<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 Lymphoma and can you explain it in depth? [/INST] Lymphoma is a group of blood and lymph tumors that develop from lymphocytes (a type of white blood cell). In current usage the name usually refers to just the cancerous versions rather than all such tumours. Signs and symptoms may include enlarged lymph nodes, fever, drenching sweats, unintended weight loss, itching, and constantly feeling tired. The enlarged lymph nodes are usually painless. The sweats are most common at night.Many subtypes of lymphomas are known. The two main categories of lymphomas are the non-Hodgkin lymphoma (NHL) (90% of cases) and Hodgkin lymphoma (HL) (10%). The World Health Organization (WHO) includes two other categories as types of lymphoma – multiple myeloma and immunoproliferative diseases. Lymphomas and leukemias are a part of the broader group of tumors of the hematopoietic and lymphoid tissues.Risk factors for Hodgkin lymphoma include infection with Epstein–Barr virus and a history of the disease in the family. Risk factors for common types of non-Hodgkin lymphomas include autoimmune diseases, HIV/AIDS, infection with human T-lymphotropic virus, immunosuppressant medications, and some pesticides. Eating large amounts of red meat and tobacco smoking may also increase the risk. Diagnosis, if enlarged lymph nodes are present, is usually by lymph node biopsy. Blood, urine, and bone marrow testing may also be useful in the diagnosis. Medical imaging may then be done to determine if and where the cancer has spread. Lymphoma most often spreads to the lungs, liver, and brain.Treatment may involve one or more of the following: chemotherapy, radiation therapy, proton therapy, targeted therapy, and surgery. In some non-Hodgkin lymphomas, an increased amount of protein produced by the lymphoma cells causes the blood to become so thick that plasmapheresis is performed to remove the protein. Watchful waiting may be appropriate for certain types. The outcome depends on the subtype with some being curable and treatment prolonging survival in most. The five-year survival rate in the United States for all Hodgkin lymphoma subtypes is 85%, while that for non-Hodgkin lymphomas is 69%. Worldwide, lymphomas developed in 566,000 people in 2012 and caused 305,000 deaths. They make up 3–4% of all cancers, making them as a group the seventh-most common form. In children, they are the third-most common cancer. They occur more often in the developed world than the developing world.

Signs and symptoms
Lymphoma may present with certain nonspecific symptoms; if the symptoms are persistent, an evaluation to determine their cause, including possible lymphoma, should be undertaken.

Lymphadenopathy or swelling of lymph nodes, is the primary presentation in lymphoma. It is generally painless.
B symptoms (systemic symptoms) – can be associated with both Hodgkin lymphoma and non-Hodgkin lymphoma. They consist of:
Fever
Night sweats
Weight loss
Other symptoms:
Anemia, bleeding, increased susceptibility to infections
Loss of appetite or anorexia
Fatigue
Respiratory distress or dyspnea
Itching

Mouth
Asymptomatic soft swelling, which may or may not be ulcerated, is primarily seen on the tonsils, buccal mucosa, palate, gums, salivary glands, tongue, the floor of the mouth, and retromolar region.

Diagnosis
Lymphoma is definitively diagnosed by a lymph-node biopsy, meaning a partial or total excision of a lymph node examined under the microscope. This examination reveals histopathological features that may indicate lymphoma. After lymphoma is diagnosed, a variety of tests may be carried out to look for specific features characteristic of different types of lymphoma. These include:

Immunophenotyping
Flow cytometry
Fluorescence in situ hybridization testing

Classification
According to the World Health Organization (WHO), lymphoma classification should reflect in which lymphocyte population the neoplasm arises. Thus, neoplasms that arise from precursor lymphoid cells are distinguished from those that arise from mature lymphoid cells. Most mature lymphoid neoplasms comprise the non-Hodgkin lymphomas. Historically, mature histiocytic and dendritic cell (HDC) neoplasms have been considered mature lymphoid neoplasms, since these often involve lymphoid tissue.Lymphoma can also spread to the central nervous system, often around the brain in the meninges, known as lymphomatous meningitis (LM).

Hodgkin lymphoma
Hodgkin lymphoma accounts for about 15% of lymphomas. It differs from other forms of lymphomas in its prognosis and several pathological characteristics. A division into Hodgkin and non-Hodgkin lymphomas is used in several of the older classification systems. A Hodgkin lymphoma is marked by the presence of a type of cell called the Reed–Sternberg cell.

Non-Hodgkin lymphomas
Non-Hodgkin lymphomas, which are defined as being all lymphomas except Hodgkin lymphoma, are more common than Hodgkin lymphoma. A wide variety of lymphomas are in this class, and the causes, the types of cells involved, and the prognoses vary by type. The number of cases per year of non-Hodgkin lymphoma increases with age. It is further divided into several subtypes.

Epstein–Barr virus-associated lymphoproliferative diseases
Epstein–Barr virus-associated lymphoproliferative diseases are a group of benign, premalignant, and malignant diseases of lymphoid cells, i.e. B cells, T cells, NK cells, and histiocytic-dendritic cells in which one or more of these cell types is infected with the Epstein–Barr virus (EBV). The virus may be responsible for the development and/or progression of these diseases. In addition to EBV-positive Hodgkin lymphomas, the World Health Organization (2016) includes the following lymphomas, when associated with EBV infection, in this group of diseases: Burkitt lymphoma; large B cell lymphoma, not otherwise specified; diffuse large B cell lymphoma associated with chronic inflammation; fibrin-associated diffuse large B cell lymphoma; primary effusion lymphoma; plasmablastic lymphoma; extranodal NK/T cell lymphoma, nasal type; peripheral T cell lymphoma, not otherwise specified; angioimmunoblastic T cell lymphoma; follicular T cell lymphoma; and systemic T cell lymphoma of childhood.

WHO classification
The WHO classification, published in 2001 and updated in 2008, is based upon the foundations laid within the "revised European–American lymphoma classification" (REAL). This system groups lymphomas by cell type (i.e. the normal cell type that most resembles the tumor) and defining phenotypic, molecular, or cytogenetic characteristics. The five groups are shown in the table. Hodgkin lymphoma is considered separately within the WHO and preceding classifications, although it is recognized as being a tumor, albeit markedly abnormal, of lymphocytes of mature B cell lineage.Of the many forms of lymphoma, some are categorized as indolent (e.g. small lymphocytic lymphoma), compatible with a long life even without treatment, whereas other forms are aggressive (e.g. Burkitts lymphoma), causing rapid deterioration and death. However, most of the aggressive lymphomas respond well to treatment and are curable. The prognosis, therefore, depends on the correct diagnosis and classification of the disease, which is established after examination of a biopsy by a pathologist (usually a hematopathologist).

Previous classifications
Several previous classifications have been used, including Rappaport 1956, Lennert/Kiel 1974, BNLI, Working formulation (1982), and REAL (1994).
The Working Formulation of 1982 was a classification of non-Hodgkin lymphoma. It excluded the Hodgkin lymphomas and divided the remaining lymphomas into four grades (low, intermediate, high, and miscellaneous) related to prognosis, with some further subdivisions based on the size and shape of affected cells. This purely histological classification included no information about cell surface markers, or genetics, and it made no distinction between T-cell lymphomas and B-cell lymphomas. It was widely accepted at the time of its publication but is now obsolete.In 1994, the Revised European-American Lymphoma (REAL) classification applied immunophenotypic and genetic features in identifying distinct clinicopathologic entities among all the lymphomas except Hodgkin lymphoma. For coding purposes, the ICD-O (codes 9590–9999) and ICD-10 (codes C81-C96) are available.

Staging
After a diagnosis and before treatment, cancer is staged. This refers to determining if the cancer has spread, and if so, whether locally or to distant sites. Staging is reported as a grade between I (confined) and IV (spread). The stage of a lymphoma helps predict a patients prognosis and is used to help select the appropriate therapy.The Ann Arbor staging system is routinely used for staging of both HL and NHL. In this staging system, stage I represents localized disease contained within a lymph node group, II represents the presence of lymphoma in two or more lymph nodes groups, III represents spread of the lymphoma to lymph nodes groups on both sides of the diaphragm, and IV indicates spread to tissue outside the lymphatic system. Different suffixes imply the involvement of different organs, for example, S for the spleen and H for the liver. Extra-lymphatic involvement is expressed with the letter E. In addition, the presence of B symptoms (one or more of the following: unintentional loss of 10% body weight in the last 6 months, night sweats, or persistent fever of 38 °C or more) or their absence is expressed with B or A, respectively.CT scan or PET scan imaging modalities are used to stage cancer. PET scanning is advised for fluorodeoxyglucose-avid lymphomas, such as Hodgkin lymphoma, as a staging tool that can even replace bone marrow biopsy. For other lymphomas, CT scanning is recommended for staging.Age and poor performance status are other established poor prognostic factors.  This means that people who are elderly or too sick to take care of themselves are more likely to die from lymphoma than others.

Differential diagnosis
Certain lymphomas (extranodal NK/T-cell lymphoma, nasal type and type II enteropathy-associated T-cell lymphoma) can be mimicked by two benign diseases which involve the excessive proliferation of non-malignant NK cells in the GI tract, natural killer cell enteropathy, a disease wherein NK cell infiltrative lesions occur in the intestine, colon, stomach, or esophagus, and lymphomatoid gastropathy, a disease wherein these cells infiltrative lesions are limited to the stomach. These diseases do not progress to cancer, may regress spontaneously and do not respond to, and do not require, chemotherapy or other lymphoma treatments.

Treatment
Prognoses and treatments are different for HL and between all the different forms of NHL, and also depend on the grade of tumour, referring to how quickly a cancer replicates. Paradoxically, high-grade lymphomas are more readily treated and have better prognoses: Burkitt lymphoma, for example, is a high-grade tumour known to double within days, and is highly responsive to treatment.

Low-grade
Many low-grade lymphomas remain indolent (growing slowly or not at all) for many years – sometimes, for the rest of the persons life. With an indolent lymphoma, such as follicular lymphoma, watchful waiting is often the initial course of action, because monitoring is less risky and less harmful than early treatment.If a low-grade lymphoma becomes symptomatic, radiotherapy or chemotherapy are the treatments of choice.  Although these treatments do not permanently cure the lymphoma, they can alleviate the symptoms, particularly painful lymphadenopathy. People with these types of lymphoma can live near-normal lifespans, even though the disease is technically incurable.
Some centers advocate the use of single agent rituximab in the treatment of follicular lymphoma rather than the wait-and-watch approach. Watchful waiting is not a desirable strategy for everyone, as it leads to significant distress and anxiety in some people. It has been called "watch and worry".

High-grade
Treatment of some other, more aggressive, forms of lymphoma can result in a cure in the majority of cases, but the prognosis for people with a poor response to therapy is worse. Treatment for these types of lymphoma typically consists of aggressive chemotherapy, including the CHOP or R-CHOP regimen. A number of people are cured with first-line chemotherapy. Most relapses occur within the first two years, and the relapse risk drops significantly thereafter. For people who relapse, high-dose chemotherapy followed by autologous stem cell transplantation is a proven approach.The treatment of side effects is also important as they can occur due to the chemotherapy or the stem cell transplantation. It was evaluated whether mesenchymal stromal cells can be used for the treatment and prophylaxis of graft-versus-host diseases. The evidence is very uncertain about the therapeutic effect of mesenchymal stromal cells to treat graft-versus-host diseases on the all-cause mortality and complete disappear of chronic acute graft-versus-host diseases. Mesenchymal stromal cells may result in little to no difference in the all-cause mortality, relapse of malignant disease and incidence of acute and chronic graft-versus-host diseases if they are used for prophylactic reason. Moreover, it was seen that platelet transfusions for people undergoing a chemotherapy or a stem cell transplantation for the prevention of bleeding events had different effects on the number of participants with a bleeding event, the number of days on which a bleeding occurred, the mortality secondary to bleeding and the number of platelet transfusions depending on the way they were used (therapeutic, depending on a threshold, different dose schedules or prophylactic).Four chimeric antigen receptor CAR-T cell therapies are FDA-approved for non-Hodgkin lymphoma, including lisocabtagene maraleucel (for relapsed or refractory large B-cell lymphoma with two failed systemic treatments), axicabtagene ciloleucel, tisagenlecleucel (for large B-cell lymphoma), and brexucabtagene autoleucel(for mantle cell lymphoma). These therapies come with certification and other restrictions.

Hodgkin lymphoma
Hodgkin lymphoma typically is treated with radiotherapy alone, as long as it is localized.Advanced Hodgkin disease requires systemic chemotherapy, sometimes combined with radiotherapy. Chemotherapy used includes the ABVD regimen, which is commonly used in the United States. Other regimens used in the management of Hodgkin lymphoma include BEACOPP and Stanford V. Considerable controversy exists regarding the use of ABVD or BEACOPP. Briefly, both regimens are effective, but BEACOPP is associated with more toxicity. Encouragingly, a significant number of people who relapse after ABVD can still be salvaged by stem cell transplant.Scientists evaluated whether positron-emission-tomography scans between the chemotherapy cycles can be used to make assumptions about the survival. The evidence is very uncertain about the effect of negative (= good prognosis) or positive (= bad prognosis) interim PET scan results on the progression-free survival. Negative interim PET scan results may result in an increase in progression-free survival compared if the adjusted result was measured. Negative interim PET scan results probably result in a large increase in the overall survival compared to those with a positive interim PET scan result.Current research evaluated whether Nivolumab can be used for the treatment of a Hodgkins lymphoma. The evidence is very uncertain about the effect of Nivolumab for patients with a Hodgkins lymphoma on the overall survival, the quality of life, the survival without a progression, the response rate (=complete disappear) and grade 3 or 4 serious adverse events.

Palliative care
Palliative care, a specialized medical care focused on the symptoms, pain, and stress of a serious illness, is recommended by multiple national cancer treatment guidelines as an accompaniment to curative treatments for people with lymphoma. It is used to address both the direct symptoms of lymphoma and many unwanted side effects that arise from treatments. Palliative care can be especially helpful for children who develop lymphoma, helping both children and their families deal with the physical and emotional symptoms of the disease </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Exploding head syndrome and can you explain it in depth? [/INST] Exploding head syndrome (EHS) is an abnormal sensory perception during sleep in which a person experiences unreal noises that are loud and of short duration when falling asleep or waking up. The noise may be frightening, typically occurs only occasionally, and is not a serious health concern. People may also experience a flash of light. Pain is typically absent.The cause is unknown. Potential organic explanations that have been investigated but found to not be a cause include ear problems, temporal lobe seizure, nerve dysfunction, or specific genetic changes. The cause of the phenomenon is psychological in nature. Potential risk factors include psychological stress. It is classified as a sleep disorder or headache disorder. People often go undiagnosed.There is no high quality evidence to support treatment. Reassurance may be sufficient. Clomipramine and calcium channel blockers have been tried. While the frequency of the condition is not well studied, some have estimated that it occurs in about 10% of people. Women are reportedly more commonly affected. The condition was initially described at least as early as 1876. The current name came into use in 1988.

Signs and symptoms
Individuals with exploding head syndrome hear or experience loud imagined noises as they are falling asleep or waking up, have a strong, often frightened emotional reaction to the sound, and do not report significant pain; around 10% of people also experience visual disturbances like perceiving visual static, lightning, or flashes of light.  Some people may also experience heat, strange feelings in their torso, or  a feeling of electrical tinglings that ascends to the head before the auditory hallucinations occur.  With the heightened arousal, people experience distress, confusion, myoclonic jerks, tachycardia, sweating, and the sensation that feels as if they have stopped breathing and have to make a deliberate effort to breathe again.The pattern of the auditory hallucinations is variable. Some people report having a total of two or four attacks followed by a prolonged or total remission, having attacks over the course of a few weeks or months before the attacks spontaneously disappear, or the attacks may even recur irregularly every few days, weeks, or months for much of a lifetime.

Causes
The cause of EHS is unknown. A number of hypotheses have been put forth with the most common being dysfunction of the reticular formation in the brainstem responsible for transition between waking and sleeping.Other theories into causes of EHS include:

Minor seizures affecting the temporal lobe
Ear dysfunctions, including sudden shifts in middle ear components or the Eustachian tube, or a rupture of the membranous labyrinth or labyrinthine fistula
Stress and anxiety
Variable and broken sleep, associated with a decline in delta sleep
Antidepressant discontinuation syndrome
Temporary calcium channel dysfunction
PTSDExploding head syndrome was first described in the 19th century, and may have first been mentioned in the 17th century. Despite evidence of EHS through centuries, some individuals hold the belief that EHS episodes are not natural events, but are the effects of directed energy weapons which create an auditory effect.  Thus, EHS has been worked into conspiracy theories, but there is no scientific evidence that EHS has non-natural origins.

Diagnosis
Classification
Exploding head syndrome is classified under other parasomnias by the 2014 International Classification of Sleep Disorders (ICSD, 3rd.Ed.) and is an unusual type of auditory hallucination in that it occurs in people who are not fully awake.According to ICD-10 and DSM-5 EHS is classified as either other specified sleep-wake disorder (codes:780.59 or G47.8) or unspecified sleep-wake disorder (codes: 780.59 or G47.9).

Treatment
As of 2018, no clinical trials had been conducted to determine what treatments are safe and effective; a few case reports had been published describing treatment of small numbers of people (two to twelve per report) with clomipramine, flunarizine, nifedipine, topiramate, carbamazepine. Studies suggest that education and reassurance can reduce the frequency of EHS episodes.  There is some evidence that individuals with EHS rarely report episodes to medical professionals.

Epidemiology
There have not been sufficient studies to make conclusive statements about how common or who is most often affected </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 Pyelectasis 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 Suberosis 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 Benign cephalic histiocytosis 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 Splenomegaly and can you explain it in depth? [/INST] Splenomegaly is an enlargement of the spleen. The spleen usually lies in the left upper quadrant (LUQ) of the human abdomen. Splenomegaly is one of the four cardinal signs of hypersplenism which include: some reduction in number of circulating blood cells affecting granulocytes, erythrocytes or platelets in any combination; a compensatory proliferative response in the bone marrow; and the potential for correction of these abnormalities by splenectomy. Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a response to hyperfunction. It is therefore not surprising that splenomegaly is associated with any disease process that involves abnormal red blood cells being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by leukemias and lymphomas. Thus, the finding of an enlarged spleen, along with caput medusae, is an important sign of portal hypertension.

Definition
The standard system for classifying splenomegaly on radiography is:
Normal (not splenomegaly): the largest dimension is less than 11 cm
Moderate splenomegaly: the largest dimension is between 11 and 20 cm
Severe splenomegaly: the largest dimension is greater than 20 cmAlso, a cutoff of a craniocaudal height of 13 cm is also used to define splenomegaly. In addition, individual intervals have been established:

For children, the cutoffs for splenomegaly are given in this table, when measuring the greatest length of the spleen between its dome and its tip, in the coronal plane through its hilum while breathing quietly.At autopsy, splenomegaly can be defined as a spleen weight above the upper limit of the standard reference range of 230 g (8.1 oz).Splenomegaly refers strictly to spleen enlargement, and is distinct from hypersplenism, which connotes overactive function by a spleen of any size. Splenomegaly and hypersplenism should not be confused.  Each may be found separately, or they may coexist. Clinically, if a spleen is palpable (felt via external examination), it means it is enlarged as it has to undergo at least twofold enlargement to become palpable </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 Inflammatory myofibroblastic tumour and can you explain it in depth? [/INST] Inflammatory myofibroblastic tumor (IMT) is a rare neoplasm of the mesodermal cells that form the connective tissues which support virtually all of the organs and tissues of the body. IMT was formerly termed inflammatory pseudotumor. Currently, however, inflammatory pseudotumor designates a large and heterogeneous group of soft tissue tumors that includes inflammatory myofibroblastic tumor, plasma cell granuloma, xanthomatous pseudotumor, solitary mast cell granuloma, inflammatory fibrosarcoma, pseudosarcomatous myofibroblastic proliferation, myofibroblastoma, inflammatory myofibrohistiocytic proliferation, and other tumors that develop from connective tissue cells. Inflammatory pseudotumour is a generic term applied to various neoplastic and non-neoplastic tissue lesions which share a common microscopic appearance consisting of spindle cells and a prominent presence of the white blood cells that populate chronic or, less commonly, acute inflamed tissues.Inflammatory myofibroblastic tumor was initially regarded as a benign tumor that most often developed in the lung and less commonly in almost any organ system or tissue. Over time, however, IMT cases occurred in which the tumor spread into local tissues, metastasized to distal tissues, recurred after treatment, or consisted of neoplastic cells that had pro-malignant chromosome abnormalities. Consequently, the World Health Organization, 2013, and current literature commonly describe inflammatory myofibroblastic tumor as a neoplasm with intermediate malignant potential or a rarely metastasizing neoplasm. In 2020, the World Health Organization reclassified IMT as a specific tumor form in the category of intermediate (rarely metastasizing) fibroblastic and myofibroblastic tumors. In all events, IMT is a rare tumor with a reported incidence in 2009 of 150–200 cases/year in the United States.IMT lesions typically consist of, and are defined by, myofibrolastic spindle cells, i.e. specialized cells that are longer than wide, have a microscopic appearance that merges the appearances of fibroblasts and smooth muscle cells (see myofibroblast), occur in normal as well as tumor tissues, and in normal tissues are commonly designated  fibroblasts. However, the lesions in some IMF cases are dominated by sheets of epithelioid cells (which may have rounded shapes) with only a minor component of spindle cells. Tumors with these characteristics  are regarded as a subtype of IMT termed epithelioid inflammatory myofibroblastic sarcoma (EIMS).The tumors in IMT and EIMS consistently contain pro-inflammatory white blood cells and in most cases tumor cells that express highly abnormal oncogenic (cancer-causing) fusion proteins such as those that contain the active portion of anaplastic lymphoma kinase (ALK). It is not clear whether this inflammation, the genetic abnormalities, or both contribute to the development of IMT but drugs blocking the activities of the fusion proteins made by these genetic abnormalities may be useful in treating the disease.

Signs and symptoms
IMT was regarded as a tumor that occurs in children or young adults and presented in the lung, mesentery, greater omentum or, less commonly, heart, liver, spleen, pancreas, colon, small intestine, spermatic cord, prostate, uterus, eye orbit, peripheral or central nervous system nerves, brain meninges, spinal cord, or other sites. However, a more recent retrospective study of 92 patients accumulated by the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute found the mean age of disease onset was 47.4 years with peak occurrences at 0 to 4, 36 to 40, and >50 years old; middle-aged individuals (41 to 64 years) represented 1/3 of all cases. In this study, the commonest sites of tumor occurrence were the lower limb and hip (22% of cases), upper limb and shoulder (12% of cases), and head, face, and neck (9% of cases). Another recent study of 25 patients found the commonest sites of IMT were the abdomen (40% of cases) and lung/thoracic wall (32% of cases). Individual IMT cases are also reported to present in the urinary bladder, anal canal, and parameningeal spaces (i.e. sites adjacent to the meninges such as the nasopharynx, middle ear, paranasal sinuses, infratemporal fossa and pterygopalatine fossa). Apparently, the age and organ/tissue distribution of IMT various with the patient population examined: in general it can present in individuals of almost any age and in almost any organ or tissue site. IMT most commonly presents as a tumor localized to a single site but may be associated with distal metastases in up to 5% of all cases or up to 10% of cases in which the tumor cells express an ALK fusion protein. The tumors range in size from 1–25 cm (average 6.5 cm) with two-thirds being 1.5–6.5 cm. In rare cases, the tumors have spontaneously regressed.Individuals with IMT present with a wide range of symptoms (e.g. pain, swelling, a mass, organ dysfunction, etc.) depending on the tumor location(s). Up to 1/3 of these individuals have symptoms of systemic inflammation such as fever, chills, night sweats, and weight loss. Rare cases of IMT have developed in individuals with: a) organizing pneumonia; b) infection by Mycobacterium avium intracellulare or Corynebacterium equi (pneumonia-causing bacteria); Campylobacter jejuni (causes gastroenteritis); Lysinibacillus sphaericus (previously termed Bacillus sphaericus, a rare cause of lung infections and sepsis); Coxiella burneti (causes Q fever); Epstein–Barr virus (causes infectious mononucleosis and Epstein–Barr virus-associated lymphoproliferative malignant diseases); and E. coli-related occlusive phlebitis of intrahepatic veins; or c) previous abdominal surgery; trauma; ventriculoperitoneal shunt in the brain; radiation therapy; and corticosteroid usage. The relationship (i.e. cause or merely association) of these disease relationships to IMT is unknown.

Molecular abnormalities
The neoplastic cells in 50–60% of IMT and all cases of EIMS express an abnormal ALK protein made by a somatic recombination in the ALK gene. ALK, i.e. anaplastic lymphoma kinase (also termed protein kinase B), is produced by the ALK gene. In IMT, the ALK gene has merged with a gene located at another site on the same or different chromosome to form a chimeric gene consisting of a part of the new gene and a part of the ALK gene coding for ALKs activity. This chimeric gene overproduces a fusion protein with excessive ALK activity. ALK is a serine/threonine-specific protein kinase that directly or indirectly stimulates PI3K/AKT/mTOR, Ras GTPase, ERKs, Janus kinase, STAT proteins, and other cell signaling elements. Activation of these elements stimulates cell growth, proliferation, survival, and other tumor-promoting behaviors. As an example of this chromosomal translocation, the ALK gene located on the short or "p" arm of chromosome 2 at position 23 (notated as 2p23) merges with the CLTC gene on the long, i.e. "q" arm of chromosome 17 at position 13 (notated 17q23) to form a chimeric gene notated as t(2;17)(p23;q23). This chimeric gene makes a CLTC-ALK fusion protein with uncontrolled ALK serine/threonine-specific protein kinase activity. Other genes that fuse with AKT found in IMT include: TFG, DCTN1, EML4, TPM3, TPM4, ATIC RANBP2 (most if not all RAMB2-ALK chimeric genes occur in the EMIS form of IMT), CARS1, and SEC31L1. IMT cases may express other chimeric genes in which the active parts of ROS1 (found in 10% of IFT cases and coding for a tyrosine kinase which promotes cell growth), PDGFRB (coding for a protein that may promote the development of cancer), and NTRK (coding for a receptor tyrosine kinase that may promote the development of cancer) merge with other genes. The fusion protein products of these chimeric genes, like those of ALK fusion proteins, are overproduced, overactive, and thereby may contribute to the development of IMT.

Diagnosis
Histopathologic examination of the tumors in IMT generally reveals myofibroblastic spindle cell sheets in a myxoid background (i.e. a background matrix containing gelatinous mucopolysaccharides and non-sulfated glycosaminoglycans); the matrix also contains inflammatory cells, particularly plasma cells and lymphocytes occasionally mixed with eosinophils and neutrophils. The epithelioid inflammatory myofibroblastic sarcoma subtype of IMT shows sheets of epithelioid to round cells within a myxoid (i.e. appears blue or purple compared to the normal red appearance of connective tissue when appropriately H&E stained and examined under the microscope), collagenous, or mixed myxoid-collagenous matrix, <5% spindle cells, and an inflammatory cell infiltrate that in most cases consists predominantly of neutrophils or, less often, small lymphocytes or eosinophils; plasma cells occur in only a minority of EIMS cases. The neoplastic cells in the tumors of 50% to 60% of IMT cases and 100% of EIMS cases express an ALK fusion protein. Other genetic abnormalities occur in these cells. Testing for the presence of the ALK fusion protein and other genetic abnormalities (see next section) can help diagnose IMT.

Treatment
Many sources recommend that localized IMT be treated with total resection of all tumorous tissues. Localized tumor recurrences may likewise be treated by total resection. There is little support for adding radiation or systemic chemotherapy to this regimen. Tumors that are not resectable, occur in inaccessible sites, are multifocal, or have metastasized are treated with aggressive therapeutic regimens.In one retrospective study, 59 patients (all <25 years old) with IMT where treated with surgery. 31 had no residual disease post-surgery; 4 of these patients had local relapses, 3 of whom were again treated surgically and 1 with surgery plus chemotherapy. Nineteen had microscopic residual disease post-surgery. Post-surgery, 6 of these patients were treated with high-dose corticosteroids; 5 with vinblastine + methotrexate chemotherapy; 3 with inhibitors of ALK; 2 with vinorelbine + low-dose cycloheximide or Ifosfamide-based chemotherapy; and 1 with cyclophosphamide + vinchristine + actinomycin D chemotherapy. Of these 19 patients, 4 had complete responses, 8 partial responses, 5 stable disease, and 2 progressive disease. Nine patients had macroscopic disease post-surgery; 5 of these patients received vincristine + methotrexate; 2 received ALK inhibitors; and 1 each received either high-dose corticosteroids or Ifosfamide-based chemotherapy. Of these 9 patients, none had complete responses; 6 had partial responses; 1 had steady disease; and 2 had progressive disease. There were no deaths among the 59 patients. The various drug regimens showed little differences in effectiveness although patients treated with ALK inhibitors trended to have longer response times. Another retrospective study evaluated the response of 17 patients (aged 22–46 years; median age 32 years) with advanced disease to Adriamycin-based chemotherapy regimens, i.e. Adriamycin alone, Adriamycin + Ifosfamide, or Adriamicin + other chemotherapy drugs. No patients had a complete response, 8 patients had partial responses, 4 patients had steady disease, and 5 patients had progressive disease. Progression-free survival and overall survival times for the group were 6.6 and 21.2 months, respectively. The study also evaluated 9 patients (aged 12–31 years, median age 16) treated with methotrexate + vinblastine, methotrexate + vinorelbine, or vinblastine + vinorelbine; 2 patients attained complete responses, 3 attained partial responses, 2 had steady disease, and 2 had progressive disease; this groups progression-free time was not reached while its overall survival time was 83.4 months. The study concluded that the Adriamycin-based and methotrexate/vinblastine/vinorelbine regimens have a high degree of activity in IMT. Due to the low numbers of patients evaluated, no conclusions could be made on which regimen(s) were most effective.In addition to the report that compared the effect of ALK-inhibitors to other therapy regimens detailed in the previous paragraph, several reports have focused primarily on small numbers of IMT patients treated with an ALK inhibitor. The European Organisation for Research and Treatment of Cancer evaluated the effect of the ALK-inhibitor, crizotinib, on 12 ALK-positive IMT adults who had persistent and/or metastatic disease following surgical and/or drug treatment: 2 patients had complete responses, 4 had partial responses, 5 had steady disease, and none had progressive disease; 9 of these patients had at least 1 year of progression-free survival but one patient died of the disease </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bile and can you explain it in depth? [/INST] Bile (from Latin bilis), or gall, is a dark-green-to-yellowish-brown fluid produced by the liver of most vertebrates that aids the digestion of lipids in the small intestine. In humans, bile is produced continuously by the liver (liver bile) and stored and concentrated in the gallbladder. After eating, this stored bile is discharged into the duodenum.The composition of hepatic bile is (97–98)% water, 0.7% bile salts, 0.2% bilirubin, 0.51% fats (cholesterol, fatty acids, and lecithin), and 200 meq/L inorganic salts. The two main pigments of bile are bilirubin, which is yellow, and its oxidised form biliverdin, which is green. When mixed, they are responsible for the brown color of feces. About 400 to 800 millilitres of bile is produced per day in adult human beings.

Function
Bile or gall acts to some extent as a surfactant, helping to emulsify the lipids in food. Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic sides facing outwards. The hydrophilic sides are negatively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles. Ordinarily, the micelles in the duodenum have a diameter around 1–50 μm in humans.The dispersion of food fat into micelles provides a greatly increased surface area for the action of the enzyme pancreatic lipase, which digests the triglycerides, and is able to reach the fatty core through gaps between the bile salts. A triglyceride is broken down into two fatty acids and a monoglyceride, which are absorbed by the villi on the intestine walls. After being transferred across the intestinal membrane, the fatty acids reform into triglycerides (re-esterified), before being absorbed into the lymphatic system through lacteals. Without bile salts, most of the lipids in food would be excreted in feces, undigested.Since bile increases the absorption of fats, it is an important part of the absorption of the fat-soluble substances, such as the vitamins A, D, E, and K.Besides its digestive function, bile serves also as the route of excretion for bilirubin, a byproduct of red blood cells recycled by the liver. Bilirubin derives from hemoglobin by glucuronidation.
Bile tends to be alkaline on average. The pH of common duct bile (7.50 to 8.05) is higher than that of the corresponding gallbladder bile (6.80 to 7.65). Bile in the gallbladder becomes more acidic the longer a person goes without eating, though resting slows this fall in pH. As an alkali, it also has the function of neutralizing excess stomach acid before it enters the duodenum, the first section of the small intestine. Bile salts also act as bactericides, destroying many of the microbes that may be present in the food.

Clinical significance
In the absence of bile, fats become indigestible and are instead excreted in feces, a condition called steatorrhea. Feces lack their characteristic brown color and instead are white or gray, and greasy. Steatorrhea can lead to deficiencies in essential fatty acids and fat-soluble vitamins. In addition, past the small intestine (which is normally responsible for absorbing fat from food) the gastrointestinal tract and gut flora are not adapted to processing fats, leading to problems in the large intestine.The cholesterol contained in bile will occasionally accrete into lumps in the gallbladder, forming gallstones. Cholesterol gallstones are generally treated through surgical removal of the gallbladder. However, they can sometimes be dissolved by increasing the concentration of certain naturally occurring bile acids, such as chenodeoxycholic acid and ursodeoxycholic acid.On an empty stomach – after repeated vomiting, for example – a persons vomit may be green or dark yellow, and very bitter. The bitter and greenish component may be bile or normal digestive juices originating in the stomach. Bile may be forced into the stomach secondary to a weakened valve (pylorus), the presence of certain drugs including alcohol, or powerful muscular contractions and duodenal spasms. This is known as biliary reflux.

Obstruction
Biliary obstruction refers to a condition when bile ducts which deliver bile from the gallbladder or liver to the duodenum become obstructed. The blockage of bile might cause a buildup of bilirubin in the bloodstream which can result in jaundice. There are several potential causes for biliary obstruction including gallstones, cancer, trauma, choledochal cysts, or other benign causes of bile duct narrowing. The most common cause of bile duct obstruction is when gallstone(s) are dislodged from the gallbladder into the cystic duct or common bile duct resulting in a blockage. A blockage of the gallbladder or cystic duct may cause cholecystitis. If the blockage is beyond the confluence of the pancreatic duct, this may cause gallstone pancreatitis. In some instances of biliary obstruction, the bile may become infected by bacteria resulting in ascending cholangitis.

Society and culture
In medical theories prevalent in the West from Classical Antiquity to the Middle Ages, the bodys health depended on the equilibrium of four "humors", or vital fluids, two of which related to bile: blood, phlegm, "yellow bile" (choler), and "black bile". These "humors" are believed to have their roots in the appearance of a blood sedimentation test made in open air, which exhibits a dark clot at the bottom ("black bile"), a layer of unclotted erythrocytes ("blood"), a layer of white blood cells ("phlegm") and a layer of clear yellow serum ("yellow bile").Excesses of black bile and yellow bile were thought to produce depression and aggression, respectively, and the Greek names for them gave rise to the English words cholera (from Greek χολή kholē, "bile") and melancholia. In the former of those senses, the same theories explain the derivation of the English word bilious from bile, the meaning of gall in English as "exasperation" or "impudence", and the Latin word cholera, derived from the Greek kholé, which was passed along into some Romance languages as words connoting anger, such as colère (French) and cólera (Spanish).

Soap
Soap can be mixed with bile from mammals, such as ox gall. This mixture, called bile soap or gall soap, can be applied to textiles a few hours before washing as a traditional and effective method for removing various kinds of tough stains.

Food
"Pinapaitan" is a dish in Philippine cuisine that uses bile as flavoring. Other areas where bile is commonly used as a cooking ingredient include Laos and northern parts of Thailand.

Bears
In regions where bile products are a popular ingredient in traditional medicine, the use of bears in bile-farming has been widespread. This practice has been condemned by activists, and some pharmaceutical companies have developed synthetic (non-ursine) alternatives.

Principal acids
See also
Bile acid sequestrant
Enterohepatic circulation
Intestinal juice

References
Seleem HM, Nada AS, Naguib MA, Abdelmaksoud OR, El-Gazzarah AR. Serum immunoglobulin G4 in patients with nonmalignant common bile duct stricture. Menoufia Med J [serial online] 2021 [cited 2022 Jan 21];34:1275-83. Available from: http://www.mmj.eg.net/text.asp?2021/34/4/1275/333263

Bibliography
Bowen, R. (2001-11-23). "Secretion of Bile and the Role of Bile Acids In Digestion". Colorado State Hypertextbook article on Bile </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 Enthesopathy and can you explain it in depth? [/INST] An enthesopathy refers to a disorder involving the attachment of a tendon or ligament to a bone. This site of attachment is known as the enthesis (pl. entheses).
If the condition is known to be inflammatory, it can more precisely be called an enthesitis.

Forms
Enthesopathy can occur at the shoulder, elbow, wrist, carpus, hip, knee, ankle, tarsus, or heel bone, among other regions. Enthesopathies may take the form of spondyloarthropathies (joint diseases of the spine) such as ankylosing spondylitis, plantar fasciitis, and Achilles tendinitis. Further examples include:
Adhesive capsulitis of shoulder
Rotator cuff syndrome of shoulder and allied disorders
Periarthritis of shoulder
Scapulohumeral fibrositis
Synovitis of hand or wrist
Periarthritis of wrist
Gluteal tendinitis
Iliac crest spur
Psoas tendinitis
Trochanteric tendinitis

Diagnosis
Mainly by clinical examination and provocative tests by counter acting the muscle action.

Treatment
The natural history of the two most common enthesopathies (plantar fasciitis and lateral epicondylitis-both mislabeled as inflammatory) is resolution over a period of about 1 year without treatment </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 Erythrasma and can you explain it in depth? [/INST] Erythrasma is a superficial skin infection that causes brown, scaly skin patches. It is caused by Corynebacterium minutissimum bacteria, a normal part of skin flora (the microorganisms that are normally present on the skin).
There are two types of erythrasma: generalized and interdigital. Interdigital is the most common bacterial infection of the feet and normally does not show any symptoms. Not only is this an aesthetically unappealing condition, but there is evidence to support that disciform erythrasma can be an early sign of type 2 diabetes mellitus. The generalized erythrasma is most commonly seen in type 2 diabetes mellitus where the lesions go beyond the areas of the body where skin is rubbing together. It is prevalent among diabetics and the obese, and in warm climates; it is worsened by wearing occlusive clothing.
The presence of erythrasma is approximately 4% and is more likely to be found in the subtropical and tropical areas compared to the rest of the world. It is found more commonly in African Americans due to the darker skin and  even though both sexes are affected, it is usually found more frequently in males for the thigh and leg regions. A great contributor to this infection is a weakened immune system which comes with aging, therefore the elderly are more susceptible to this disease than the young; this does not mean the young cannot be affected. The epidemiology background of erythrasma remains partially unsolved.

Signs and symptoms
Lesions of erythrasma are initially pink, but progress quickly to become brown and scaly (as skin starts to shed), which are sharply distinguished. Erythrasmic patches are typically found in moist and intertriginous areas (skin fold areas—e.g. armpit, groin, under breast) and can be well-defined patches or irregular. The most common is interdigital erythrasma, which is of the foot, and may present as a scaling, fissuring, and chronic non-resolving break down of the toe web interspaces. The slightly webbed spaces between toes, or other body region skin folds, make it difficult to distinguish from various Tinea. The patient is commonly otherwise asymptomatic.

Cause
Erythrasma is caused by Corynebacterium minutissimum. This bacterium tends to thrive in mostly moist and warm environments. Great contributors are poor hygiene, obesity, hyperhidrosis (excessive sweating), aging, diabetes mellitus, and a poorly functioning immune system. Only some of the causable factors can be modified to reduce risk. Hygiene can be improved, along with avoiding moist and warm environments.

Diagnosis
The differential diagnosis for erythrasma includes psoriasis, candidiasis, dermatophytosis, and intertrigo. The diagnosis can be made on the clinical picture alone. However, a simple side-room investigation with a Woods lamp is additionally useful in diagnosing erythrasma. The ultraviolet light of a Woods lamp causes the organism to fluoresce a characteristic coral red color, differentiating it from other skin conditions such as tinea versicolor, which may fluoresce a copper-orange color. Another route to differentiate erythrasma would be through bacterial and mycology related cultures to compare/contrast normal results to these findings. These are both non-invasive routes.
Erythrasma is often mistakenly diagnosed as dermatophytic infection which is a fungal infection and not a bacterial infection. The difference here is that fungi are multicellular and eukaryotes while bacteria are single celled prokaryotes. This is vital to differentiate because of the way they reproduce will indicate how the infection will spread throughout the human body.

Mechanism
Corynebacterium minutissimum is the bacterium that causes this infection, often club shaped rods when observed under a microscope following a staining procedure, which is a result of snapping division which makes them look like a picket fence. This bacterium is gram positive, which means it has a very thick cell wall that cannot be easily penetrated. Electron microscopy confirms the bacterial nature of erythrasma, it shows decreased electron density in keratinized cells at the sites of proliferation. This means that the bacterium causes erythrasma by breaking down keratin Fibrils in the skin. Corynebacterium minutissimum consumes carbohydrates such as glucose, dextrose, sucrose, maltose, and mannitol.Erythrasma manifests mostly in slightly webbed spaces between toes (or other body region skin folds like the thighs/groin area) in warm atmospheric regions, and is more prevalent in dark skinned humans. As a person ages, they are more susceptible to this infection. This bacterium is not only found in warm atmospheric regions, but also warm and sweaty parts of the human body. Corynebacterium minutissimum survives the best here due to the encouraged fungal growth in these regions and allows it to replicate. It is more prevalent in African Americans due to their skin pigmentation.

Treatment
Initial treatments for minor erythrasma can begin with keeping the area clean and dry and with antibacterial soaps. The next level is treated with topical fusidic acid and an antibacterial solution such as clindamycin to eradicate the bacteria. For aggressive types of erythrasma, oral antibiotics such as macrolides (erythromycin or azithromycin) can be prescribed </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 Critical illness polyneuropathy and can you explain it in depth? [/INST] Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are overlapping syndromes of diffuse, symmetric, flaccid muscle weakness occurring in critically ill patients and involving all extremities and the diaphragm with relative sparing of the cranial nerves. CIP and CIM have similar symptoms and presentations and are often distinguished largely on the basis of specialized electrophysiologic testing or muscle and nerve biopsy. The causes of CIP and CIM are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome. Corticosteroids and neuromuscular blocking agents, which are widely used in intensive care, may contribute to the development of CIP and CIM, as may elevations in blood sugar, which frequently occur in critically ill patients.CIP was first described by Charles F. Bolton in a series of five patients.Combined CIP and CIM was first described by Nicola Latronico in a series of 24 patients.

Signs and symptoms
People with CIP/CIM have diffuse, symmetric, flaccid muscle weakness. CIP/CIM typically develops in the setting of a critical illness and immobilization, so patients with CIP/CIM are often receiving treatment in the intensive care unit (ICU).Weakness (motor deficits) occurs in generalized fashion, rather than beginning in one region of the body and spreading.  Limb and respiratory (diaphragm) muscles are especially affected.  The muscles of the face are usually spared, but in rare cases, the eye muscles may be weakened, leading to ophthalmoplegia.Respiratory difficulties can be caused by atrophy of the muscles between the ribs (intercostals), atrophy of the diaphragm muscle, and degeneration of the nerve that stimulates the diaphragm (phrenic nerve).  This can prolong the time it takes to wean a person off of a breathing machine (mechanical ventilation) by as much as 7 – 13 days.Deep tendon reflexes may be lost or diminished, and there may be bilateral symmetric flaccid paralysis of the arms and legs. The nervous system manifestations are typically limited to peripheral nerves, as the central nervous system is usually unaffected.

Cause
The causes of CIP and CIM are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome.

Pathology
Nerve biopsy would show axonal neuropathy, but it is no longer indicated. A muscle biopsy of critical illness myopathy would show selective loss of thick filaments in muscle, demonstrating the loss of myosin and the presence of muscle cell death (necrosis). When muscles lose stimulation from neurons, they can undergo degeneration. However, when critical illness myopathy occurs, it is not solely due to loss of innervation of the muscle.  With critical illness myopathy, no other cause of the muscle degeneration can be found.Unlike Guillain Barre Syndrome, another neurological disorder that causes weakness, patients with critical illness polyneuropathy do not have loss of the myelin sheath that normally surrounds neurons (demyelination).

Diagnosis
CIP and CIM are a major cause of ICU-acquired weakness (ICUAW). Current guidelines recommend a clinical diagnosis of ICUAW, made by manually testing the muscle strength with the use of the Medical Research Council (MRC) sum score or handgrip dynamometry.CIP/CIM is often not identified until a patient is unable to be successfully weaned from a mechanical ventilator. Early detection of the condition is difficult, because these patients are often sedated and intubated, and thus unable to cooperate with a thorough neuromuscular physical examination. The use of conventional nerve conduction studies is time-consuming and requires specialized personnel; however, simplified electrophysiologic tests can be used as screening tools in the critically ill to confirm or exclude CIP/CIM. The peroneal nerve test is a validated, high-sensitivity, minimally invasive, non-volitional and quick diagnostic test which can accurately exclude CIP/CIM if the result is normal. Moreover, patients with disuse atrophy and muscle deconditioning have normal electrophysiological tests even if muscle strength is severely reduced Hence, these tests are important to define the cause of muscle weakness and can be helpful to refine the prognosis.

Laboratory values
The serum creatine phosphokinase (CPK) can be mildly elevated.  While the CPK is often a good marker for damage to muscle tissue, it is not a helpful marker in CIP/CIM, because CIP/CIM is a gradual process and does not usually involve significant muscle cell death (necrosis).  Also, even if necrosis is present, it may be brief and is therefore easily missed.  If a lumbar puncture (spinal tap) is performed, the protein level in the cerebral spinal fluid would be normal.

Screening
Initial screening for CIP/CIM may be performed using an objective scoring system for muscle strength. The Medical Research Council (MRC) score is one such tool, and sometimes used to help identify CIP/CIM patients in research studies.  The MRC score involves assessing strength in 3 muscle groups in the right and left sides of both the upper and lower extremities.  Each muscle tested is given a score of 0–5, giving a total possible score of 60.  An MRC score less than 48 is suggestive of CIP/CIM.  However, the tool requires that patients be awake and cooperative, which is often not the case.  Also, the screening tool is non-specific, because it does not identify the cause a persons muscle weakness.Once weakness is detected, the evaluation of muscle strength should be repeated several times.  If the weakness persists, then a muscle biopsy, a nerve conduction study (electrophysiological studies), or both should be performed.

Prognosis
CIP/CIM can lead to difficulty weaning a person from a mechanical ventilator, and is associated with increased length of stay in the ICU and increased mortality (death).  It can lead to impaired rehabilitation.  Since CIP/CIM can lead to decreased mobility (movement), it increases the risk of pneumonia, deep vein thrombosis, and pulmonary embolism.
Critically ill people that are in a coma can become completely paralyzed from CIP/CIM. Improvement usually occurs in weeks to months, as the innervation to the muscles are restored. About half of patients recover fully.

Epidemiology
While the exact incidence is unknown, estimates range from 33 - 57 percent of patients staying in the ICU for longer than 7 days. More exact data is difficult to obtain, since variation exists in defining the condition.
The three main risk factors for CIP and CIM are sepsis and systemic inflammatory response syndrome (SIRS), and multi-organ failure.  Reported rates of CIP/CIM in people with sepsis and SIRS range from 68 to 100 percent </s>