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Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders. Page 180. ISBN 0-7216-2921-0 . ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). ... St. Louis: Mosby. ISBN 1-4160-2999-0 . This dermatology article is a stub .
Interstitial granulomatous dermatitis with arthritis is a rare rheumatologic disease characterized by the occurrence of inflammatory arthritis in association with large, erythematous, symmetrical cutaneous lesions (ranging from typical, but infrequent, cord-like lesions on the flanks to more common violaceous plaques on the trunk and limbs) featuring a typical histologic infiltrate mainly constituted of histiocytes.
Lippincott Williams & Wilkins. p. 1152. ISBN 0-7817-7513-2 . ^ Pryse-Phillips, William (2003). ... Oxford University Press US. p. 587. ISBN 0-19-515938-1 . ^ Bradley, Walter George (2004). ... Lippincott Williams & Wilkins. p. 2695. ISBN 0-7817-5777-0 . ^ Miller, Neil R.; Frank Burton Walsh; Valérie Biousse; William Fletcher Hoyt (2005). ... Lippincott Williams & Wilkins. p. 1289. ISBN 0-7817-4811-9 . ^ a b Loder, Elizabeth; Dawn A. ... McGraw-Hill Professional. p. 127. ISBN 0-07-105467-7 . ^ G. D. Schott (2007).
See also: Hypertensive emergency and Hypertensive urgency Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110—sometimes termed malignant or accelerated hypertension) is referred to as a hypertensive crisis , as blood pressure at this level confers a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches (22% of cases)  and dizziness than the general population.  Other symptoms accompanying a hypertensive crisis may include visual deterioration due to retinopathy, breathlessness due to heart failure, or a general feeling of malaise due to kidney failure.  Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.  A " hypertensive emergency " is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic.  This may include hypertensive encephalopathy , caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). ... New York, NY: McGraw-Hill. pp. 1463–81. ISBN 978-0-07-139140-5 . ^ a b O'Brien, Eoin; Beevers, D.
In contrast ostium secundum defects have an axis between 0 degrees and 180 degrees with most cases to the right of 100 degrees. ... Baltimore: Williams & Wilkins. pp. 52 . ISBN 978-0-683-30272-1 . ^ Q21.2 Sources Pryor R, Woodwork MB, Blount SG: Electrocardiographic Changes in Atrial Septal Defects:Ostium Secundum versus Ostium Primum defect.
Auditory brainstem responses revealed that Nesp4 -/- mice, but not Nesp +/- mice, developed hearing loss that progressed to all frequencies by postnatal day 60. At postnatal day 0, Nesp4 -/- cochlea appeared normal; however, with onset of detectable hearing, Nesp4 -/- outer hair cells showed progressive degeneration, from the base to the apex, with concomitant redistribution of nuclei from the base of outer hair cells to a more apical position. Disruption of the inner hair cells was delayed to postnatal day 180. Sun1 -/- animals showed a similar overall phenotype, with hearing loss and degeneration of cochlear outer hair cells.
Di Barletta et al. (2006) reported a 6-year-old boy with a history of effort-induced syncopal episodes from 3 years of age, in whom exercise stress testing demonstrated rapid PVT; Holter monitoring showed several runs of asymptomatic polymorphic and bidirectional sustained VT at rates of 170 to 180 bpm during outdoor play. The authors also described an unrelated 17-year-old girl with onset of syncopal episodes at 4 years of age and PVT of up to 200 bpm on ECG, in whom antiarrhythmic therapy and left cardiac sympathetic denervation were unsuccessful and who ultimately required an implantable cardioverter defibrillator. ... Mapping Lahat et al. (2001) performed genomewide linkage analysis in 7 consanguineous Bedouin families segregating catecholamine-induced PVT in an autosomal recessive fashion and mapped the disease locus to a 16-Mb interval on chromosome 1p21-p13, with a maximum lod score of 8.24 obtained at D1S189 (theta = 0). Molecular Genetics Lahat et al. (2001) analyzed the CASQ2 gene in members of 7 consanguineous Bedouin families in Israel with CPVT and identified homozygosity for a mutation (N307H; 114251.0001) in all affected individuals.
The bidirectional tachycardia is defined as a ventricular arrhythmia with an alternating 180°-QRS axis on a beat-to-beat basis; some individuals may have polymorphic VT without a "stable" QRS vector alternans. ... If the affected individual continues exercising, the duration of the runs of VT progressively increases and VT may become sustained. An alternating 180°-QRS axis on a beat-to-beat basis, so-called bidirectional VT, is often the distinguishing presentation of CPVT arrhythmias.
A number sign (#) is used with this entry because catecholaminergic polymorphic ventricular tachycardia-1 (CPVT1) is caused by heterozygous mutation in the cardiac ryanodine receptor gene (RYR2; 180902) on chromosome 1q43. Description Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an arrhythmogenic disorder of the heart characterized by a reproducible form of polymorphic ventricular tachycardia induced by physical activity, stress, or catecholamine infusion, which can deteriorate into ventricular fibrillation. Patients present with recurrent syncope, seizures, or sudden death after physical activity or emotional stress. Typically, clinical cardiologic examinations, such as baseline ECG and echocardiogram, reveal mostly normal findings, and postmortem examinations, when carried out, have not disclosed any significant morphologic alterations in the fine structure of the heart, with the exception of mild fatty myocardial infiltration in a few patients. The hallmark of CPVT comprises ventricular arrhythmias of varying morphology not present under resting conditions but appearing only with physical exercise, excitement, or catecholamine administration.
A rare, severe genetic arrhythmogenic disorder of the structurally normal heart characterized by catecholamine-induced ventricular tachycardia (VT) manifesting as syncope and sudden death in young individuals. Epidemiology The prevalence of catecholaminergic polymorphic ventricular tachycardia (CPVT) is estimated to be 1/10,000. Both sexes are equally affected. Clinical description Typical age of onset of CPVT is between 7 and 15 years of age. Exercise- or emotion-induced syncopal spells are frequently the first symptom. In a subset of patients (10-20%), the disease is clinically silent, presenting only in the event of sudden death.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic disorder that causes an abnormally fast and irregular heart rhythm in response to physical activity or emotional stress. Signs and symptoms include light-headedness, dizziness, and fainting. Symptoms most often develop between 7 to 9 years of age. If untreated CPVT can cause a heart attack and death. CPVT is caused by mutations in the RYR2 or CASQ2 genes. When a RYR2 gene mutation is involved, the condition is passed through families in an autosomal dominant fashion. When CASQ2 gene mutations are involved, the condition is inherited in an autosomal recessive fashion.
A number sign (#) is used with this entry because of evidence that catecholaminergic polymorphic ventricular tachycardia-4 (CPVT4) is caused by heterozygous mutation in the calmodulin gene (CALM1; 114180) on chromosome 14q32. For a general phenotypic description and a discussion of genetic heterogeneity of CPVT, see 604772. Clinical Features Nyegaard et al. (2012) studied a large 4-generation Swedish family with a history of ventricular arrhythmias, syncope, and sudden death, predominantly in association with physical exercise or stress. The proband was a 42-year-old man who first developed syncope at 12 years of age while playing football; electrocardiogram (ECG) at that time showed bradycardia with a prominent U-wave in leads V2 and V3, without evidence of QT prolongation. He had a history of loss of consciousness on at least 4 occasions during physical activity and once in connection with a fire alarm.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a condition characterized by an abnormal heart rhythm (arrhythmia). As the heart rate increases in response to physical activity or emotional stress, it can trigger an abnormally fast heartbeat called ventricular tachycardia. Episodes of ventricular tachycardia can cause light-headedness, dizziness, and fainting (syncope). In people with CPVT, these episodes typically begin in childhood. If CPVT is not recognized and treated, an episode of ventricular tachycardia may cause the heart to stop beating (cardiac arrest), leading to sudden death. Researchers suspect that CPVT may be a significant cause of sudden death in children and young adults without recognized heart abnormalities.
A number sign (#) is used with this entry because of evidence that catecholaminergic polymorphic ventricular tachycardia-3 (CPVT3) is caused by homozygous mutation in the TECRL gene (617242) on chromosome 4q13. Description Catecholaminergic polymorphic ventricular tachycardia-3 (CPVT3) is characterized by overlapping features of long QT syndrome (see 192500) and CPVT. Affected individuals exhibit adrenergic ventricular tachycardia associated with a high prevalence of cardiac arrest and sudden cardiac death, with recurrent atrial tachycardia sometimes triggering the ventricular arrhythmias. In addition, affected individuals have a normal or mildly prolonged QTc on baseline electrocardiography, with a paradoxical QT increase during adrenergic simulation (summary by Devalla et al., 2016). For a general phenotypic description and a discussion of genetic heterogeneity of CPVT, see 604772.
A number sign (#) is used with this entry because of evidence that catecholaminergic polymorphic ventricular tachycardia-5 with or without muscle weakness (CPVT5) is caused by homozygous or compound heterozygous mutation in the triadin gene (TRDN; 603283) on chromosome 6q22. For a general phenotypic description and a discussion of genetic heterogeneity of CPVT, see 604772. Clinical Features Roux-Buisson et al. (2012) studied 2 families with cardiac arrhythmias. In the first family, which originated from the French West Indies, the 2-year-old proband experienced syncope followed by cardiac arrest after a shock while playing with his 7-year-old brother. Resting electrocardiogram (ECG) after resuscitation showed numerous polymorphic or bidirectional ventricular extra beats and runs of polymorphic ventricular tachycardia.
Hopefully, after this, the eye will focus all light on the same location at the retina, and the patient's vision will be less blurred. [ medical citation needed ] In against-the-rule astigmatism, a plus cylinder is added in the horizontal axis (or a minus cylinder in the vertical axis).  Axis is always recorded as an angle in degrees, between 0 and 180 degrees in a counter-clockwise direction. Both 0 and 180 degrees lie on a horizontal line at the level of the center of the pupil, and as seen by an observer, 0 lies on the right of both the eyes. [ medical citation needed ] Irregular astigmatism, which is often associated with prior ocular surgery or trauma, is also a common naturally occurring condition.  The two steep hemimeridians of the cornea, 180° apart in regular astigmatism, may be separated by less than 180° in irregular astigmatism (called nonorthogonal irregular astigmatism); and/or the two steep hemimeridians may be asymmetrically steep—that is, one may be significantly steeper than the other (called asymmetric irregular astigmatism). ... Lippincott Williams & Wilkins. pp. 173–. ISBN 978-0-7817-4206-1 . ^ Carlo Cavallotti; Luciano Cerulli (31 May 2008). ... Ophthalmology . 93 (11): 1461–5. doi : 10.1016/s0161-6420(86)33545-0 . PMID 3808608 . ^ Brookman, KE (1993). ... Notes and Records of the Royal Society of London . 21 (2): 180–199. doi : 10.1098/rsnr.1966.0017 .
Overview Astigmatism (uh-STIG-muh-tiz-um) is a common and generally treatable imperfection in the curvature of the eye that causes blurred distance and near vision. Astigmatism occurs when either the front surface of the eye (cornea) or the lens inside the eye has mismatched curves. Instead of having one curve like a round ball, the surface is egg-shaped. This causes blurred vision at all distances. Astigmatism is often present at birth and may occur in combination with nearsightedness or farsightedness. Often it's not pronounced enough to require corrective action. When it is, treatment options are corrective lenses or surgery.
Description Astigmatism (from the Greek 'a' meaning absence and 'stigma' meaning point) is a condition in which the parallel rays of light entering the eye through the refractive media are not focused on a single point. Both corneal and noncorneal factors contribute to refractive astigmatism. Corneal astigmatism is mainly the result of an aspheric anterior surface of the cornea, which can be measured readily by means of a keratometer; in a small fraction of cases (approximately 1 in 10) the effect is neutralized by the back surface. The curvature of the back surface of the cornea is not considered in most studies, because it is more difficult to measure; moreover, in the case of severe corneal astigmatism, there is evidence that both surfaces have the same configuration. Noncorneal factors are errors in the curvature of the 2 surfaces of the crystalline lens, irregularity in the refractive index of the lens, and an eccentric lens position.
Affluenza: How to Be Successful and Stay Sane . Vermilion . ISBN 978-0-09-190011-3 . ^ James, Oliver (2008). The Selfish Capitalist . Vermilion . ISBN 978-0-09-192381-5 . ^ James, Oliver (2007). ... London: Vermilion. p. 344 . ISBN 978-0-09-190010-6 . 1. The mean prevalence of emotional distress for the six English-speaking nations combined was 21.6%. ... (Archive is the same work, but on a different website) Further reading [ edit ] The Circle of Simplicity , Cecile Andrews, ISBN 0-06-092872-7 The Golden Ghetto: The Psychology of Affluence , Jessie H. O'Neill, ISBN 978-0-9678554-0-0 Voluntary Simplicity , Duane Elgin, ISBN 0-688-12119-5 Voluntary Simplicity , Daniel Doherty & Amitai Etzioni, ISBN 0-7425-2066-8 How Much Is Too Much?
New York City: Viking Adult . p. 3. ISBN 978-0-670-03855-8 . ^ "The Plague of Justinian". ... New York City: Viking Adult . pp. 321–322. ISBN 978-0-670-03855-8 . ^ Charles-Edwards, Wales and the Britons , p. 216 ^ Russell, Josiah C. (1968). ... Plague and the End of Antiquity: The Pandemic of 541–750 . Cambridge. ISBN 978-0-521-84639-4 . Moorhead, J. (1994). ... New York: Bantam Doubleday Dell. ISBN 978-0-385-12122-4 . Orent, Wendy (2004). ... New York: Simon & Schuster. ISBN 978-0-7432-3685-0 . Russell, J. C. (1958).
The Guardian . London. ^ a b Mass Murderers ISBN 0-7835-0004-1 p. 169 ^ Courtroom Television Network (2005). ... The Guardian . London. ^ Mass Murderers ISBN 0-7835-0004-1 p. 12 ^ a b Mass Murderers , p. 172 ISBN 0-7835-0004-1 ^ a b "Michael Ryan, the Hungerford UK Mass Murderer – Whatever Moves – Crime Library on" . ... Retrieved 17 January 2011 . ^ Mass Murderers ISBN 0-7835-0004-1 p. 174 ^ Mass Murderers , p. 173 ISBN 0-7835-0004-1 ^ Mass Murderers ISBN 0-7835-0004-1 p. 178 ^ "HUNGERFORD MASSACRE ANNIVERSARY" . www.itnsource.com . ^ a b "Hungerford Report Ryan Police August Pistol 1987 Station" . ... Retrieved 17 January 2011 . ^ a b Mass Murderers ISBN 0-7835-0004-1 p. 179 ^ Mass Murderers ISBN 0-7835-0004-1 p. 179–180 ^ Mass Murderers ISBN 0-7835-0004-1 p. 180 ^ "The Glasgow Herald – Google News Archive Search" . news.google.com . ^ Mass Murderers ISBN 0-7835-0004-1 p. 184 ^ Michael Ryan – The Hungerford UK Mass Murderer Archived 29 April 2006 at the Wayback Machine . ... Routledge; 2Rev Ed editio. pp. 63–77. ISBN 0-415-22513-2 . CS1 maint: extra text: authors list ( link ) Webster, Duncan (May 1989).
Biology of Brassica Coenospecies . Elsevier. pp. 186 –189. ISBN 978-0-444-50278-0 . ^ Schnable P, Wise RP (May 1998). ... Trends in Plant Science . 3 (5): 175–180. doi : 10.1016/S1360-1385(98)01235-7 . ^ Weider C, Stamp P, Christov N, Hüsken A, Foueillassar X, Camp K, Munsch M (2009).
Clinical Strabismus Management: Principles and Surgical Techniques . David Hunter. p. 27. ISBN 978-0-7216-7673-9 . ^ Arthur L. Rosenbaum; Alvina Pauline Santiago (1999). Clinical Strabismus Management: Principles and Surgical Techniques . David Hunter. p. 28. ISBN 978-0-7216-7673-9 . ^ D.S. Burger; R. London (1993). ... Journal of the American Optometric Association (review). 64 (3): 176–180. PMID 8454834 . ^ Hadid OH, Wride NK, Griffiths PG, Strong NP, Clarke MP (July 2008).
Basic Skills in Interpreting Laboratory Data . ISBN 978-1-58528-180-0 . Retrieved 23 May 2013 . ^ Person—microalbumin level (measured) at Australian Institute of Health and Welfare. 01/03/2005 ^  Justesen, T.; Petersen, J.; Ekbom, P.; Damm, P.; Mathiesen, E. (2006).
Clinical Features Bierzynska et al. (2017) reported 3 children, including 2 sisters (patients 175 and 175S) born of consanguineous parents and an unrelated child (patient 180), with NPHS15. The patients presented with proteinuria and hypoalbuminemia within the first 4 months of life. ... Patient 175 had rapid disease progression, resulting in end-stage renal failure necessitating renal transplant at age 3.5 years, whereas patient 175S had a more benign course and had not had renal transplant by age 2.3 years. Patient 180 had persistent proteinuria with only mild renal impairment until age 9 years; he did not need a renal transplant. Renal biopsy of patient 175 showed marked glomerular lobulation with fibrosis or global sclerosis, and interstitial fibrosis. Renal biopsy of patient 180 showed minimal change disease and 2 of 59 glomeruli with global sclerosis. ... Patient 175S had some minor cardiac abnormalities, including mild peripheral branch pulmonary stenosis and patent foramen ovale, possibly unrelated to the renal disorder. Patient 180 had polydactyly and pyloric stenosis, but no other features of a characterized syndrome.