<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 Granulomatous meningoencephalitis and can you explain it in depth? [/INST] Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) of dogs and, rarely, cats. It is a form of meningoencephalitis.  GME is likely second only to encephalitis caused by canine distemper virus as the most common cause of inflammatory disease of the canine CNS.  The disease is more common in female dogs of young and middle age.  It has a rapid onset.  The lesions of GME exist mainly in the white matter of the cerebrum, brainstem, cerebellum, and spinal cord.  The cause is only known to be noninfectious and is considered at this time to be idiopathic.  Because lesions resemble those seen in allergic meningoencephalitis, GME is thought to have an immune-mediated cause, but it is also thought that the disease may be based on an abnormal response to an infectious agent.  One study searched for viral DNA from canine herpesvirus, canine adenovirus, and canine parvovirus in brain tissue from dogs with GME, necrotizing meningoencephalitis, and necrotizing leukoencephalitis (see below for the latter two conditions), but failed to find any.

Types of GME
Disseminated – This is a diffuse disease throughout the CNS.  It was previously known as inflammatory reticulosis.  There is an accumulation of mononuclear cells and neutrophils around the blood vessels (perivascular) of the CNS.  Meningitis is seen with this form of GME and causes fever and neck pain.  It has an acute progression over a few weeks.  Symptoms include incoordination, nystagmus, head tilt, seizures, and depression.
Focal – The disease presents as a granuloma, which mimics a tumor.  It usually is found in the cerebrum or cerebellopontine angle.  Symptoms may be acute or develop slowly over several months and depend on the location of the lesion.
Ocular – This is an uncommon form of GME and is characterized by sudden blindness caused by optic neuritis.  The disease is bilateral.  Ocular GME is considered to be an extension of CNS disease.  The blood vessels of the posterior segment of the eye and anterior uvea have the same infiltrates of inflammatory cells as the intracranial vessels.  Uveitis, retinal detachment, and secondary glaucoma may be seen.

Diagnosis and treatment
Cerebrospinal fluid (CSF) analysis shows a large number of white blood cells.  Typically small mature lymphocytes are the majority of cells seen, with monocytes and neutrophils making up the rest.  Definitive diagnosis is based on histopathology, either a brain biopsy or post-mortem evaluation (necropsy).  A CT scan or MRI will show patchy, diffuse, or multifocal lesions.  For a number of years, the basic treatment was some type of corticosteroid in combination with one or more immunosuppressive drugs, typically cytosine arabinoside and/or cyclosporine or other medications such as azathioprine, cyclophosphamide, or procarbazine, of which were usually added one at a time to the corticosteroid until a successful combination was found.  There is evidence that treatment with radiation therapy for focal GME provides the longest periods of remission.

Pug dog encephalitis
Pug dog encephalitis (PDE) is an idiopathic inflammatory disease primarily affecting the prosencephalon (forebrain and thalamus).  It is also known as necrotizing meningoencephalitis.  The disease may be inherited in Pugs and Maltese and has been diagnosed in other breeds as well (Yorkies, Chihuahuas).  The prevalence of PDE in pugs is about 1%. It differs in pathology from GME by more tissue breakdown and increased eosinophils (white blood cells).  CSF analysis is also unique among inflammatory CNS diseases in dogs in that the cells are predominantly lymphocytes, instead of a mixed population of mononuclear cells.  In Maltese and Pugs, there is extensive necrosis and inflammation of the gray matter of the cerebrum and subcortical white matter.  The most common early symptoms are related to forebrain disease and include seizures and dementia, and later circling, head tilt, and blindness with normal pupillary light reflexes may be seen </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 1q21.1 deletion syndrome and can you explain it in depth? [/INST] 1q21.1 deletion syndrome is a rare aberration of chromosome 1. A human cell has one pair of identical chromosomes on chromosome 1. With the 1q21.1 deletion syndrome, one chromosome of the pair is not complete, because a part of the sequence of the chromosome is missing. One chromosome has the normal length and the other is too short.
In 1q21.1, the 1 stands for chromosome 1, the q stands for the long arm of the chromosome and 21.1 stands for the part of the long arm in which the deletion is situated.
The syndrome is a form of the 1q21.1 copy number variations, and it is a deletion in the distal area of the 1q21.1 part. The CNV leads to a very variable phenotype, and the manifestations in individuals are quite variable. Some people who have the syndrome can function in a normal way, while others have symptoms of intellectual impairment and various physical anomalies.1q21.1 microdeletion is a very rare chromosomal condition. Only 46 individuals with this deletion have been reported in medical literature as of August 2011.

Symptoms and signs
Recognised symptoms are:
Only one set of genes on the two chromosomes function (haploinsufficiency)
Thrombocytopenia-absent radius (TAR syndrome), in case of a class II-deletion
Neurological-psychiatric problems: schizophrenia; epilepsy; learning problems; cognitive disabilities — mild to moderate; developmental delay — mild to moderate (milestones like sitting, standing and walking; come at a later period in childhood); children show an ataxic gait and fall down a lot
Dysmorphism: slightly unusual facial appearance; disturbed growth; skeletal malformations; small head (microcephaly); prominent forehead; bulbous nose; deep-set eyes; broad thumbs; broad toes; squint; very flexible joints; clavicular pseudoarthrosis (the collarbone doesnt develop normally) (class II-deletion); an extra transverse crease of the fifth finger (class II-deletion)); problems with the development of the vagina (Müllerian aplasia)
Eyes: cataracts
Heart abnormalities and cardiovascular anomalies (30% of the cases): anomalous origin of the coronary artery (Class II-deletion)
Kidneys: missing kidney or floating kidneys
Cancer: neuroblastoma
Sleep disturbancesIt is not clear whether the list of symptoms is complete. Very little information is known about the syndrome. The syndrome can have completely different effects on members of the same family.A common deletion is between 1.0–1.9Mb. Mefford states that the standard for a deletion is 1.35Mb. The largest deletion seen on a living human is over 5 Mb.

Cause
Meiosis is the process of dividing cells in humans. In meiosis, the chromosome pairs split and a representative of each pair goes to one daughter cell. In this way the number of chromosomes will be halved in each cell, while all the parts on the chromosome (genes) remain, after being randomized. Which information of the parent cell ends up in the daughter cell is purely decided by chance. Besides this random process, there is a second random process. In this second random process the DNA will be scrambled in a way that pieces are omitted (deletion), added (duplication), moved from one place to another (translocation) and inverted (inversion). This is a common process, which leads to about 0.4% variation in the DNA.A problem of the second random process is that genetic mistakes can occur. Because of the deletion and duplication process, the chromosomes that come together in a new cell may be shorter or longer. The result of this spontaneous change in the structure of DNA is a so-called copy number variation. Due to the copy number variation chromosomes of different sizes can be combined in a new cell. If this occurs around conception, the result will be a first cell of a human with a genetic variation. This can be either positive or negative. In positive cases this new human will be capable of a special skill that is assessed positively, for example, in sports or science. In negative cases, you have to deal with a syndrome or a severe disability, as in this case the 1q21.1 deletion syndrome.Based on the meiotic process, the syndrome may occur in two ways.
a spontaneous deviation (a de novo situation): two chromosomes come together of which one has a copy number variation as a result of the meiosis process.
a parent is unknowingly the carrier of a chromosome with a copy number variation and passes it at conception to the child, with different consequences for the child.Due to this genetic misprint, the embryo may experience problems in the development during the first months of pregnancy. Approximately 20 to 40 days after fertilization, something goes wrong in the construction of the body parts and brain, which leads to a chain reaction.

Genetics
The structure of 1q21.1
The structure of 1q21.1 is complex. The area has a size of approximately 6 Megabase (Mb) (from 141.5 Mb to 147.9 Mb). Within 1q21.1 there are two areas where the CNVs can be found: the proximal area or TAR area (144.1 to 144.5) and the distal area (144.7 to 145.9). The 1q21.1 deletion syndrome will commonly be found in the distal area, but an overlap with the TAR-area is possible. 1q21.1 has multiple repetitions of the same structure (areas with the same color in the picture have equal structures) Only 25% of the structure is not duplicated. There are several gaps in the sequence. There is no further information available about the DNA-sequence in those areas up until now. The gaps represent approximately 700 Kilobase. New genes are expected in the gaps. Because the gaps are still a topic of research, it is hard to find the exact start and end markers of a deletion. The area of 1q21.1 is one of the most difficult parts of the human genome to map.Because of the repetitions in 1q21.1, there is a larger chance of an unequal crossing-over during meiosis. CNVs occur due to non-allelic homologous recombination mediated by low copy repeats (sequentially similar regions).

Typing
A common deletion is restricted to the distal area. This is a Class I-deletion.In some cases the deletion is so large that the proximal area is involved as well, the so-called Class II-deletion. There are some complex cases in which both the proximal area and the distal area are affected, while the area in between is normal. There are also some a-typical variants.

Related genes
Genes related to 1q21.1 deletion in the distal area are PDE4DIP, HYDIN2, PRKAB2, PDIA3P, FMO5, CHD1L, BCL9, ACP6, GJA5, GJA8, NBPF10, GPR89B, GPR89C, PDZK1P1 and NBPF11.

Diagnostics
A de novo-situation appears in about 75% of the cases. In 25% of the cases, one of the parents is carrier of the syndrome, without any effect on the parent. Sometimes adults have mild problems with the syndrome. To find out whether either of the parents carries the syndrome, both parents have to be tested. In several cases, the syndrome was identified with the child, because of a developmental disorder or another problem, and later it appeared that the parent was affected as well. In families where both parents have tested negative for the syndrome, chances of a second child with the syndrome are extremely low. If the syndrome was found in the family, chances of a second child with the syndrome are 50%, because the syndrome is autosomal dominant. The effect of the syndrome on the child cannot be predictedThe syndrome can be detected with fluorescence in situ hybridization. For parents with a child with the syndrome, it is advisable to consult a physician before another pregnancy.

Management
Treatment of cause: Due to the genetic cause, no treatment of the cause is possible.Treatment of manifestations: routine treatment of ophthalmologic, cardiac, and neurologic findings; speech, occupational, and physical therapies as appropriate; specialized learning programs to meet individual needs; antiepileptic drugs or antipsychotic medications as needed.Surveillance: routine pediatric care; routine developmental assessments; monitoring of specific identified medical issues.

Prevalence
As of October 2012, Unique, an international rare chromosome disorder group and registry, has 64 genetically confirmed cases of this deletion worldwide.

Research
On several locations in the world people are studying on the subject of 1q21.1 deletion syndrome. The syndrome was identified for the first time with people with heart abnormalities. The syndrome has later been found in patients with schizophrenia. Research is done on patients with a symptom of the syndrome, to find more patients with the syndrome.There may be a relation between autism and schizophrenia. Literature shows that nine locations have been found on the DNA where the syndromes related to autism or schizophrenia can be found, the so-called "hotspots": 1q21.1, 3q29, 15q13.3, 16p11.2, 16p13.1, 16q21, 17p12, 21q11.2 and 21q13.3. With a number of hotspots, either autism and schizophrenia were observed depending on the copy-number variation (CNV) at that location.Statistical research showed that schizophrenia is more common in combination with 1q21.1 deletion syndrome. On the other side, autism is significantly more common with 1q21.1 duplication syndrome. Further research confirmed that the odds on a relation between schizophrenia and deletions at 1q21.1, 3q29, 15q13.3, 22q11.21 en Neurexin 1 (NRXN1) and duplications at 16p11.2 are at 7.5% or higher.

Common variations in the BCL9 gene, which is in the distal area, confer risk of schizophrenia and may also be associated with bipolar disorder and major depressive disorder.Research is done on 10–12 genes on 1q21.1 that produce DUF1220-locations. DUF1220 is an unknown protein, which is active in the neurons of the brain near the neocortex. Based on research on apes and other mammals, it is assumed that DUF1220 is related to cognitive development (man: 212 locations; chimpanzee: 37 locations; monkey: 30 locations; mouse: 1 location). It appears that the DUF1220-locations on 1q21.1 are in areas that are related to the size and the development of the brain. The aspect of the size and development of the brain is related to autism (macrocephaly) and schizophrenia (microcephaly) </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 Community-acquired pneumonia and can you explain it in depth? [/INST] Community-acquired pneumonia (CAP) refers to pneumonia (any of several lung diseases) contracted by a person outside of the healthcare system. In contrast, hospital-acquired pneumonia (HAP) is seen in patients who have recently visited a hospital or who live in long-term care facilities. CAP is common, affecting people of all ages, and its symptoms occur as a result of oxygen-absorbing areas of the lung (alveoli) filling with fluid. This inhibits lung function, causing dyspnea, fever, chest pains and cough.
CAP, the most common type of pneumonia, is a leading cause of illness and death worldwide. Its causes include bacteria, viruses, fungi and parasites. CAP is diagnosed by assessing symptoms, performing a physical examination, by x-ray or by sputum examination. Patients with CAP sometimes require hospitalization, and it is treated primarily with antibiotics, antipyretics and cough medicine. Some forms of CAP can be prevented by vaccination and by abstaining from tobacco products.

Signs and symptoms
Common symptoms
Coughing which produces greenish or yellow sputum
A high fever, accompanied by sweating, chills and shivering
Sharp, stabbing chest pains
Rapid, shallow, often painful breathing

Less-common symptoms
Coughing up blood (hemoptysis)
Headaches, including migraines
Loss of appetite
Excessive fatigue
Bluish skin (cyanosis)
Nausea
Vomiting
Diarrhea
Joint pain (arthralgia)
Muscle aches (myalgia)
Rapid heartbeat
Dizziness or lightheadedness

In the elderly
New or worsening confusion
Hypothermia
Poor coordination, which may lead to falls

In infants
Unusual sleepiness
Yellowing of the skin (jaundice)
Difficulty feeding

Complications
Major complications of CAP include:

Sepsis - A life-threatening reaction to infection. A common cause of sepsis is bacterial pneumonia, frequently the result of infection with streptococcus pneumoniae. Patients with sepsis require intensive care with blood pressure monitoring and support against hypotension. Sepsis can cause liver, kidney and heart damage.
Respiratory failure - CAP patients often have dyspnea, which may require support. Non-invasive machines (such as bilevel positive airway pressure), a tracheal tube or a ventilator may be used.
Pleural effusion and empyema - Microorganisms from the lung may trigger fluid collection in the pleural cavity, or empyema. Pleural fluid, if present, should be collected with a needle and examined. Depending on the results, complete drainage of the fluid with a chest tube may be necessary to prevent proliferation of the infection.  Antibiotics, which do not penetrate the pleural cavity well, are less effective.
Abscess - A pocket of fluid and bacteria may appear on X-ray as a cavity in the lung. Abscesses, typical of aspiration pneumonia, usually contain a mixture of anaerobic bacteria. Although antibiotics can usually cure abscesses, sometimes they require drainage by a surgeon or radiologist.

Causes
Many different microorganisms can cause CAP.  However, the most common cause is Streptococcus pneumoniae. Certain groups of people are more susceptible to CAP-causing pathogens - infants, adults with chronic conditions (such as chronic obstructive pulmonary disease), and senior citizens. Alcoholics and others with compromised immune systems are more likely to develop CAP from Haemophilus influenzae or Pneumocystis jirovecii. A definitive cause is identified in only half the cases.

Neonates and infants
It is possible for a fetus to develop a lung infection before birth by aspirating infected amniotic fluid or through a blood-borne infection which crossed the placenta. Infants can also inhale contaminated fluid from the vagina at birth. The most prevalent pathogen causing CAP in newborns is Streptococcus agalactiae, also known as group-B streptococcus (GBS). GBS causes more than half of CAP in the first week after birth. Other bacterial causes of neonatal CAP include Listeria monocytogenes and a variety of mycobacteria. CAP-causing viruses may also be transferred from mother to child; herpes simplex virus, the most common, is life-threatening, and adenoviridae, mumps and enterovirus can also cause pneumonia. Another cause of neonatal CAP is Chlamydia trachomatis, which, though acquired at birth, does not cause pneumonia until two to four weeks later. It usually presents with no fever and a characteristic, staccato cough.
CAP in older infants reflects increased exposure to microorganisms, with common bacterial causes including Streptococcus pneumoniae, Escherichia coli, Klebsiella pneumoniae, Moraxella catarrhalis and Staphylococcus aureus. Maternally-derived syphilis is also a cause of CAP in infants. Viral causes include human respiratory syncytial virus (RSV), human metapneumovirus, adenovirus, human parainfluenza viruses, influenza and rhinovirus, and RSV is a common source of illness and hospitalization in infants. CAP caused by fungi or parasites is not usually seen in otherwise-healthy infants.

Children
Although children older than one month tend to be at risk for the same microorganisms as adults, children under five years of age are much less likely to have pneumonia caused by Mycoplasma pneumoniae, Chlamydophila pneumoniae or Legionella pneumophila than older children. In contrast, older children and teenagers are more likely to acquire Mycoplasma pneumoniae and Chlamydophila pneumoniae than adults.

Adults
A full spectrum of microorganisms is responsible for CAP in adults, and patients with certain risk factors are more susceptible to infections by certain groups of microorganisms. Identifying people at risk for infection by these organisms aids in appropriate treatment.
Many less-common organisms can cause CAP in adults; these may be determined by identifying specific risk factors, or when treatment for more common causes fails.

Risk factors
Some patients have an underlying problem which increases their risk of infection. Some risk factors are:

Obstruction - When part of the airway (bronchus) leading to the alveoli is obstructed, the lung cannot eliminate fluid; this can lead to pneumonia. One cause of obstruction, especially in young children, is inhalation of a foreign object such as a marble or toy. The object lodges in a small airway, and pneumonia develops in the obstructed area of the lung. Another cause of obstruction is lung cancer, which can block the flow of air.
Lung disease - Patients with underlying lung disease are more likely to develop pneumonia. Diseases such as emphysema and habits such as smoking result in more frequent and more severe bouts of pneumonia. In children, recurrent pneumonia may indicate cystic fibrosis or pulmonary sequestration.
Immune problems - Immune-deficient patients, such as those with HIV/AIDS, are more likely to develop pneumonia. Other immune problems that increase the risk of developing pneumonia range from severe childhood immune deficiencies, such as Wiskott–Aldrich syndrome, to the less severe common variable immunodeficiency.

Pathophysiology
The symptoms of CAP are the result of lung infection by microorganisms and the response of the immune system to the infection. Mechanisms of infection are different for viruses and other microorganisms.

Viruses
Up to 20 percent of CAP cases can be attributed to viruses. The most common viral causes are influenza, parainfluenza, human respiratory syncytial virus, human metapneumovirus and adenovirus. Less common viruses which may cause serious illness include chickenpox, SARS, avian flu and hantavirus.Typically, a virus enters the lungs through the inhalation of water droplets and invades the cells lining the airways and the alveoli. This leads to cell death; the cells are killed by the virus or they self-destruct. Further lung damage occurs when the immune system responds to the infection. White blood cells, particularly lymphocytes, activate chemicals known as cytokines which cause fluid to leak into the alveoli. The combination of cell destruction and fluid-filled alveoli interrupts the transportation of oxygen into the bloodstream. In addition to their effects on the lungs, many viruses affect other organs. Viral infections weaken the immune system, making the body more susceptible to bacterial infection, including bacterial pneumonia.

Bacteria and fungi
Although most cases of bacterial pneumonia are caused by Streptococcus pneumoniae, infections by atypical bacteria such as Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila can also cause CAP. Enteric gram-negative bacteria, such as Escherichia coli and Klebsiella pneumoniae, are a group of bacteria that typically live in the large intestine; contamination of food and water by these bacteria can result in outbreaks of pneumonia. Pseudomonas aeruginosa, an uncommon cause of CAP, is a difficult bacteria to treat.
Bacteria and fungi typically enter the lungs by inhalation of water droplets, although they can reach the lung through the bloodstream if an infection is present. In the alveoli, bacteria and fungi travel into the spaces between cells and adjacent alveoli through connecting pores. The immune system responds by releasing neutrophil granulocytes, white blood cells responsible for attacking microorganisms, into the lungs. The neutrophils engulf and kill the microorganisms, releasing cytokines which activate the entire immune system. This response causes fever, chills and fatigue, common symptoms of CAP. The neutrophils, bacteria and fluids leaked from surrounding blood vessels fill the alveoli, impairing oxygen transport. Bacteria may travel from the lung to the bloodstream, causing septic shock (very low blood pressure which damages the brain, kidney, and heart).

Parasites
A variety of parasites can affect the lungs, generally entering the body through the skin or by being swallowed. They then travel to the lungs through the blood, where the combination of cell destruction and immune response disrupts oxygen transport.

Diagnosis
Patients with symptoms of CAP require evaluation. Diagnosis of pneumonia is made clinically, rather than on the basis of a particular test. Evaluation begins with a physical examination by a health provider, which may reveal fever, an increased respiratory rate (tachypnea), low blood pressure (hypotension), a fast heart rate (tachycardia) and changes in the amount of oxygen in the blood. Palpating the chest as it expands and tapping the chest wall to identify dull, non-resonant areas can identify stiffness and fluid, signs of CAP. Listening to the lungs with a stethoscope (auscultation) can also reveal signs associated with CAP. A lack of normal breath sounds or the presence of crackles can indicate fluid consolidation. Increased vibration of the chest when speaking, known as tactile fremitus, and increased volume of whispered speech during auscultation can also indicate the presence of fluid.Several tests can identify the cause of CAP. Blood cultures can isolate bacteria or fungi in the bloodstream. Sputum Gram staining and culture can also reveal the causative microorganism. In severe cases, bronchoscopy can collect fluid for culture. Special tests, such as urinalysis, can be performed if an uncommon microorganism is suspected.
Chest X-rays and X-ray computed tomography (CT) can reveal areas of opacity (seen as white), indicating consolidation. CAP does not always appear on x-rays, sometimes because the disease is in its initial stages or involves a part of the lung not clearly visible on x-ray. In some cases, chest CT can reveal pneumonia not seen on x-rays. However, congestive heart failure or other types of lung damage can mimic CAP on x-ray.When signs of pneumonia are discovered during evaluation, chest X-rays and examination of the blood and sputum for infectious microorganisms may be done to support a diagnosis of CAP. The diagnostic tools employed will depend on the severity of illness, local practices and concern about complications of the infection. All patients with CAP should have their blood oxygen monitored with pulse oximetry. In some cases, arterial blood gas analysis may be required to determine the amount of oxygen in the blood. A complete blood count (CBC) may reveal extra white blood cells, indicating infection.

Prevention
CAP may be prevented by treating underlying illnesses that increasing its risk, by smoking cessation, and by vaccination. Vaccination against haemophilus influenzae and streptococcus pneumoniae in the first year of life has been protective against childhood CAP. A vaccine against streptococcus pneumoniae, available for adults, is recommended for healthy individuals over 65 and all adults with COPD, heart failure, diabetes mellitus, cirrhosis, alcoholism, cerebrospinal fluid leaks or who have had a splenectomy. Re-vaccination may be required after five or ten years.Patients who have been vaccinated against streptococcus pneumoniae, health professionals, nursing-home residents and pregnant women should be vaccinated annually against influenza. During an outbreak, drugs such as amantadine, rimantadine, zanamivir and oseltamivir have been demonstrated to prevent influenza.

Treatment
CAP is treated with an antibiotic that kills the infecting microorganism; treatment also aims at managing complications. If the causative microorganism is unidentified, which is often the case, the laboratory identifies the most effective antibiotic; this may take several days.
Health professionals consider a persons risk factors for various organisms when choosing an initial antibiotic. Additional consideration is given to the treatment setting; most patients are cured by oral medication, while others must be hospitalized for intravenous therapy or intensive care.
Current treatment guidelines recommend a beta lactam, like amoxicillin and a macrolide, like azithromycin or clarithromycin, or a quinolone, such as levofloxacin. Doxycycline is the antibiotic of choice in the UK for atypical bacteria, due to increased clostridium difficile colitis in hospital patients linked to the increased use of clarithromycin.
Ceftriaxone and azithromycin are often used to treat community acquired pneumonia, which usually present with a few days of cough, fever, and shortness of breath. Chest x-ray typically reveals a lobar infiltrate (rather than diffuse).

Newborns
Most newborn infants with CAP are hospitalized, receiving IV ampicillin and gentamicin for at least ten days to treat the common causative agents streptococcus agalactiae, listeria monocytogenes and escherichia coli. To treat the herpes simplex virus, IV acyclovir is administered for 21 days.

Children
Treatment of CAP in children depends on the childs age and the severity of illness. Children under five are not usually treated for atypical bacteria. If hospitalization is not required, a seven-day course of amoxicillin is often prescribed, with co-trimaxazole as an alternative when there is allergy to penicillins. Further studies are needed to confirm the efficacy of newer antibiotics.  With the increase in drug-resistant Streptococcus pneumoniae, antibiotics such as cefpodoxime may become more popular. Hospitalized children receive intravenous ampicillin, ceftriaxone or cefotaxime, and a recent study found that a three-day course of antibiotics seems sufficient for most mild-to-moderate CAP in children.

Adults
In 2001 the American Thoracic Society, drawing on the work of the British and Canadian Thoracic Societies, established guidelines for the management of adult CAP by dividing patients into four categories based on common organisms:
Healthy outpatients without risk factors: This group (the largest) is composed of otherwise-healthy patients without risk factors for DRSP, enteric gram-negative bacteria, pseudomonas or other, less common, causes of CAP. Primary microorganisms are viruses, atypical bacteria, penicillin-sensitive streptococcus pneumoniae and haemophilus influenzae. Recommended drugs are macrolide antibiotics, such as azithromycin or clarithromycin, for seven to ten days. A shorter course of these antibiotics has been investigated, however, there is not sufficient evidence to make recommendations.
Outpatients with underlying illness or risk factors: Although this group does not require hospitalization, they have underlying health problems such as emphysema or heart failure or are at risk for DRSP or enteric gram-negative bacteria. They may be treated with a quinolone active against streptococcus pneumoniae (such as levofloxacin) or a β-lactam antibiotic (such as cefpodoxime, cefuroxime, amoxicillin or amoxicillin/clavulanic acid) and a macrolide antibiotic, such as azithromycin or clarithromycin, for seven to ten days.
Hospitalized patients without risk for pseudomonas: This group requires intravenous antibiotics, with a quinolone active against streptococcus pneumoniae (such as levofloxacin), a β-lactam antibiotic (such as cefotaxime, ceftriaxone, ampicillin/sulbactam or high-dose ampicillin plus a macrolide antibiotic (such as azithromycin or clarithromycin) for seven to ten days.
Intensive-care patients at risk for pseudomonas aeruginosa: These patients require antibiotics targeting this difficult-to-eradicate bacterium. One regimen is an intravenous antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an IV antipseudomonal fluoroquinolone such as levofloxacin. Another is an IV antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an aminoglycoside such as gentamicin or tobramycin, plus a macrolide (such as azithromycin) or a nonpseudomonal fluoroquinolone such as ciprofloxacin.For mild-to-moderate CAP, shorter courses of antibiotics (3–7 days) seem to be sufficient.Some patients with CAP will be at increased risk of death despite antimicrobial treatment. A key reason for this is the hosts exaggerated inflammatory response.  There is a tension between controlling the infection on one hand and minimizing damage to other tissues on the other. Some recent research focuses on immunomodulatory therapy that can modulate the immune response in order to reduce injury to the lung and other affected organs such as the heart. Although the evidence for these agents has not resulted in their routine use, their potential benefits are promising.

Hospitalization
Some CAP patients require intensive care, with clinical prediction rules such as the pneumonia severity index and CURB-65 guiding the decision whether or not to hospitalize. Factors increasing the need for hospitalization include:

Age greater than 65
Underlying chronic illnesses
Respiratory rate greater than 30 per minute
Systolic blood pressure less than 90 mmHg
Heart rate greater than 125 per minute
Temperature below 35 or over 40 °C
Confusion
Evidence of infection outside the lungLaboratory results indicating hospitalization include:

Arterial oxygen tension less than 60 mm Hg
Carbon dioxide over 50 mmHg or pH under 7.35 while breathing room air
Hematocrit under 30 percent
Creatinine over 1.2 mg/dl or blood urea nitrogen over 20 mg/dl
White-blood-cell count under 4 × 10^9/L or over 30 × 10^9/L
Neutrophil count under 1 x 10^9/LX-ray findings indicating hospitalization include:

Involvement of more than one lobe of the lung
Presence of a cavity
Pleural effusion

Prognosis
The CAP outpatient mortality rate is less than one percent, with fever typically responding within the first two days of therapy, and other symptoms abating in the first week. However, X-rays may remain abnormal for at least a month. Hospitalized patients have an average mortality rate of 12 percent, with the rate rising to 40 percent for patients with bloodstream infections or those who require intensive care. Factors increasing mortality are identical to those indicating hospitalization.
When CAP does not respond to treatment, this may indicate a previously unknown health problem, a treatment complication, inappropriate antibiotics for the causative organism, a previously unsuspected microorganism (such as tuberculosis) or a condition mimicking CAP (such as granuloma with polyangiitis). Additional tests include X-ray computed tomography, bronchoscopy or lung biopsy.

Epidemiology
CAP is common worldwide, and is a major cause of death in all age groups. In children, most deaths (over two million a year) occur in the newborn period </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 Myxoid cyst 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 Parakeratosis 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 Mitochondrial encephalomyopathy 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 Pycnodysostosis and can you explain it in depth? [/INST] Pycnodysostosis (from Greek: πυκνός (puknos) meaning "dense", dys ("defective"), and ostosis ("condition of the bone")), is a lysosomal storage disease of the bone caused by a mutation in the gene that codes the enzyme cathepsin K. It is also known as PKND and PYCD.

History
The disease was first described by Maroteaux and Lamy in 1962 at which time it was defined by the following characteristics: dwarfism; osteopetrosis; partial agenesis of the terminal digits of the hands and feet; cranial anomalies, such as persistence of fontanelles and failure of closure of cranial sutures; frontal and occipital bossing; and hypoplasia of the angle of the mandible. The defective gene responsible for the disease was discovered in 1996. The French painter Henri de Toulouse Lautrec (1864-1901) is believed to have had the disease.

Signs and symptoms
Pycnodysostosis causes the bones to be abnormally dense; the last bones of the fingers (the distal phalanges) to be unusually short; and delays the normal closure of the connections (sutures) of the skull bones in infancy, so that the "soft spot" (fontanelle) on top of the head remains widely open. Because of the bone denseness, those with the syndrome suffer from fractures.Those with the syndrome have brittle bones which easily break, especially in the legs and feet.
Other abnormalities involve the head and face, teeth, collar bones, skin, and nails. The front and back of the head are prominent. Within the open sutures of the skull, there may be many small bones (called wormian bones). The midface is less full than usual. The nose is prominent. The jaw can be small. The palate is narrow and grooved. There will be delay in fall of milk teeth. The permanent teeth can also be slow to appear. The permanent teeth are commonly irregular and teeth may be missing (hypodontia). The collar bones are often underdeveloped and malformed. The nails are flat, grooved, and dysplastic. High bone density, Acro-osteolysis and obtuse mandibular angle are the characteristic radiological findings of this disorder.Pycnodysostosis also causes problems that may become evident with time. Aside from the broken bones, the distal phalanges and the collar bone can undergo slow progressive deterioration. Vertebral defects may permit the spine to curve laterally resulting in scoliosis. The dental problems often require orthodontic care and cavities are common.
Patients with PYCD are at a high risk of severe obstructive sleep apnea (OSA) due to upper airway obstructions </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 Hyperdontia and can you explain it in depth? [/INST] Hyperdontia is the condition of having supernumerary teeth, or teeth that appear in addition to the regular number of teeth (32 in the average adult). They can appear in any area of the dental arch and can affect any dental organ. The opposite of hyperdontia is hypodontia, where there is a congenital lack of teeth, which is a condition seen more commonly than hyperdontia. The scientific definition of hyperdontia is "any tooth or odontogenic structure that is formed from tooth germ in excess of usual number for any given region of the dental arch." The additional teeth, which may be few or many, can occur on any place in the dental arch. Their arrangement may be symmetrical or non-symmetrical.

Signs and symptoms
The presence of a supernumerary tooth, particularly when seen in young children, is associated with a disturbance of the maxillary incisor region. This commonly results in the impaction of the incisors during the mixed dentition stage. The study debating this also considered many other factors such as: the patients age, number, morphology, growth orientation and position of the supernumerary tooth. Alongside this issue, the presence of an extra tooth can impede the eruption of adjacent additional or normal teeth. Therefore, the presence of a supernumerary tooth when found must be approached with the appropriate treatment plan, incorporating the likelihood of incisal crowding. In some individuals, the additional teeth can erupt far from the dental arch, within the maxillary sinus. The extra teeth may also migrate to a different location after development. In some cases, supernumerary teeth can lead to the formation of cysts. Crowding is also frequently seen in people with hyperdontia.

Causes
There is evidence of hereditary factors along with some evidence of environmental factors leading to this condition. While a single excess tooth is relatively common, multiple hyperdontia is rare in people with no other associated diseases or syndromes. Many supernumerary teeth never erupt, but they may delay eruption of nearby teeth or cause other dental or orthodontic problems. Molar-type extra teeth are the most common type. Dental X-rays are often used to diagnose hyperdontia.
It is suggested that supernumerary teeth develop from a third tooth bud arising from the dental lamina near the regular tooth bud or possibly from splitting the regular tooth bud itself. Supernumerary teeth in deciduous (baby) teeth are less common than in permanent teeth.

Related conditions
Hyperdontia is seen in a number of disorders, including Gardners syndrome and cleidocranial dysostosis, where multiple supernumerary teeth are seen that are usually impacted.Other associated conditions are: Cleidocranial dysplasia, Ehlers–Danlos syndrome Type III, Ellis–van Creveld syndrome, Gardners syndrome, Goldenhar syndrome, Hallermann–Streiff syndrome, Orofaciodigital syndrome type I, Incontinentia pigmenti, Marfan syndrome, Nance–Horan syndrome, and Tricho-rhino-phalangeal syndrome Type 1.

Diagnosis
Supernumerary teeth may be detected by taking two different dental X-rays at different angles. Examples of this may be an intra-oral X-ray (one that is taken inside the mouth) and a panoramic radiograph </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 Metamorphopsia and can you explain it in depth? [/INST] Metamorphopsia is a type of distorted vision in which a grid of straight lines appears wavy and parts of the grid may appear blank. People can first notice they suffer with the condition when looking at mini-blinds in their home. For example, straight lines might be wavy or bendy. Things may appear closer or further than they are.

Initially characterized in the 1800s, metamorphopsia was described as one of the primary and most notable indications of myopic and senile maculopathies. Metamorphopsia can present itself as unbalanced vision, resulting from small unintentional movements of the eye as it tries to stabilize the field of vision </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 Asteroid hyalosis 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 Corneal ectatic disorders 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 Anagen effluvium and can you explain it in depth? [/INST] Anagen effluvium is the pathologic loss of anagen or growth-phase hairs.  Classically, it is caused by radiation therapy to the head and systemic chemotherapy, especially with alkylating agents.: 753–4 Anagen effluvium is due to an acute injury to the hair follicles by an endogenous or exogenous cause, resulting in sudden diffuse shedding of structurally damaged hairs. Diffuse alopecia (hair loss) may occur over a period of days. The alopecia is non-scarring.

Pathophysiology
Any insult that impairs mitosis of hair follicle keratinocytes can cause anagen effluvium. Disruption to cell division in the hair matrix makes the hair narrowed at its base and susceptible to breakage just above the zone of keratinisation. The necrotic matrix forms plugs consisting of melanin, keratin and inner root sheath which are extruded through the follicular opening. This process is known as trichomalacia. The main causes of anagen effluvium are an infection, a drug, a toxin, radiation or an autoimmune disease.Toxins that can interrupt hair growth include:

Chemotherapy agents, usually prescribed to treat cancer, especially when multiple drugs are used or they are in high dose. Severe hair loss is reported from doxorubicin, the nitrosoureas, and cyclophosphamide. Other causes are bleomycin, dactinomycin, daunorubicin, systemic fluorouracil, and high-dose methotrexate.
Other medicines such as colchicine and ciclosporin (ciclosporin more often causes increased hair growth)
Poisons such as thallium, arsenic, gold and bismuth.

Evaluation
A biopsy is rarely necessary, as a diagnosis can usually be made on history and physical exam findings alone. If a biopsy is requested or necessary for diagnosis, it can help exclude telogen effluvium. In anagen effluvium, histopathologic evaluation of a punch biopsy of the scalp will exhibit a normal anagen-to-telogen ratio, which is less than 15% telogen hair follicles. If greater than 15% of the hair follicles are in the telogen phase, this more supports a diagnosis of telogen effluvium.

Treatment
The management of anagen effluvium should be aimed at limiting the amount of time the patient has alopecia. To date, several agents have been studied; unfortunately, no treatment appears to be effective in preventing or stopping the hair loss </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 Hypophosphatemia and can you explain it in depth? [/INST] Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. Symptoms may include weakness, trouble breathing, and loss of appetite. Complications may include seizures, coma, rhabdomyolysis, or softening of the bones.Causes include alcohol use disorder, refeeding in those with malnutrition, recovery from diabetic ketoacidosis, burns, hyperventilation, and certain medications. It may also occur in the setting of hyperparathyroidism, hypothyroidism, and Cushing syndrome. It is diagnosed based on a blood phosphate concentration of less than 0.81 mmol/L (2.5 mg/dL). When levels are below 0.32 mmol/L (1.0 mg/dL) it is deemed to be severe.Treatment depends on the underlying cause. Phosphate may be given by mouth or by injection into a vein. Hypophosphatemia occurs in about 2% of people within hospital and 70% of people in the intensive care unit (ICU).

Signs and symptoms
Muscle dysfunction and weakness – This occurs in major muscles, but also may manifest as: diplopia, low cardiac output, dysphagia, and respiratory depression due to respiratory muscle weakness.
Mental status changes – This may range from irritability to gross confusion, delirium, and coma.
White blood cell dysfunction, causing worsening of infections.
Instability of cell membranes due to low adenosine triphosphate (ATP) levels – This may cause rhabdomyolysis with increased serum levels of creatine phosphokinase, and also hemolytic anemia.
Increased affinity for oxygen in the blood caused by decreased production of 2,3-bisphosphoglyceric acid.

Causes
Refeeding syndrome – This causes a demand for phosphate in cells due to the action of hexokinase, an enzyme that attaches phosphate to glucose to begin metabolism of glucose. Also, production of ATP when cells are fed and recharge their energy supplies requires phosphate. A similar mechanism is seen in the treatment of diabetic ketoacidosis, which can be complicated by respiratory failure in these cases due to respiratory muscle weakness.
Respiratory alkalosis – Any alkalemic condition moves phosphate out of the blood into cells. This includes most common respiratory alkalemia (a higher than normal blood pH from low carbon dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes).  This phenomenon is seen because in respiratory alkalosis carbon dioxide (CO2) decreases in the extracellular space, causing intracellular CO2 to freely diffuse out of the cell.  This drop in intracellular CO2 causes a rise in cellular pH which has a stimulating effect on glycolysis.  Since the process of glycolysis requires phosphate (the end product is adenosine triphosphate), the result is a massive uptake of phosphate into metabolically active tissue (such as muscle) from the serum.  However, that this effect is not seen in metabolic alkalosis, for in such cases the cause of the alkalosis is increased bicarbonate rather than decreased CO2.  Bicarbonate, unlike CO2, has poor diffusion across the cellular membrane and therefore there is little change in intracellular pH.
Alcohol use disorder – Alcohol impairs phosphate absorption. People who excessively consume alcohol are usually also malnourished with regard to minerals </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 Umbilical cord prolapse and can you explain it in depth? [/INST] Umbilical cord prolapse is when the umbilical cord comes out of the uterus with or before the presenting part of the baby. The concern with cord prolapse is that pressure on the cord from the baby will compromise blood flow to the baby. It usually occurs during labor but can occur anytime after the rupture of membranes.The greatest risk factors are an abnormal position of the baby within the uterus and a premature or small baby. Other risk factors include a multiple pregnancy, more than one previous delivery, and too much amniotic fluid. Whether medical rupture of the amniotic sac is a risk is controversial. The diagnosis should be suspected if there is a sudden decrease in the babys heart rate during labor. Seeing or feeling the cord confirms the diagnosis.Management focuses on quick delivery, usually by cesarean section. Filling the bladder or pushing up the baby by hand is recommended until this can take place. Sometimes women will be placed in a knee-chest position or the Trendelenburg position in order to help prevent further cord compression. With appropriate management, the majority of cases have good outcomes.Umbilical cord prolapse occurs in about 1 in 500 pregnancies. The risk of death of the baby is about 10%. However, much of this risk is due to congenital anomalies or prematurity. It is considered an emergency.

Signs and symptoms
The first sign of umbilical cord prolapse is usually a sudden and severe decrease in fetal heart rate that does not immediately resolve. On fetal heart tracing (a linear recording of the fetal heart rate) this would usually look like moderate to severe variable decelerations. In overt cord prolapse, the cord can be seen or felt on the vulva or vagina.A majority of umbilical cord prolapse cases happen during the second stage of labor.

Risk factors
Risk factors that are associated with umbilical cord prolapse tend to make it difficult for the baby from appropriately engaging and filling the maternal pelvis or are related to abnormalities of the umbilical cord. The two major categories of risk factors are spontaneous and iatrogenic (those that result from medical intervention).

spontaneous factors:
fetal malpresentation: abnormal fetal lie tends to result in space below the baby in the maternal pelvis, which can then be occupied by the cord.
polyhydramnios, or an abnormally high amount of amniotic fluid
prematurity: likely related to increased chance of malpresentation and relative polyhydramnios.
low birth weight: usually described as <2500g at birth, though some studies will use <1500g. Cause is likely similar to those for prematurity.
multiple gestation, or being pregnant with more than one baby at a given time: more likely to occur in the baby that is not born first.
spontaneous rupture of membranes: about half of prolapses occur within 5 minutes of membrane rupture, two-thirds within 1 hour, 95% within 24 hours.
treatment associated factors:
artificial rupture of membranes
placement of internal monitors (for example, internal scalp electrode or intrauterine pressure catheter)
manual rotation of fetal head

Diagnosis
Umbilical cord prolapse should always be considered a possibility when there is a sudden decrease in fetal heart rate or variable decelerations, particularly after the rupture of membranes. With overt prolapses, the diagnosis can be confirmed if the cord can be felt on vaginal examination. Without overt prolapse, the diagnosis can only be confirmed after a cesarean section, though even then it will not always be evident at time of procedure.

Classification
There are three types of umbilical prolapse that can occur:
overt umbilical cord prolapse: descent of the umbilical cord past the presenting fetal part. In this case, the cord is through the cervix and into or beyond the vagina. Overt umbilical cord prolapse requires rupture of membranes. This is the most common type of cord prolapse.
occult umbilical prolapse: descent of the umbilical cord alongside the presenting fetal part, but has not advanced past the presenting fetal part. Occult umbilical prolapse can occur with both intact or ruptured membranes.
funic (cord) presentation: presence of the umbilical cord between the presenting fetal part and fetal membranes. In this case, the cord has not passed the opening of the cervix. In funic presentation, the membranes are not yet ruptured.

Management
The typical treatment of umbilical cord prolapse in the setting of a viable pregnancy involves immediate delivery by the quickest and safest route possible. This usually requires cesarean section, especially if the woman is in early labor. Occasionally, vaginal delivery will be attempted if clinical judgment determines that is a safer or quicker method.Other interventions during management of cord prolapse are typically used to decrease the chance of complications while preparations for delivery are being made. These interventions are focused on reducing pressure on the cord to prevent fetal complications from cord compression. The following maneuvers are among those used in clinical practice:

Manual elevation of the presenting fetal part.
Repositioning of the mother to be in the knee-chest position or Trendelenburg position (head down with feet elevated), lying on left side is usually preferred.
Filling of the bladder using a foley catheter can help elevate the presenting fetal part and lift it off the cord.
Use of tocolytics (medications to suppress labor) have been proposed, usually done in addition to bladder filling rather than as a stand-alone intervention.If the mother is far from delivery, funic reduction (manually placing the cord back into the uterine cavity) has been attempted, with successful cases reported. However, this is not currently recommended by the Royal College of Obstetricians and Gynaecologists (RCOG), as there is insufficient evidence to support this maneuver.

Outcomes
The primary concern with umbilical cord prolapse is inadequate blood supply, and thus oxygen, to the baby if the cord becomes compressed </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 Coronary artery disease and can you explain it in depth? [/INST] Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), myocardial ischemia, or simply heart disease, involves the reduction of blood flow to the heart muscle due to build-up of atherosclerotic plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, myocardial infarction, and sudden cardiac death. A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. Occasionally it may feel like heartburn. Usually symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest. Shortness of breath may also occur and sometimes no symptoms are present. In many cases, the first sign is a heart attack. Other complications include heart failure or an abnormal heartbeat.Risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, and excessive alcohol consumption. A number of tests may help with diagnoses including: electrocardiogram, cardiac stress testing, coronary computed tomographic angiography, and coronary angiogram, among others.Ways to reduce CAD risk include eating a healthy diet, regularly exercising, maintaining a healthy weight, and not smoking. Medications for diabetes, high cholesterol, or high blood pressure are sometimes used. There is limited evidence for screening people who are at low risk and do not have symptoms. Treatment involves the same measures as prevention. Additional medications such as antiplatelets (including aspirin), beta blockers, or nitroglycerin may be recommended. Procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG) may be used in severe disease. In those with stable CAD it is unclear if PCI or CABG in addition to the other treatments improves life expectancy or decreases heart attack risk.In 2015, CAD affected 110 million people and resulted in 8.9 million deaths. It makes up 15.6% of all deaths, making it the most common cause of death globally. The risk of death from CAD for a given age decreased between 1980 and 2010, especially in developed countries. The number of cases of CAD for a given age also decreased between 1990 and 2010. In the United States in 2010, about 20% of those over 65 had CAD, while it was present in 7% of those 45 to 64, and 1.3% of those 18 to 45; rates were higher among men than women of a given age.

Signs and symptoms
The narrowing of coronary arteries reduces the supply of oxygen-rich blood flowing to the heart, which becomes more pronounced during strenuous activities during which the heart beats faster. For some, this causes severe symptoms, while others experience no symptoms at all.The most common symptom is chest pain or discomfort that occurs regularly with activity, after eating, or at other predictable times; this phenomenon is termed stable angina and is associated with narrowing of the arteries of the heart. Angina also includes chest tightness, heaviness, pressure, numbness, fullness, or squeezing. Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction. In adults who go to the emergency department with an unclear cause of pain, about 30% have pain due to coronary artery disease. Angina, shortness of breath, sweating, nausea or vomiting, and lightheadedness are signs of a heart attack, or myocardial infarction, and immediate emergency medical services are crucial.

Symptoms in women
Symptoms in women can differ from those in men, and the most common symptom reported by women of all races is shortness of breath. Other symptoms more commonly reported by women than men are extreme fatigue, sleep disturbances, indigestion, and anxiety. However, some women do experience irregular heartbeat, dizziness, sweating, and nausea. Burning, pain, or pressure in the chest or upper abdomen that can travel to the arm or jaw can also be experienced in women, but it is less commonly reported by women than men. On average, women experience symptoms 10 years later than men. Women are less likely to recognize symptoms and seek treatment.

Risk factors
Coronary artery disease has a number of well determined risk factors. Some of these include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, family history, psychological stress and excessive alcohol. About half of cases are linked to genetics. Smoking and obesity are associated with about 36% and 20% of cases, respectively. Smoking just one cigarette per day about doubles the risk of CAD. Lack of exercise has been linked to 7–12% of cases. Exposure to the herbicide Agent Orange may increase risk. Rheumatologic diseases such as rheumatoid arthritis, systemic lupus erythematosus, psoriasis, and psoriatic arthritis are independent risk factors as well.Job stress appears to play a minor role accounting for about 3% of cases. In one study, women who were free of stress from work life saw an increase in the diameter of their blood vessels, leading to decreased progression of atherosclerosis. In contrast, women who had high levels of work-related stress experienced a decrease in the diameter of their blood vessels and significantly increased disease progression. Having a type A behavior pattern, a group of personality characteristics including time urgency, competitiveness, hostility, and impatience, is linked to an increased risk of coronary disease.

Blood fats
High blood cholesterol (specifically, serum LDL concentrations; also referred to as LDL-C to denote low-density lipoprotien cholesterol). HDL (high density lipoprotein) has a protective effect over development of coronary artery disease.
High blood triglycerides may play a role.
High levels of lipoprotein(a), a compound formed when LDL cholesterol combines with a protein known as apolipoprotein(a).Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed. Saturated fat is still a concern.

Genetics
The heritability of coronary artery disease has been estimated between 40% and 60%. Genome-wide association studies have identified over 160 genetic susceptibility loci for coronary artery disease.

Other
Endometriosis in women under the age of 40.
Depression and hostility appear to be risks.
The number of categories of adverse childhood experiences (psychological, physical, or sexual abuse; violence against mother; or living with household members who used substances, mentally ill, suicidal, or incarcerated) showed a graded correlation with the presence of adult diseases including coronary artery (ischemic heart) disease.
Hemostatic factors: High levels of fibrinogen and coagulation factor VII are associated with an increased risk of CAD.
Low hemoglobin.
In the Asian population, the b fibrinogen gene G-455A polymorphism was associated with the risk of CAD.

Pathophysiology
Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the hearts muscle cells. The hearts muscle cells may die from lack of oxygen and this is called a myocardial infarction (commonly referred to as a heart attack). It leads to damage, death, and eventual scarring of the heart muscle without regrowth of heart muscle cells. Chronic high-grade narrowing of the coronary arteries can induce transient ischemia which leads to the induction of a ventricular arrhythmia, which may terminate into a dangerous heart rhythm known as ventricular fibrillation, which often leads to death.Typically, coronary artery disease occurs when part of the smooth, elastic lining inside a coronary artery (the arteries that supply blood to the heart muscle) develops atherosclerosis. With atherosclerosis, the arterys lining becomes hardened, stiffened, and accumulates deposits of calcium, fatty lipids, and abnormal inflammatory cells – to form a plaque. Calcium phosphate (hydroxyapatite) deposits in the muscular layer of the blood vessels appear to play a significant role in stiffening the arteries and inducing the early phase of coronary arteriosclerosis. This can be seen in a so-called metastatic mechanism of calciphylaxis as it occurs in chronic kidney disease and hemodialysis. Although these people have kidney dysfunction, almost fifty percent of them die due to coronary artery disease. Plaques can be thought of as large "pimples" that protrude into the channel of an artery, causing partial obstruction to blood flow. People with coronary artery disease might have just one or two plaques, or might have dozens distributed throughout their coronary arteries. A more severe form is chronic total occlusion (CTO) when a coronary artery is completely obstructed for more than 3 months.Cardiac syndrome X is chest pain (angina pectoris) and chest discomfort in people who do not show signs of blockages in the larger coronary arteries of their hearts when an angiogram (coronary angiogram) is being performed. The exact cause of cardiac syndrome X is unknown. Explanations include microvascular dysfunction or epicardial atherosclerosis. For reasons that are not well understood, women are more likely than men to have it; however, hormones and other risk factors unique to women may play a role.

Diagnosis
For symptomatic people, stress echocardiography can be used to make a diagnosis for obstructive coronary artery disease. The use of echocardiography, stress cardiac imaging, and/or advanced non-invasive imaging is not recommended on individuals who are exhibiting no symptoms and are otherwise at low risk for developing coronary disease.The diagnosis of "Cardiac Syndrome X" – the rare coronary artery disease that is more common in women, as mentioned, is a diagnosis of exclusion. Therefore, usually, the same tests are used as in any person with the suspected of having coronary artery disease:
Baseline electrocardiography (ECG)
Exercise ECG – Stress test
Exercise radioisotope test (nuclear stress test, myocardial scintigraphy)
Echocardiography (including stress echocardiography)
Coronary angiography
Intravascular ultrasound
Magnetic resonance imaging (MRI)The diagnosis of coronary disease underlying particular symptoms depends largely on the nature of the symptoms. The first investigation is an electrocardiogram (ECG/EKG), both for "stable" angina and acute coronary syndrome. An X-ray of the chest and blood tests may be performed.

Stable angina
In "stable" angina, chest pain with typical features occurring at predictable levels of exertion, various forms of cardiac stress tests may be used to induce both symptoms and detect changes by way of electrocardiography (using an ECG), echocardiography (using ultrasound of the heart) or scintigraphy (using uptake of radionuclide by the heart muscle). If part of the heart seems to receive an insufficient blood supply, coronary angiography may be used to identify stenosis of the coronary arteries and suitability for angioplasty or bypass surgery.Stable coronary artery disease (SCAD) is also often called stable ischemic heart disease (SIHD). A 2015 monograph explains that "Regardless of the nomenclature, stable angina is the chief manifestation of SIHD or SCAD." There are U.S. and European clinical practice guidelines for SIHD/SCAD.

Acute coronary syndrome
Diagnosis of acute coronary syndrome generally takes place in the emergency department, where ECGs may be performed sequentially to identify "evolving changes" (indicating ongoing damage to the heart muscle). Diagnosis is clear-cut if ECGs show elevation of the "ST segment", which in the context of severe typical chest pain is strongly indicative of an acute myocardial infarction (MI); this is termed a STEMI (ST-elevation MI) and is treated as an emergency with either urgent coronary angiography and percutaneous coronary intervention (angioplasty with or without stent insertion) or with thrombolysis ("clot buster" medication), whichever is available. In the absence of ST-segment elevation, heart damage is detected by cardiac markers (blood tests that identify heart muscle damage). If there is evidence of damage (infarction), the chest pain is attributed to a "non-ST elevation MI" (NSTEMI). If there is no evidence of damage, the term "unstable angina" is used. This process usually necessitates hospital admission and close observation on a coronary care unit for possible complications (such as cardiac arrhythmias – irregularities in the heart rate). Depending on the risk assessment, stress testing or angiography may be used to identify and treat coronary artery disease in patients who have had an NSTEMI or unstable angina.

Risk assessment
There are various risk assessment systems for determining the risk of coronary artery disease, with various emphasis on different variables above. A notable example is Framingham Score, used in the Framingham Heart Study. It is mainly based on age, gender, diabetes, total cholesterol, HDL cholesterol, tobacco smoking, and systolic blood pressure. When it comes to predicting risk in younger adults (18–39 years old), Framingham Risk Score remains below 10-12% for all deciles of baseline-predicted risk.Polygenic score is another way of risk assessment. In one study the relative risk of incident coronary events was 91% higher among participants at high genetic risk than among those at low genetic risk.

Prevention
Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided. Prevention involves adequate physical exercise, decreasing obesity, treating high blood pressure, eating a healthy diet, decreasing cholesterol levels, and stopping smoking. Medications and exercise are roughly equally effective. High levels of physical activity reduce the risk of coronary artery disease by about 25%. Life’s Essential 8 are the key measures for improving and maintaining cardiovascular health, as defined by the American Heart Association. AHA added sleep as a factor influencing heart health in 2022.Most guidelines recommend combining these preventive strategies. A 2015 Cochrane Review found some evidence that counseling and education to bring about behavioral change might help in high-risk groups. However, there was insufficient evidence to show an effect on mortality or actual cardiovascular events.In diabetes mellitus, there is little evidence that very tight blood sugar control improves cardiac risk although improved sugar control appears to decrease other problems such as kidney failure and blindness. The World Health Organization (WHO) recommends "low to moderate alcohol intake" to reduce risk of coronary artery disease while high intake increases the risk.

Diet
A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death. Vegetarians have a lower risk of heart disease, possibly due to their greater consumption of fruits and vegetables. Evidence also suggests that the Mediterranean diet and a high fiber diet lower the risk.The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause a precursor to atherosclerosis and increase the risk of coronary artery disease.Evidence does not support a beneficial role for omega-3 fatty acid supplementation in preventing cardiovascular disease (including myocardial infarction and sudden cardiac death). There is tentative evidence that intake of menaquinone (Vitamin K2), but not phylloquinone (Vitamin K1), may reduce the risk of CAD mortality.

Secondary prevention
Secondary prevention is preventing further sequelae of already established disease. Effective lifestyle changes include:

Weight control
Smoking cessation
Avoiding the consumption of trans fats (in partially hydrogenated oils)
Decreasing psychosocial stress
ExerciseAerobic exercise, like walking, jogging, or swimming, can reduce the risk of mortality from coronary artery disease. Aerobic exercise can help decrease blood pressure and the amount of blood cholesterol (LDL) over time. It also increases HDL cholesterol.Although exercise is beneficial, it is unclear whether doctors should spend time counseling patients to exercise. The U.S. Preventive Services Task Force found "insufficient evidence" to recommend that doctors counsel patients on exercise but "it did not review the evidence for the effectiveness of physical activity to reduce chronic disease, morbidity, and mortality", only the effectiveness of counseling itself. The American Heart Association, based on a non-systematic review, recommends that doctors counsel patients on exercise.Psychological symptoms are common in people with CHD, and while many psychological treatments may be offered following cardiac events, there is no evidence that they change mortality, the risk of revascularization procedures, or the rate of non-fatal myocardial infarction.Antibiotics for secondary prevention of coronary heart disease
Antibiotics may help patients with coronary disease to reduce the risk of heart attacks and strokes. However, the latest evidence suggests that antibiotics for secondary prevention of coronary heart disease are harmful with increased mortality and occurrence of stroke. So, the use of antibiotics is not currently supported for preventing secondary coronary heart disease.

Neuropsychological Assessment
A thorough systematic review found that indeed there is a link between a CHD condition and brain dysfunction in females/women. Consequently, since research is showing that cardiovascular diseases, like CHD, can play a role as a precursor for dementia, like Alzheimers disease, individuals with CHD should have a neuropsychological assessment.

Treatment
There are a number of treatment options for coronary artery disease:
Lifestyle changes
Medical treatment – commonly prescribed drugs (e.g., cholesterol lowering medications, beta-blockers, nitroglycerin, calcium channel blockers, etc.);
Coronary interventions as angioplasty and coronary stent;
Coronary artery bypass grafting (CABG)

Medications
Statins, which reduce cholesterol, reduce the risk of coronary artery disease
Nitroglycerin
Calcium channel blockers and/or beta-blockers
Antiplatelet drugs such as aspirinIt is recommended that blood pressure typically be reduced to less than 140/90 mmHg. The diastolic blood pressure however should not be lower than 60 mmHg. Beta blockers are recommended first line for this use.

Aspirin
In those with no previous history of heart disease, aspirin decreases the risk of a myocardial infarction but does not change the overall risk of death. It is thus recommended only in adults who are at increased risk for coronary artery disease where increased risk is defined as "men older than 90 years of age, postmenopausal women, and younger persons with risk factors for coronary artery disease (for example, hypertension, diabetes, or smoking) who are at increased risk for heart disease and may wish to consider aspirin therapy". More specifically, high-risk persons are "those with a 5-year risk ≥ 3%".

Anti-platelet therapy
Clopidogrel plus aspirin (dual anti-platelet therapy) reduces cardiovascular events more than aspirin alone in those with a STEMI. In others at high risk but not having an acute event, the evidence is weak. Specifically, its use does not change the risk of death in this group. In those who have had a stent, more than 12 months of clopidogrel plus aspirin does not affect the risk of death.

Surgery
Revascularization for acute coronary syndrome has a mortality benefit. Percutaneous revascularization for stable ischaemic heart disease does not appear to have benefits over medical therapy alone. In those with disease in more than one artery, coronary artery bypass grafts appear better than percutaneous coronary interventions. Newer "anaortic" or no-touch off-pump coronary artery revascularization techniques have shown reduced postoperative stroke rates comparable to percutaneous coronary intervention. Hybrid coronary revascularization has also been shown to be a safe and feasible procedure that may offer some advantages over conventional CABG though it is more expensive.

Epidemiology
As of 2010, CAD was the leading cause of death globally resulting in over 7 million deaths. This increased from 5.2 million deaths from CAD worldwide in 1990. It may affect individuals at any age but becomes dramatically more common at progressively older ages, with approximately a tripling with each decade of life. Males are affected more often than females.It is estimated that 60% of the worlds cardiovascular disease burden will occur in the South Asian subcontinent despite only accounting for 20% of the worlds population. This may be secondary to a combination of genetic predisposition and environmental factors. Organizations such as the Indian Heart Association are working with the World Heart Federation to raise awareness about this issue.Coronary artery disease is the leading cause of death for both men and women and accounts for approximately 600,000 deaths in the United States every year. According to present trends in the United States, half of healthy 40-year-old men will develop CAD in the future, and one in three healthy 40-year-old women. It is the most common reason for death of men and women over 20 years of age in the United States.

Society and culture
Names
Other terms sometimes used for this condition are "hardening of the arteries" and "narrowing of the arteries". In Latin it is known as morbus ischaemicus cordis (MIC).

Support groups
The Infarct Combat Project (ICP) is an international nonprofit organization founded in 1998 which tries to decrease ischemic heart diseases through education and research.

Industry influence on research
In 2016 research into the archives of theSugar Association, the trade association for the sugar industry in the US, had sponsored an influential literature review published in 1965 in the New England Journal of Medicine that downplayed early findings about the role of a diet heavy in sugar in the development of CAD and emphasized the role of fat; that review influenced decades of research funding and guidance on healthy eating.

Research
Research efforts are focused on new angiogenic treatment modalities and various (adult) stem-cell therapies </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 Multiple endocrine neoplasia type 2 and can you explain it in depth? [/INST] Multiple endocrine neoplasia type 2 (also known as "Pheochromocytoma and amyloid producing medullary thyroid carcinoma", "PTC syndrome," and "Sipple syndrome") is a group of medical disorders associated with tumors of the endocrine system. The tumors may be benign or malignant (cancer).  They generally occur in endocrine organs (e.g. thyroid, parathyroid, and adrenals), but may also occur in endocrine tissues of organs not classically thought of as endocrine.MEN2 is a sub-type of MEN (multiple endocrine neoplasia) and itself has sub-types, as discussed below.

Signs and symptoms
MEN2 can present with a sign or symptom related to a tumor or, in the case of multiple endocrine neoplasia type 2b, with characteristic musculoskeletal and/or lip and/or gastrointestinal findings. Medullary thyroid carcinoma (MTC) represents the most frequent initial diagnosis. Occasionally pheochromocytoma or primary hyperparathyroidism may be the initial diagnosis.Pheochromocytoma occurs in 33-50% of MEN2 cases. In MEN2A, primary hyperparathyroidism occurs in 10–50% of cases and is usually diagnosed after the third decade of life. Rarely, it may present in childhood or be the sole clinical manifestation of this syndrome.MEN2A associates medullary thyroid carcinoma with pheochromocytoma in about 20–50% of cases and with primary hyperparathyroidism in 5–20% of cases. MEN2B associates medullary thyroid carcinoma with pheochromocytoma in 50% of cases, with marfanoid habitus and with mucosal and digestive neurofibromatosis.In familial isolated medullary thyroid carcinoma the other components of the disease are absent.
In a review of 85 patients 70 had MEN2A and 15 had MEN2B. The initial manifestation of MEN2 was medullary thyroid carcinoma in 60% of patients, medullary thyroid carcinoma synchronous with pheochromocytoma in 34% and pheochromocytoma alone in 6%. 72% had bilateral pheochromocytomas.

Causes
The table in the multiple endocrine neoplasia article lists the genes involved in the various MEN syndromes.  Most cases of MEN2 derive from a variation in the RET proto-oncogene, and are specific for cells of neural crest origin.  A database of MEN-implicated RET mutations is maintained by the University of Utah Department of Physiology.The protein produced by the RET gene plays an important role in the TGF-beta (transforming growth factor beta) signaling system.  Because the TGF-beta system operates in nervous tissues throughout the body, variations in the RET gene can have effects in nervous tissues throughout the body. MEN2 generally results from a gain-of-function variant of a RET gene.  Other diseases, such as Hirschsprung disease, result from loss-of-function variants.  OMIM # 164761 lists the syndromes associated with the RET gene.

Genetics
When inherited, multiple endocrine neoplasia type 2 is transmitted in an autosomal dominant pattern, which means affected people have one affected parent, and possibly affected siblings and children </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 Dependent personality disorder and can you explain it in depth? [/INST] Dependent personality disorder (DPD) is characterized by a pervasive psychological dependence on other people. This personality disorder is a long-term condition in which people depend on others to meet their emotional and physical needs, with only a minority achieving normal levels of independence. Dependent personality disorder is a cluster C personality disorder, which is characterized by excessive fear and anxiety. It begins prior to early adulthood, and it is present in a variety of contexts and is associated with inadequate functioning. Symptoms can include anything from extreme passivity, devastation or helplessness when relationships end, avoidance of responsibilities and severe submission.

Signs and symptoms
People who have dependent personality disorder are overdependent on other people when it comes to making decisions. They cannot make a decision on their own as they need constant approval from other people. Consequently, individuals diagnosed with DPD tend to place needs and opinions of others above their own as they do not have the confidence to trust their decisions. This kind of behaviour can explain why people with DPD tend to show passive and clingy behaviour. These individuals display a fear of separation and cannot stand being alone. When alone, they experience feelings of isolation and loneliness due to their overwhelming dependence on other people. Generally people with DPD are also pessimistic: they expect the worst out of situations or believe that the worst will happen. They tend to be more introverted and are more sensitive to criticism and fear rejection.

Risk factors
People with a history of neglect and an abusive upbringing are more susceptible to develop DPD, specifically those involved in long-term abusive relationships. Those with overprotective or authoritarian parents are also more at risk to develop DPD. Having a family history of anxiety disorder can play a role in the development of DPD as a 2004 twin study found a 0.81 heritability for personality disorders collectively.

Causes
The exact cause of dependent personality disorder is unknown. A study in 2012 estimated that between 55% and 72% of the risk of the condition is inherited from ones parents. The difference between a "dependent personality" and a "dependent personality disorder" is somewhat subjective, which makes diagnosis sensitive to cultural influences such as gender role expectations.
Dependent traits in children tended to increase with parenting behaviours and attitudes characterized by overprotectiveness and authoritarianism. Thus the likelihood of developing dependent personality disorder increased, since these parenting traits can limit them from developing a sense of autonomy, rather teaching them that others are powerful and competent.Traumatic or adverse experiences early in an individuals life, such as neglect and abuse or serious illness, can increase the likelihood of developing personality disorders, including dependent personality disorder, later on in life. This is especially prevalent for those individuals who also experience high interpersonal stress and poor social support.There is a higher frequency of the disorder seen in women than men, hence expectations relating to gender role may contribute to some extent.

Diagnosis
Clinicians and clinical researchers conceptualize dependent personality disorder in terms of four related components:

Cognitive: a perception of oneself as powerless and ineffectual, coupled with the belief that other people are comparatively powerful and potent.
Motivational: a desire to obtain and maintain relationships with protectors and caregivers.
Behavioral: a pattern of relationship-facilitating behavior designed to strengthen interpersonal ties and minimize the possibility of abandonment and rejection.
Emotional: fear of abandonment, fear of rejection, and anxiety regarding evaluation by figures of authority.

American Psychiatric Association and DSM
The Diagnostic and Statistical Manual of Mental Disorders (DSM) contains a dependent personality disorder diagnosis. It refers to a pervasive and excessive need to be taken care of which leads to submissive and clinging behavior and fears of separation. This begins prior to early adulthood and can be present in a variety of contexts.In the DSM Fifth Edition (DSM-5), there is one criterion by which there are eight features of dependent personality disorder. The disorder is indicated by at least five of the following factors:
Has difficulty making everyday decisions without an excessive amount of advice and reassurance from others.
Needs others to assume responsibility for most major areas of their life.
Has difficulty expressing disagreement with others because of fear of loss of support or approval.
Has difficulty initiating projects or doing things on their own (because of a lack of self confidence in judgment or abilities rather than a lack of motivation or energy).
Goes to excessive lengths to obtain nurturance and support from others, to the point of volunteering to do things that are unpleasant.
Feels uncomfortable or helpless when alone because of exaggerated fears of being unable to care for themselves.
Urgently seeks another relationship as a source of care and support when a close relationship ends.
Is unrealistically preoccupied with fears of being left to take care of themselves.The diagnosis of personality disorders in the fourth edition Diagnostic and Statistical Manual of Mental Disorders, including dependent personality disorder, was found to be problematic due to reasons such as excessive diagnostic comorbidity, inadequate coverage, arbitrary boundaries with normal psychological functioning, and heterogeneity among individuals within the same categorial diagnosis.

World Health Organization
The World Health Organizations ICD-10 lists dependent personality disorder as F60.7 Dependent personality disorder:
It is characterized by at least 4 of the following:
Encouraging or allowing others to make most of ones important life decisions;
Subordination of ones own needs to those of others on whom one is dependent, and undue compliance with their wishes;
Unwillingness to make even reasonable demands on the people one depends on;
Feeling uncomfortable or helpless when alone, because of exaggerated fears of inability to care for oneself;
Preoccupation with fears of being abandoned by a person with whom one has a close relationship, and of being left to care for oneself;
Limited capacity to make everyday decisions without an excessive amount of advice and reassurance from others.Associated features may include perceiving oneself as helpless, incompetent, and lacking stamina.
Includes:

Asthenic, inadequate, passive, and self-defeating personality (disorder)
It is a requirement of ICD-10 that a diagnosis of any specific personality disorder also satisfies a set of general personality disorder criteria.

SWAP-200
The SWAP-200 is a diagnostic tool that was proposed with the goal of overcoming limitations, such as limited external validity for the diagnostic criteria for dependent personality disorder, to the DSM. It serves as a possible alternative nosological system that emerged from the efforts to create an empirically based approach to personality disorders – while also preserving the complexity of clinical reality. Dependent personality disorder is considered a clinical prototype in the context of the SWAP-200. Rather than discrete symptoms, it provides composite description characteristic criteria – such as personality tendencies.Based on the Q-Sort method and prototype matching, the SWAP-200 is a personality assessment procedure relying on an external observers judgment. It provides:

A personality diagnosis expressed as the matching with ten prototypical descriptions of DSM-IV personality disorders.
A personality diagnosis based on the matching of the patient with 11 Q-factors of personality derived empirically.
A dimensional profile of healthy and adaptive functioning.The traits that define dependent personality disorder according to SWAP-200 are:

They tend to become attached quickly and/or intensely, developing feelings and expectations that are not warranted by the history or context of the relationship.
Since they tend to be ingratiating and submissive, people with DPD tend to be in relationships in which they are emotionally or physically abused.
They tend to feel ashamed, inadequate, and depressed.
They also feel powerless and tend to be suggestible.
They are often anxious and tend to feel guilty.
These people have difficulty acknowledging and expressing anger and struggle to get their own needs and goals met.
Unable to soothe or comfort themselves when distressed, they require involvement of another person to help regulate their emotions.

Psychodynamic Diagnostic Manual
The Psychodynamic Diagnostic Manual (PDM) approaches dependent personality disorder in a descriptive, rather than prescriptive sense and has received empirical support. The Psychodynamic Diagnostic Manual includes two different types of dependent personality disorder:
Passive-aggressive
Counter-dependent The PDM-2 adopts and applies a prototypic approach, using empirical measures like the SWAP-200. It was influenced by a developmental and empirically grounded perspective, as proposed by Sidney Blatt. This model is of particular interest when focusing on dependent personality disorder, claiming that psychopathology comes from distortions of two main coordinates of psychological development:

The anaclitic/introjective dimension.
The relatedness/self-definition dimension.The anaclitic personality organization in individuals exhibits difficulties in interpersonal relatedness, exhibiting the following behaviours:

Preoccupation with relationships
Fear of abandonment and of rejection
Seeking closeness and intimacy
Difficulty managing interpersonal boundaries
Tend to have an anxious-preoccupied attachment style.Introjective personality style is associated with problems in self-definition.

Differential diagnosis
There are similarities between individuals with dependent personality disorder and individuals with borderline personality disorder, in that they both have a fear of abandonment. Those with dependent personality disorder do not exhibit impulsive behaviour, unstable affect, and poor self-image experienced by those with borderline personality disorder, differentiating the two disorders.

Treatment
People who have DPD are generally treated with psychotherapy. The main goal of this therapy is to make the individual more independent and help them form healthy relationships with the people around them. This is done by improving their self-esteem and confidence.Medication can be used to treat patients with depression or anxiety because of their DPD, but this does not treat the core problems caused by DPD.

Epidemiology
Based on a recent survey of 43,093 Americans, 0.49% of adults meet diagnostic criteria for DPD (National Epidemiologic Survey on Alcohol and Related Conditions; NESARC; Grant et al., 2004).
Traits related to DPD, like most personality disorders, emerge in childhood or early adulthood. Findings from the NESArC study found that 18 to 29 year olds have a greater chance of developing DPD. DPD is more common among women compared to men as 0.6% of women have DPD compared to 0.4% of men.A 2004 twin study suggests a heritability of 0.81 for developing dependent personality disorder. Because of this, there is significant evidence that this disorder runs in families.Children and adolescents with a history of anxiety disorders and physical illnesses are more susceptible to acquiring this disorder.

Millons subtypes
Psychologist Theodore Millon identified five adult subtypes of dependent personality disorder. Any individual dependent may exhibit none or one of the following:

History
The conceptualization of dependency, within classical psychoanalytic theory, is directly related to Freuds oral psychosexual stage of development. Frustration or over-gratification was said to result in an oral fixation and in an oral type of character, characterized by feeling dependent on others for nurturance and by behaviours representative of the oral stage. Later psychoanalytic theories shifted the focus from a drive-based approach of dependency to the recognition of the importance of early relationships and establishing separation from these early caregivers, in which the exchanges between the caregiver and the child become internalized, and the nature of these interactions becomes part of the concepts of the self and of others.

References
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Millon, Theodore (1981). Disorders of Personality: DSM-III, Axis II. New York: Wiley. ISBN 978-0-471-06403-9.
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Millon, Theodore; Millon, Carrie M.; Meagher, Sarah; Grossman, Seth; Ramnath, Rowena (2004). Personality Disorders in Modern Life. Wiley. ISBN 978-0-471-66850-3.
Millon, Theodore (2006). "Personality Subtypes".
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Benjamin, Lorna Smith (1993) </s>