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For example, ICD-10 classifies " vasculitis limited to skin " with skin conditions (under "L"), and "necrotizing vasculopathies" (corresponding to systemic vasculitis ) with musculoskeletal system and connective tissue conditions (under "M"). Arteritis/phlebitis on their own are classified with circulatory conditions (under "I"). ... Retrieved 19 August 2015 . ^ Millet A, Pederzoli-Ribeil M, Guillevin L, Witko-Sarsat V, Mouthon L (2013) Antineutrophil cytoplasmic antibody-associated vasculitides: is it time to split up the group? ... PMID 25337761 . ^ Dellavedova L, Carletto M, Faggioli P, Sciascera A, Del Sole A, Mazzone A, Maffioli LS (2015).
Vasculitis represents a clinically heterogenous group of diseases of multifactorial etiology characterized by inflammation of either large-sized vessels (large-vessel vasculitis, e.g. Giant-cell arteritis and Takayasu arteritis; see these terms), medium-sized vessels (medium-vessel vasculitis e.g. polyarteritis nodosa and Kawasaki disease; see these terms), or small-sized vessels (small-vessel vasculitis, e.g. granulomatosis with polyangiitis, microscopic polyangiitis, immunoglobulin A vasculitis, and cutaneous leukocytoclastic angiitis; see these terms). Vasculitis occurs at any age, may be acute or chronic, and manifests with general symptoms such as fever, weight loss and fatigue, as well as more specific clinical signs depending on the type of vessels and organs affected. The degree of severity is variable, ranging from life or sight threatening disease (e.g. Behçet disease, see this term) to relatively minor skin disease.
Overview Vasculitis involves inflammation of the blood vessels. The inflammation can cause the walls of the blood vessels to thicken, which reduces the width of the passageway through the vessel. If blood flow is restricted, it can result in organ and tissue damage. There are many types of vasculitis, and most of them are rare. Vasculitis might affect just one organ, or several. The condition can be short term or long lasting. Vasculitis can affect anyone, though some types are more common among certain age groups. Depending on the type you have, you may improve without treatment. Most types require medications to control the inflammation and prevent flare-ups.
. ^ a b McCue ME, Valberg SJ, Jackson M, Borgia L, Lucio M, Mickelson JR (January 2009). ... J Vet Intern Med . 18 (6): 887–894. doi : 10.1111/j.1939-1676.2004.tb02637.x . ^ Corte FD, Valberg SJ, Mickelson JR, Hower-Moritz M (July 1999). "Blood glucose clearance after feeding and exercise in polysaccharide storage myopathy" .
. ^ Metherell LA, Naville D, Halaby G, Begeot M, Huebner A, Nürnberg G, Nürnberg P, Green J, Tomlinson JW, Krone NP, Lin L, Racine M, Berney DM, Achermann JC, Arlt W, Clark AJ (October 2009). ... Fertil Steril . 91 (3): 934.e15–8. doi : 10.1016/j.fertnstert.2008.07.1770 . PMID 18829024 . ^ Abdulhadi-Atwan M, Jean A, Chung WK, Meir K, Ben Neriah Z, Stratigopoulos G, Oberfield SE, Fennoy I, Hirsch HJ, Bhangoo A, Ten S, Lerer I, Zangen DH (October 2007).
A disorder that is one of the most severe forms of congenital adrenal hyperplasia (CAH) characterized by severe adrenal insufficiency and sex reversal in males. Epidemiology The prevalence is unknown but it is extremely rare and is more common in people of Japanese, Korean and Palestinian ancestry. Clinical description Age of onset typically occurs in the antenatal period but congenital anomalies are typically seen in the perinatal period. Boys are not virilized and demonstrate a complete girl phenotype. The external genitalia of girls are normal. Hypoglycemic seizures, vomiting or symptoms of dehydration are common manifestations in the first few weeks of life and can be life threatening.
.; Scarpa, Aldo; Sundin, Anders; Perren, Aurel; Gross, David; O’Connor, Juan M. (2006). "Gastrinoma (Duodenal and Pancreatic)" . ... Saunders, p. 473, ISBN 978-1-4160-4059-0 , retrieved 2020-12-18 ^ a b Falconi, M.; Eriksson, B.; Kaltsas, G.; Bartsch, D. K.; Capdevila, J.; Caplin, M.; Kos-Kudla, B.; Kwekkeboom, D.; Rindi, G.; Klöppel, G.; Reed, N. (2016).
Zollinger-Ellison syndrome (ZES) is characterized by severe peptic disease (ulcers/esophageal disease) caused by hypergastrinemia secondary to a gastrinoma resulting in increased gastric acid secretion. Epidemiology Annual incidence is estimated at 1-2 cases per million. The condition is slightly more common in females than males (sex ratio of 1.3:1). Clinical description ZES is usually diagnosed in the fifth decade of life. Abdominal pain (typically in the upper abdomen) and diarrhea are the most frequent manifestations. Heartburn is often present (44% of cases). Other signs include nausea, vomiting, malabsorption, and weight loss.
Zollinger-Ellison syndrome (ZES) is a condition in which tumors called gastrinomas in the pancreas and duodenum (part of the small intestine) cause high levels of the hormone gastrin in the blood. High levels of gastrin then cause production of too much stomach acid. Signs and symptoms may include abdominal pain, peptic ulcers , vomiting blood, and diarrhea. The tumors are sometimes cancerous and may spread to other areas of the body. In most cases, the cause of ZES is unknown. However, about 25-30% of gastrinomas are caused by an inherited condition called multiple endocrine neoplasia type 1 (MEN1) .
Massey University . ^ Mathew, R. J.; Weinman, M. L.; Semchuk, K. M.; Levin, B. L. ... PMID 15178463 . ^ Taylor, Joanne E.; Sullman, Mark J. M. (May 2009). "What does the Driving and Riding Avoidance Scale (DRAS) measure?".
Anti-itch drug Toxin List of cutaneous conditions References [ edit ] ^ Gross, Michael; Baer, Harold; Fales, Henry M (1975). "Urushiols of poisonous anacardiaceae". ... ISBN 978-0-7234-0839-0 . ^ Kalergis, Alexis M; López, Carolina B; Becker, Maria I; Diaz, Marisol I; Sein, Jorge; Garbarino, Juan A; De Ioannes, Alfredo E (Jan 1997). ... Retrieved 2010-06-04 . ^ Stibich, A. S.; Yagan, M.; Sharma, V.; Herndon, B. & Montgomery, C. (2001).
ISSN 0091-7370 . PMID 9098513 . ^ Harada, M. (1995-01-01). "Minamata disease: methylmercury poisoning in Japan caused by environmental pollution". ... Retrieved 2016-04-14 . ^ Braun, Joe M.; Yolton, Kimberly; Dietrich, Kim N.; Hornung, Richard; Ye, Xiaoyun; Calafat, Antonia M.; Lanphear, Bruce P. (2009-12-01).
These hip dislocations are typically posterior, and a direct result of motor vehicle traffic collisions. [4] Other animals [ edit ] Main article: Dislocation of hip in animals References [ edit ] ^ a b c d e f g h i j k l m n "Hip Dislocation" . AAOS . June 2014 . ... Retrieved 1 March 2015 . ^ Persiani P, Molayem I, Calistri A, Rosi S, Bove M, Villani C (October 2008). "Hip subluxation and dislocation in cerebral palsy: outcome of bone surgery in 21 hips" (PDF) . ... Lea's son & co. ^ a b c d e f g h i j k l m Hip Dislocation Treatment & Management at eMedicine External links [ edit ] Classification D ICD - 10 : S73.0 , Q65.0 - Q65.2 ICD - 9-CM : 835 OMIM : 142700 MeSH : D006618 DiseasesDB : 3056 External resources eMedicine : emerg/144 v t e Congenital malformations and deformations of musculoskeletal system / musculoskeletal abnormality Appendicular limb / dysmelia Arms clavicle / shoulder Cleidocranial dysostosis Sprengel's deformity Wallis–Zieff–Goldblatt syndrome hand deformity Madelung's deformity Clinodactyly Oligodactyly Polydactyly Leg hip Hip dislocation / Hip dysplasia Upington disease Coxa valga Coxa vara knee Genu valgum Genu varum Genu recurvatum Discoid meniscus Congenital patellar dislocation Congenital knee dislocation foot deformity varus Club foot Pigeon toe valgus Flat feet Pes cavus Rocker bottom foot Hammer toe Either / both fingers and toes Polydactyly / Syndactyly Webbed toes Arachnodactyly Cenani–Lenz syndactylism Ectrodactyly Brachydactyly Stub thumb reduction deficits / limb Acheiropodia Ectromelia Phocomelia Amelia Hemimelia multiple joints Arthrogryposis Larsen syndrome RAPADILINO syndrome Axial Skull and face Craniosynostosis Scaphocephaly Oxycephaly Trigonocephaly Craniofacial dysostosis Crouzon syndrome Hypertelorism Hallermann–Streiff syndrome Treacher Collins syndrome other Macrocephaly Platybasia Craniodiaphyseal dysplasia Dolichocephaly Greig cephalopolysyndactyly syndrome Plagiocephaly Saddle nose Vertebral column Spinal curvature Scoliosis Klippel–Feil syndrome Spondylolisthesis Spina bifida occulta Sacralization Thoracic skeleton ribs : Cervical Bifid sternum : Pectus excavatum Pectus carinatum v t e Dislocations / subluxations , sprains and strains Joints and ligaments Head and neck Dislocation of jaw Whiplash Shoulder and upper arm GH ( Dislocated shoulder ) AC ( Separated shoulder ) ALPSA lesion SLAP tear Bankart lesion Elbow and forearm Pulled elbow Gamekeeper's thumb Hip and thigh Hip dislocation Knee and leg Tear of meniscus Anterior cruciate ligament injury Unhappy triad Patellar dislocation Knee dislocation Ankle and foot Sprained ankle ( High ankle sprain ) Turf toe Muscles and tendons Shoulder and upper arm Rotator cuff tear Hip and thigh Pulled hamstring Knee and leg Patellar tendon rupture Achilles tendon rupture Shin splints
. ^ a b c d [1] at NLM Genetics Home Reference ^ Tassabehji M, Fang ZM, Hilton EN, et al. (August 2008). ... PMID 12188968 . ^ Papanastassiou ID, Baaj AA, Dakwar E, Eleraky M, Vrionis FD (March 2011). "Failure of cervical arthroplasty in a patient with adjacent segment disease associated with Klippel-Feil syndrome" . ... PMID 9875048 . ^ Angeli, E., Wagner, J., Lawrick, E., Moore, K., Anderson, M., Soderland, L., & Brizee, A. (2010, May 5).
A number sign (#) is used with this entry because of evidence that Klippel-Feil syndrome-2 (KFS2) is caused by homozygous mutation in the MEOX1 gene (600147) on chromosome 17q21. Description Klippel-Feil syndrome (KFS) is a congenital anomaly characterized by a defect in the formation or segmentation of the cervical vertebrae, resulting in a fused appearance. The clinical triad consists of short neck, low posterior hairline, and limited neck movement, although less than 50% of patients demonstrate all 3 clinical features (Tracy et al., 2004). Clarke et al. (1998) proposed a classification system for KFS in which an autosomal recessive form is characterized by the most rostral fusion at C1 and the presence of severe associated anomalies, including short neck, cardiac defects, and craniofacial anomalies. For a general description and a discussion of genetic heterogeneity of Klippel-Feil syndrome, see KFS1 (118100).
A number sign (#) is used with this entry because Klippel-Feil syndrome-1 is caused by heterozygous mutation in the GDF6 gene (601147) on chromosome 8q22. Description Klippel-Feil syndrome (KFS) is a congenital anomaly characterized by a defect in the formation or segmentation of the cervical vertebrae, resulting in a fused appearance. The clinical triad consists of short neck, low posterior hairline, and limited neck movement, although less than 50% of patients demonstrate all 3 clinical features (Tracy et al., 2004). Genetic Heterogeneity of Klippel-Feil Syndrome Additional forms of KFS include autosomal recessive KFS2 (214300), caused by mutation in the MEOX1 gene (600147) on chromosome 17q21, autosomal dominant KFS3 (613702), caused by mutation in the GDF3 gene (606522) on chromosome 12p13, and autosomal recessive KFS4 (616549), caused by mutation in the MYO18B gene (607295) on chromosome 22q12. See also MURCS association (601076), in which Klippel-Feil anomaly is associated with urogenital anomalies.
Klippel Feil syndrome (KFS) is a condition affecting the development of the bones in the spine. People with KFS are born with abnormal fusion of at least two spinal bones (vertebrae) in the neck. Common features may include a short neck, low hairline at the back of the head, and restricted movement of the upper spine. Some people with KFS have no symptoms. Others may have frequent headaches, back and neck pain, and other nerve issues. People with KFS are at risk for severe spinal injury. KFS can occur along with other types of birth defects, and sometimes KFS occurs as a feature of another disorder or syndrome.
Klippel-Feil Syndrome is characterised by improper segmentation of cervical segments resulting in congenitally fused cervical vertebrae. Epidemiology The prevalence has been estimated at 1 in 50,000. Clinical description The syndrome was first reported in 1912 by Maurice Klippel and André Feil and is often associated with the classic clinical triad of manifestations consisting of a low posterior hairline, short neck, and limited neck range of motion. However, subsequent studies have shown that only 34% to 74% of patients present with such findings. The phenotypic expression of Klippel-Feil syndrome is variable, occurring with or without extraskeletal manifestations or any additional spinal abnormalities. Etiology The syndrome is caused by failure of cervical segmentation in the early stages of pregnancy but the exact aetiology and mode of inheritance remain unknown.
A number sign (#) is used with this entry because Klippel-Feil syndrome-3 (KFS3) is caused by heterozygous mutation in the GDF3 gene (606522) on chromosome 12p13. Description Klippel-Feil syndrome is a congenital anomaly characterized by a defect in the formation or segmentation of the cervical vertebrae, resulting in a fused appearance. The clinical triad consists of short neck, low posterior hairline, and limited neck movement, although less than 50% of patients demonstrate all 3 clinical features (Tracy et al., 2004). For a general description and a discussion of genetic heterogeneity of Klippel-Feil syndrome, see KFS1 (118100). Clinical Features Ye et al. (2010) described a 3-generation North American family with a spectrum of ocular and skeletal phenotypes.
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In rare cases, physicians may conduct tests to see whether the cause of the bloody sputum is a serious condition such as tuberculosis or lung cancer . [ citation needed ] Epidemiology [ edit ] Acute bronchitis is one of the most common diseases. [3] [13] About 5% of adults are affected and about 6% of children have at least one episode a year. [7] [8] It occurs more often in the winter. [7] In infants under one year of age, acute bronchitis was the most common reason for admission to the hospital after an emergency department visit in the US in 2011. [24] References [ edit ] ^ a b c d e f g h i j k l m n o p Albert, RH (1 December 2010). ... Brent; Redding, Gregory R.; Gibson, Peter G.; Marchant, Julie M.; Grimwood, Keith (March 2016). "Protracted bacterial bronchitis: The last decade and the road ahead" . ... Retrieved 24 January 2019 . ^ Smith, Susan M.; Fahey, Tom; Smucny, John; Becker, Lorne A. (19 June 2017).
Disorder in which a cyst forms in the spinal cord Syringomyelia An idiopathic syrinx Pronunciation / s ɪ ˌ r ɪ ŋ ɡ ə m aɪ ˈ iː l i ə , - ɡ oʊ -/ [1] [2] Specialty Neurosurgery Syringomyelia is a generic term referring to a disorder in which a cyst or cavity forms within the spinal cord . ... Archived from the original on 2012-07-08 . Retrieved 2009-02-12 . ^ Brewis M, Poskanzer DC, Rolland C, et al., "Neurological disease in an English city". ... Japanese Journal of Clinical Urology , Vol.60, No. 6, pp 413-415, 2006. ISSN 0385-2393 . ^ Hirsch M, et al. Neuropathic osteoarthropathy of the shoulder secondary to syringomyelia. https://doi.org/10.1016/j.diii.2020.09.010 ^ "Neuropathic Arthropathy of the Shoulder (Charcot Shoulder): Clinical Commentary" Medscape.
A rare central nervous system malformation characterized by a fluid-filled longitudinally oriented cavity (syrinx) within the spinal cord, which may or may not communicate with the central canal, does not have an ependymal lining, and is either idiopathic or seen as a familial malformation. Clinical manifestations in symptomatic patients include neuropathic pain, as well as sensory and motor disturbances. Typical presentations may be cape-like loss of pain and temperature sensation along the torso and arms, or disproportionately greater motor impairment in upper compared to lower extremities.
Syringomyelia is characterised by cerebrospinal fluid (CSF)-filled cavities (syrinx) inside the spinal cord, either as a result of a known cause (secondary syringomyelia, SS) or, more rarely, due to an unknown cause (primary syringomyelia, PS). Epidemiology Estimated prevalence is 8.4/100 000. Cases of autosomal recessive familial syringomyelia have been reported with an estimated incidence of 2% of all syringomyelia cases. Clinical description Although syringomyelia can lead to disruption of neural connections in the spinal cord and to neurological damage, 50% of patients (when all types of syrinxes are considered) will experience no or only mild disability. In symptomatic patients, onset is usually marked by pain and sensory disturbances, varying from complete absence of sensation, pins and needles or temperature sensing alterations, to increased sensation to stimuli. Although there are no clear clinical clues at neurological examination, a `cape-like' sensory dissociation (loss of the ability to distinguish between hot and cold with intact light-touch sensation in the upper limbs and torso), as well as reduced upper limb reflexes, are quite specific initial findings when present.
References [ edit ] ^ a b c d e f g h i j k l m Gooskens SL, Houwing ME, Vujanic GM, Dome JS, Diertens T, Coulomb-l'Herminé A, Godzinski J, Pritchard-Jones K, Graf N, van den Heuvel-Eibrink MM (2017). ... PMID 22579455 . ^ Alavi S, Khoddami M, Yazdi MK, Dehghanian P, Esteghamati S (2013). ... National Cancer Institute (US). 2002. ^ Laetsch TW, Nagasubramanian R, Casanova M (2017). "Targeting NTRK fusions for the treatment of congenital mesoblastic nephroma".
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