Ernest Tyzzer in 1917 when his entire colony of Japanese waltzing mice suddenly died. Upon closer observation, Tyzzer discovered necrotic lesions and spore-forming bacillus in the livers of the deceased mice </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 Optic neuritis and can you explain it in depth? [/INST] Optic neuritis describes any condition that causes inflammation of the optic nerve; it may be associated with demyelinating diseases, or infectious or inflammatory processes.It is also known as optic papillitis (when the head of the optic nerve is involved), neuroretinitis (when there is a combined involvement of optic disc and surrounding retina in the macular area) and retrobulbar neuritis (when the posterior part of the nerve is involved). Prelaminar optic neuritis describes involvement of the non-myelinated axons in the retina. It is most often associated with multiple sclerosis, and it may lead to complete or partial loss of vision in one or both eyes. Other causes include:
Hereditary optic neuritis (Lebers disease)
Parainfectious optic neuritis (associated with viral infections such as measles, mumps, chickenpox, whooping cough and glandular fever)
Infectious optic neuritis (sinus related or associated with cat scratch fever, tuberculosis, lyme disease and cryptococcal meningitis in AIDS patients
Autoimmune causes (sarcoidosis, systemic lupus erythematosus, PAN, MOG Antibody disease, granulomatosis with polyangiitis)
Diabetes Mellitus
Low phosphorus levels
HyperkalaemiaPartial, transient vision loss (lasting less than one hour) can be an indication of early onset multiple sclerosis.

Signs and symptoms
Major symptoms are sudden loss of vision (partial or complete), sudden blurred or "foggy" vision, and pain on movement of the affected eye. Early symptoms that require investigation include symptoms from multiple sclerosis (twitching, lack of coordination, slurred speech, frequent episodes of partial vision loss or blurred vision), episodes of "disturbed/blackened" rather than blurry indicate moderate stage and require immediate medical attention to prevent further loss of vision. Other early symptoms are reduced night vision, photophobia and red eyes. Many patients with optic neuritis may lose some of their color vision in the affected eye (especially red), with colors appearing subtly washed out compared to the other eye. Patients may also experience difficulties judging movement in depth which can be particular troublesome during driving or sport (Pulfrich effect). Likewise transient worsening of vision with increase of body temperature (Uhthoffs phenomenon) and glare disability are a frequent complaint. However, several case studies in children have demonstrated the absence of pain in more than half of cases (approximately 60%) in their pediatric study population, with the most common symptom reported simply as "blurriness." Other remarkable differences between the presentation of adult optic neuritis as compared to pediatric cases include more often unilateral optic neuritis in adults, while children much predominantly present with bilateral involvement.
On medical examination the head of the optic nerve can easily be visualized by a slit lamp with a high positive lens or by using direct ophthalmoscopy; however, frequently there is no abnormal appearance of the nerve head in optic neuritis (in cases of retrobulbar optic neuritis), though it may be swollen in some patients (anterior papillitis or more extensive optic neuritis). In many cases, only one eye is affected and patients may not be aware of the loss of color vision until they are asked to close or cover the healthy eye.

Cause
The optic nerve comprises axons that emerge from the retina of the eye and carry visual information to the primary visual nuclei, most of which is relayed to the occipital cortex of the brain to be processed into vision. Inflammation of the optic nerve causes loss of vision, usually because of the swelling and destruction of the myelin sheath covering the optic nerve.
The most common cause is multiple sclerosis or ischemic optic neuropathy due to thrombosis or embolism of the vessel that supplies the optic nerve. Up to 50% of patients with MS will develop an episode of optic neuritis, and 20-30% of the time optic neuritis is the presenting sign of MS. The presence of demyelinating white matter lesions on brain MRI at the time of presentation of optic neuritis is the strongest predictor for developing clinically definite MS. Almost half of the patients with optic neuritis have white matter lesions consistent with multiple sclerosis.
Some other common causes of optic neuritis include infection (e.g. a tooth abscess in the upper jaw, syphilis, Lyme disease, herpes zoster), autoimmune disorders (e.g. lupus, neurosarcoidosis, neuromyelitis optica), methanol poisoning, Vitamin B12 deficiency, beriberi, dysautonomia (i.e. autonomic nervous system dysfunction), and diabetes, or an injury to the eye. In neuromyelitis optica higher AQP4 autoantibody levels are associated with the occurrence of optic neuritis.Less common causes are: papilledema, brain tumor or abscess in the occipital region, cerebral trauma or hemorrhage, meningitis, arachnoidal adhesions, sinus thrombosis, liver dysfunction, or late stage kidney disease.

Demyelinating recurrent optic neuritis and non-demyelinating (CRION)
The repetition of an idiopathic optic neuritis is considered a distinct clinical condition, and when it shows demyelination, it has been found to be associated to anti-MOG and AQP4-negative neuromyelitis opticaWhen an inflammatory recurrent optic neuritis is not demyelinating, it is called "Chronic relapsing inflammatory optic neuropathy" (CRION)When it is anti-MOG related, it is demyelinating and it is considered inside the anti-MOG associated inflammatory demyelinating diseases.
Some reports point to the possibility to establish a difference via OCT

Treatment
In most MS-associated optic neuritis, visual function spontaneously improves over 2–3 months, and there is evidence that corticosteroid treatment does not affect the long term outcome. However, for optic neuritis that is not MS-associated (or atypical optic neuritis) the evidence is less clear and therefore the threshold for treatment with intravenous corticosteroids is lower </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 Oculocerebrorenal syndrome and can you explain it in depth? [/INST] Oculocerebrorenal syndrome (also called Lowe syndrome) is a rare X-linked recessive disorder characterized by congenital cataracts, hypotonia, intellectual disability, proximal tubular acidosis, aminoaciduria and low-molecular-weight proteinuria. Lowe syndrome can be considered a cause of Fanconi syndrome (bicarbonaturia, renal tubular acidosis, potassium loss and sodium loss).

Signs and symptoms
Boys with Lowe syndrome are born with cataracts in both eyes; glaucoma is present in about half of the individuals with Lowe syndrome, though usually not at birth. While not present at birth, kidney problems develop in many affected boys at about one year of age. Renal pathology is characterized by an abnormal loss of certain substances into the urine, including bicarbonate, sodium, potassium, amino acids, organic acids, albumin, calcium and L-carnitine. This problem is known as Fanconi-type renal tubular dysfunction.

Genetics
This syndrome is caused by mutations in the OCRL gene which encodes an inositol polyphosphate-5-phosphatase. At least one mechanism by which these mutations cause this syndrome is by loss of its Rab-binding domain.This protein is associated with the primary cilia of the retinal pigment epithelial cells, fibroblasts and kidney tubular cells </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 Glycogen storage disease 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 Cryptotia 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 Cerebrospinal fluid rhinorrhoea and can you explain it in depth? [/INST] Cerebrospinal fluid rhinorrhoea (CSF rhinorrhoea) refers to the drainage of cerebrospinal fluid through the nose (rhinorrhoea). It is typically caused by a basilar skull fracture, which presents complications such as infection. It may be diagnosed using brain scans (prompted based on initial symptoms), and by testing to see if discharge from the nose is cerebrospinal fluid </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 Osteopathia striata with cranial sclerosis 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 Schizotypal personality disorder and can you explain it in depth? [/INST] Schizotypal personality disorder (STPD or SPD), also known as schizotypal disorder, is a mental and behavioural disorder. DSM classification describes the disorder specifically as a personality disorder characterized by thought disorder, paranoia, a characteristic form of social anxiety, derealization, transient psychosis, and unconventional beliefs. People with this disorder feel pronounced discomfort in forming and maintaining social connections with other people, primarily due to the belief that other people harbour negative thoughts and views about them. Peculiar speech mannerisms and socially unexpected modes of dress are also characteristic. Schizotypal people may react oddly in conversations, not respond, or talk to themselves. They frequently interpret situations as being strange or having unusual meaning for them; paranormal and superstitious beliefs are common. Schizotypal people usually disagree with the suggestion their thoughts and behaviour are a disorder, and seek medical attention for depression or anxiety instead. Schizotypal personality disorder occurs in approximately 3% of the general population and is more commonly diagnosed in males.The term "schizotype" was first coined by Sandor Rado in 1956 as an abbreviation of "schizophrenic phenotype". STPD is classified as a cluster A personality disorder, also known as the "odd or eccentric" cluster.

Causes
Genetic
Schizotypal personality disorder is widely understood to be a "schizophrenia spectrum" disorder. Rates of schizotypal personality disorder are much higher in relatives of individuals with schizophrenia than in the relatives of people with other mental illnesses or in people without mental illness. Technically speaking, schizotypal personality disorder may also be considered an "extended phenotype" that helps geneticists track the familial or genetic transmission of the genes that are implicated in schizophrenia pathogenesis. But there is also a genetic connection of STPD to mood disorders and depression in particular. Prediction of schizophrenia based on schizotypal traits has a higher accuracy for individuals with high genetic risk for STPD.

Social and environmental
Unique environmental factors, which differ from shared sibling experiences, have been found to play a role in the development of STPD and its dimensions. There is now evidence to suggest that parenting styles, early separation, trauma/maltreatment history (especially early childhood neglect) can lead to the development of schizotypal traits. Neglect or abuse, trauma, or family dysfunction during childhood may increase the risk of developing schizotypal personality disorder. There is also evidence indicating insults in the prenatal environment could have an effect on development of STPD. Over time, children learn to interpret social cues and respond appropriately but for unknown reasons this process does not work well for people with this disorder.Schizotypal personality disorders are characterized by a common attentional impairment in various degrees that could serve as a marker of biological susceptibility to STPD. The reason is that an individual who has difficulties taking in information may find it difficult in complicated social situations where interpersonal cues and attentive communications are essential for quality interaction. This might eventually cause the individual to withdraw from most social interactions, thus leading to asociality.

Diagnosis
Screening
There are various methods of screening for schizotypal personality. The Schizotypal Personality Questionnaire (SPQ) measures nine traits of STPD using a  self-report assessment. The nine traits referenced are Ideas of Reference, Excessive Social Anxiety, Odd Beliefs or Magical Thinking, Unusual Perceptual Experiences, Odd or Eccentric Behavior, No Close Friends, Odd Speech, Constricted Affect, and Suspiciousness. A study found that of the participants who scored in the top 10th percentile of all the SPQ scores, 55% were clinically diagnosed with STPD. A method that measures the risk for developing psychosis through self-reports is the Wisconsin Schizotypy Scale (WSS). The WSS divides schizotypal personality traits into 4 scales for Perceptual Aberration, Magical Ideation, Revised Social Anhedonia, and Physical Anhedonia. A comparison of the SPQ and the WSS suggests that these measures should be cautiously used for screening purposes of STPD.

STPD as a Personality Disorder
DSM-5
In the American Psychiatric Associations DSM-5, schizotypal personality disorder is defined as a "pervasive pattern of social and interpersonal deficits marked by acute discomfort with, and reduced capacity for, close relationships as well as by cognitive or perceptual distortions and eccentricities of behavior, beginning by early adulthood and present in a variety of contexts."At least five of the following symptoms must be present:

ideas of reference
strange beliefs or magical thinking that influences behavior and is inconsistent with subcultural norms (e.g., superstitiousness, belief in clairvoyance, telepathy, or “sixth sense”, bizarre fantasies or preoccupations)
abnormal perceptual experiences, including bodily illusions
strange thinking and speech (e.g., vague, circumstantial, metaphorical, overelaborate, or stereotyped)
suspiciousness or paranoid ideation
inappropriate or constricted affect
strange behavior or appearance
lack of close friends
excessive social anxiety that does not diminish with familiarity and tends to be associated with paranoid fears rather than negative judgments about selfThese symptoms must not occur only during the course of a disorder with similar symptoms (such as schizophrenia or autism spectrum disorder).

STPD as a Clinical Disorder
ICD-10
The World Health Organizations ICD-10 uses the name schizotypal disorder (F21). It is classified as a clinical disorder associated with schizophrenia, rather than a personality disorder as in DSM-5.The ICD definition is:

A disorder characterized by eccentric behavior and anomalies of thinking and affect which resemble those seen in schizophrenia, though no definite and characteristic schizophrenic anomalies have occurred at any stage. There is no dominant or typical disturbance, but any of the following may be present:
Inappropriate or constricted affect (the individual appears cold and aloof);
Behavior or appearance that is odd, eccentric or peculiar;
Poor rapport with others and a tendency to withdraw socially;
Odd beliefs or magical thinking, influencing behavior and inconsistent with subcultural norms;
Suspiciousness or paranoid ideas;
Obsessive ruminations without inner resistance;
Unusual perceptual experiences including somatosensory (bodily) or other illusions, depersonalization or derealization;
Vague, circumstantial, metaphorical, over-elaborate or stereotyped thinking, manifested by odd speech or in other ways, without gross incoherence;
Occasional transient quasi-psychotic episodes with intense illusions, auditory or other hallucinations and delusion-like ideas, usually occurring without external provocation.
The disorder runs a chronic course with fluctuations of intensity. Occasionally it evolves into overt schizophrenia. There is no definite onset and its evolution and course are usually those of a personality disorder. It is more common in individuals related to people with schizophrenia and is believed to be part of the genetic "spectrum" of schizophrenia.

Diagnostic guidelines
This diagnostic rubric is not recommended for general use because it is not clearly demarcated either from simple schizophrenia or from schizoid or paranoid personality disorders, or possibly autism spectrum disorders as currently diagnosed. If the term is used, three or four of the typical features listed above should have been present, continuously or episodically, for at least two years. The individual must never have met criteria for schizophrenia itself. A history of schizophrenia in a first-degree relative gives additional weight to the diagnosis but is not a prerequisite.

Subtypes
Theodore Millon proposes two subtypes of schizotypal personality. Any individual with schizotypal personality disorder may exhibit either one of the following somewhat different subtypes (Note that Millon believes it is rare for a personality with one pure variant, but rather a mixture of one major variant with one or more secondary variants):

Treatment
Medication
STPD is rarely seen as the primary reason for treatment in a clinical setting, but it often occurs as a comorbid finding with other mental disorders. When patients with STPD are prescribed pharmaceuticals, they are usually prescribed neuroleptics of the sort used to treat schizophrenia; however, the use of neuroleptic drugs in the schizotypal population is in great doubt. While people with schizotypal personality disorder and other attenuated psychotic-spectrum disorders may have a good outcome with neuroleptics in the short term, long-term followup suggests significant impairment in daily functioning compared to schizotypal and even schizophrenic people without neuroleptic drug exposure. Antidepressants are also sometimes prescribed, whether for STPD proper or for comorbid anxiety and depression.

Therapy
According to Theodore Millon, schizotypal personality disorder is one of the easiest personality disorders to identify but one of the most difficult to treat with psychotherapy. Persons with STPD usually consider themselves to be simply eccentric or nonconformist; the degree to which they consider their social nonconformity a problem differs from the degree to which it is considered a problem in psychiatry. It is difficult to gain rapport with people with STPD due to the fact that increasing familiarity and intimacy usually increase their level of anxiety and discomfort.Group therapy is recommended for persons with STPD only if the group is well structured and supportive. Otherwise, it could lead to loose and tangential ideation. Support is especially important for schizotypal patients with predominant paranoid symptoms, because they will have a lot of difficulties even in highly structured groups.

Comorbidity
Schizotypal personality disorder frequently co-occurs with major depressive disorder, dysthymia and social phobia. Furthermore, sometimes schizotypal personality disorder can co-occur with obsessive–compulsive disorder, and its presence appears to affect treatment outcome adversely. Some people with a clinical diagnosis of OCD have been found to also possess many schizotypal personality traits resulting in what can be called ‘schizotypal OCD’. Without proper treatment, STPD tendencies, such as magical thinking and paranoid ideation, could worsen the symptoms of OCD in an individual. There may also be an association with bipolar disorder </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 Bronchopneumonia 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 Nephritic syndrome and can you explain it in depth? [/INST] Nephritic syndrome  is a syndrome comprising signs of nephritis, which is kidney disease involving inflammation. It often occurs in the glomerulus, where it is called glomerulonephritis. Glomerulonephritis is characterized by inflammation and thinning of the glomerular basement membrane and the occurrence of small pores in the podocytes of the glomerulus. These pores become large enough to permit both proteins and red blood cells to pass into the urine (yielding proteinuria and hematuria, respectively). By contrast, nephrotic syndrome is characterized by proteinuria and a constellation of other symptoms that specifically do not include hematuria. Nephritic syndrome, like nephrotic syndrome, may involve low level of albumin in the blood due to the protein albumin moving from the blood to the urine.

Signs and symptoms
Historically, nephritic syndrome has been characterized by blood in the urine (hematuria), high blood pressure (hypertension), decreased urine output <400 ml/day (oliguria), red blood cell casts, pyuria, and mild to moderate proteinuria. If the condition is allowed to progress without treatment, it can eventually lead to azotemia and uremic symptoms. This constellation of symptoms contrasts with the classical presentation of nephrotic syndrome (excessive proteinuria >3.5 g/day, low plasma albumin levels (hypoalbuminemia) <3 g/L, generalized edema, and hyperlipidemia).Signs and symptoms that are consistent with nephritic syndrome include:

Hematuria (red blood cells in the urine)
Proteinuria (protein in the urine) ranging from sub-nephrotic (<3.5 g/day) to >10 g/day, although it is rarely above nephrotic range proteinuria levels.
Hypertension resting blood pressure is persistently at or above 130/80 or 140/90 mmHg.
Blurred vision
Azotemia (increased plasma Urea and Creatinine)
Oliguria (low urine output <400 ml/day)
Red blood cell casts (seen with urinalysis and microscopy)
Pyuria (white blood cells or pus in the urine)

Causes
Nephritic syndrome is caused by extensive inflammatory damage to the glomerulus capillaries, which is associated with a variety of medical conditions that we will discuss. Furthermore, the cause of this inflammation can be infectious, autoimmune, or thrombotic. The causative conditions can be divided conveniently between age groups as follows, though it is important to note that many of the conditions listed in children/adolescents can also occur in adults with lower frequency, and vice versa:

Children/adolescents
IgA nephropathy (Note: Contrast time of onset with Post-streptococcal Glomerulonephritis) - Most commonly diagnosed in children who recently had an upper respiratory tract infection (URI). Symptoms typically present within 1–2 days of a non-specific URI with severe flank/abdominal pain, gross hematuria (characterized by dark brown or red colored urine), and edema of the hands, feet, and/or face.
Post-streptococcal glomerulonephritis (PSGN) - Similar to IgA nephropathy, post-streptococcal glomerulonephritis (PSGN) most often occurs in children who have recently had an upper respiratory infection (URI). In contrast with IgA nephropathy, however, PSGN typically presents 2–3 weeks after recovering from an URI that was caused specifically by a Streptococcus bacteria. The symptoms at onset are very similar to IgA nephropathy and include abdominal pain, hematuria, edema, and oliguria.
Henoch–Schönlein purpura (HSP) - Often considered a systemic form of IgA nephropathy, Henoch–Schönlein purpura (HSP) is a systemic small-vessel vasculitis that is characterized by deposition of IgA antibody immune complexes in different key areas throughout the body. Most often, the condition presents in children with palpable purpura, abdominal pain, and arthritis. When the kidneys are affected, the IgA immune complexes deposit in the glomerulus very similarly to IgA nephropathy and will present in a similar way.
Hemolytic uremic syndrome - Most cases occur immediately following infectious diarrhea caused by a specific type of E. coli (O157:H7). The bacteria produces a toxin that causes widespread inflammation and numerous blood clots in small blood vessels (thrombotic microangiopathy). When the inflammation reaches the kidney, or the by-products of systemic inflammation build up in the kidney, the patient will begin showing signs of nephritic syndrome or potentially acute kidney failure (elevated creatinine, BUN, etc.).

Adults
Goodpasture syndrome - This is a rare autoimmune disease where autoantibodies are produced that target the glomerular basement membrane in both the lungs and the kidneys. The damage to the basement membrane causes bleeding, and the disease often presents in patients as hematuria and haemoptysis (coughing up blood). If not treated promptly with plasmapharesis to remove the autoantibodies, it can lead to permanent damage in the lungs/kidneys.
Systemic Lupus Erythematosus (SLE) - Better known as simply "Lupus", this autoimmune disease can affect nearly every major system in the human body and the kidneys are no exception. Autoantibodies produced in SLE can form immune complexes that deposit along the glomerular basement membrane and cause glomerular inflammation which leads to a nephritic syndrome.
Rapidly progressive glomerulonephritis - This is a syndrome of the kidney that is characterized by rapid loss of kidney function (usually >50% decline in glomerular filtration rate (GFR) within 3 months) with glomerular crescent formation frequently seen on kidney biopsy. Without treatment, it will quickly lead to kidney failure and potentially death within months. This syndrome has numerous underlying causes that can also cause nephritic syndrome, so this may be more of an association than a cause.
Infective endocarditis - Infection that affects the inner lining of the heart (endocardium) and can potentially cause a thrombus to form on one or more heart valves and, if left untreated, can cause septic emboli that can have many systemic effects, including deposition into the glomerulus, causing glomerulonephritis and nephritic syndrome.
Cryoglobulinemia - Antibodies that are sensitive to the cold can become activated in cold conditions and cause an increase in blood viscosity (hyperviscosity syndrome) as well as forming immune complexes that can deposit in the small blood vessels and can cause nephritic syndrome when this occurs in the kidneys.
Membranoproliferative glomerulonephritis (MPGN) - Another type of glomerulonephritis that is caused primarily by immune complex deposition in the glomerular mesangium and glomerular basement membrane thickening, which activates the complement cascade and damages the glomerulus. This damage leads to inflammation in the glomerulus and can present with a nephritic syndrome.
Other ANCA small-vessel vasculitides - The conditions included in this category are eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis, and granulomatosis with polyangiitis.

Pathophysiology
The pathophysiology of nephritic syndrome is dependent on the underlying disease process, which can vary depending on what condition the nephritic syndrome is secondary to. More specifically, different diseases (many of which are mentioned above in the Causes section) affect different segments of the glomerulus and cause disease-specific segments of the glomerulus to become inflamed. Most often, it is dependent on what part of the glomerulus is damaged by antibody-antigen complex (immune complex) deposition. In all cases, however, the inflammatory processes in the glomerulus cause the capillaries to swell and the pores between podocytes become large enough that inappropriate contents in the blood plasma (i.e. red blood cells, protein, etc.) will begin to spill into the urine. This causes a decrease in glomerular filtration rate (GFR) and, if left untreated over time, will eventually produce uremic symptoms and retention of sodium and water in the body, leading to both edema and hypertension.

Diagnosis
The diagnostic approach to nephritic syndrome includes evaluating the patient for any suspected underlying pathology that could cause a nephritic syndrome.

Physical examination
If the person in the office is being examined by a physician, some physical exam findings consistent with nephritic syndrome include the following:

Edema - This could present as generalized edema (anasarca) or specific swelling of the hands, feet, and/or face.
Other signs of fluid overload - Diffuse rales (crackles) may be heard at bilateral lung bases or diffusely in all lung fields on auscultation with a stethoscope. Jugular venous distention (JVD) may also be appreciated when visualizing the veins of the neck on physical exam.
Elevated blood pressure - Measured at least two separate times with at least two minutes between measurements using a sphygmomanometer or equivalent method.
Abnormal heart sounds - If the underlying cause is cardiac in nature (such as infective endocarditis), then you may appreciate abnormal heart sounds during auscultation of the heart.

Laboratory testing
If the physician is suspicious of a possible nephritic syndrome, then he/she may order some common lab tests including:

Serum electrolytes - The kidney is one of the main regulators of electrolytes in the human body and measuring the different electrolyte levels using either a basic metabolic panel (BMP) or comprehensive metabolic panel (CMP) can be a useful indicator of the underlying pathology.
Serum creatinine - Also measured using a BMP or CMP, creatinine is one of the most important indicators of current kidney function and is used to calculate the glomerular filtration rate (GFR). An elevated creatinine level is considered abnormal and may indicate decreased kidney function.
Blood urea nitrogen (BUN) - Also measured using a BMP or CMP, blood urea nitrogen is an indicator of how much nitrogen is in the blood at the time of the phlebotomy. The kidney is responsible for excreting nitrogenous substances in the urine, so an elevated BUN usually indicates that the kidney is not functioning appropriately.
Urine Analysis (Urinalysis) - After the patient provides a urine specimen, it is sent to the lab for analysis using a variety of methods including urine dipstick testing and microscopic examination. Because the kidney is responsible for making urine, analyzing the urine directly can provide crucial data that can help the physician diagnose nephritic syndrome. Some findings on urinalysis that are consistent with nephritic syndrome include red blood cells (hematuria), red blood cell casts, proteinuria, and possibly white blood cells (pyuria).If nephritic syndrome is identified and diagnosed, then it is important for the physician to determine the underlying cause. To do this, he/she may order any of a large variety of relevant lab tests, some of which are included here:

Blood culture - This is the process where a sample of the patients blood is sent to the microbiology lab to attempt to isolate and grow any bacteria that may be circulating in the blood, in order to identify the pathogen. This is helpful if the physician suspects infection as the underlying cause of the nephritic syndrome.
Antinuclear antibody (ANA) titer - ANA is commonly positive in patients who have an underlying autoimmune disease, so this test is useful if the physician suspects an underlying autoimmune disease (refer to the Causes section above for examples) as the cause of the presenting nephritic syndrome. If positive, then the physician may order additional tests to determine which autoimmune condition is the cause and how best to treat it.
Antiglomerular basement membrane (anti-GBM) antibody - If positive, this is highly indicative of Goodpastures syndrome and can be used to guide treatment.
Antineutrophil cytoplasmic antibody (ANCA) - If positive, this indicates that there is likely an underlying vasculitis that may be causing the acute nephritic syndrome.
Serum complement (C3 and C4) - Complement factors bind to antibodies to form immune complexes and a decreased serum complement level could indicate that the complement is being consumed at a higher rate due to the formation of immune complexes leading to deposition in the glomerulus of the kidney.

Invasive testing
A kidney biopsy will provide a fully definitive diagnosis of nephritic syndrome and may also reveal the underlying cause of the nephritic syndrome depending on the underlying pathological process. On biopsy, a patient with nephritic syndrome would show inflammation of numerous glomeruli.

Treatment
When a patient is confirmed to have nephritic syndrome, the main goal of treatment (regardless of the underlying cause) is to control elevated blood pressures and reduce active inflammation in the kidney itself. Most often, the patient will need to be admitted to the hospital for close monitoring to ensure the efficacy of treatment and make adjustments as needed. Some treatment modalities commonly used to meet these goals include:

Bed rest during the recovery process to ensure administration of optimal medical therapy with as low of a risk as possible for any exacerbating factors (falls, infection, etc.).
Fluid restriction to minimize the risk of edema (if not already present) or to reduce any active edema that may be present.
A special diet during the hospital stay that restricts sodium, potassium, and fluids in conjunction with the previously mentioned fluid restriction in an attempt to control symptoms of fluid overload.
Administration of diuretics if patient is showing signs of fluid overload. This will cause excess fluids to be excreted in the urine and may lessen the workload placed on the kidney, allowing it to recover from the inflammatory damage.
Administration of antihypertensives to alleviate hypertension and maintain a normal blood pressure during the recovery process.
Administration of anti-inflammatory medications (such as steroids or NSAIDs) to reduce active inflammation in the kidney.
If the patient is showing signs of kidney failure or end-organ damage, the treatment team may opt to utilize kidney dialysis temporarily (or permanently, in some severe cases) to decrease stress on the kidneys and allow for optimal recovery.Once the acute phase of the nephritic syndrome is controlled, it is crucial to determine the underlying pathology that caused the onset of the acute nephritic syndrome and to treat that condition. If the underlying cause is not determined and treated appropriately, it increases the risk of a recurrence of nephritic syndrome or chronic kidney disease (CKD) in the future.

Prognosis
Because nephritic syndrome is a syndrome and not a disease, the prognosis depends on the underlying cause. Generally, the prognosis of nephritic syndrome in children is better than it is in adults.

Epidemiology
According to the CDC, nephritis/nephrosis/nephritic syndrome was the 9th leading cause of death in the United States in 2017. It was listed as the cause of death for 50,633 out of the total 2,813,503 deaths reported in 2017.

Geography
The southeast region of the United States reported a significantly higher death rate due to kidney disease than any other region in 2017 </s>


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<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 Cross syndrome 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 Mineral deficiency 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 Congenital cataract and can you explain it in depth? [/INST] Congenital cataracts refers to a lens opacity which is present at birth. Congenital cataracts cover a broad spectrum of severity: whereas some lens opacities do not progress and are visually insignificant, others can produce profound visual impairment.
Congenital cataracts may be unilateral or bilateral. They can be classified by morphology, presumed or defined genetic cause, presence of specific metabolic disorders, or associated ocular anomalies or systemic findings.

Signs and symptoms
Congenital cataracts occur in a variety of morphologic configurations, including lamellar, polar, sutural, coronary, cerulean, nuclear, capsular, complete, membranous.

Cause
In general, approximately one-third of congenital cataracts are a component of a more extensive syndrome or disease (e.g., cataract resulting from congenital rubella syndrome), one-third occur as an isolated inherited trait, and one-third result from undetermined causes. Metabolic diseases tend to be more commonly associated with bilateral cataracts.

Genetics
Approximately 50% of all congenital cataract cases may have a genetic cause which is quite heterogeneous </s>