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Books on the topic 'Inflammation of the nasal mucosa'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Eriksson, Catarina. Herbicide-induced toxicity in the nasal olfactory mucosa: Studies on Dichlobenil and Chlorthiamid. Sveriges Lantbruksuniversitet, 1995.

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2

Division, Medicode (Firm) Med-Index, ed. Midface--sinus & nasal mucosa. Medicode, Med-Index Division, 1994.

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3

Drake-Lee, A. B. Nasal mast cells: A preliminary report on their ultrastructure. Headley Brothers, 1987.

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4

Winther, Birgit. Effects on the nasal mucosa of upper respiratory viruses (common cold). Lægeforeningen, 1993.

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5

Torben, Lildholdt, and Mygind Niels, eds. Nasal polyposis: An inflammatory disease and its treatment. Munksgaard, 1997.

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6

H, Stead Ron, ed. Neuro-immuno-physiology of the gastrointestinal mucosa: Implications for inflammatory diseases. New York Academy of Sciences, 1992.

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7

Falk Symposium (133rd 2004 Berlin, Germany). Mechanisms of intestinal inflammation: Implications for therapeutic intervention in IBD : proceedings of Falk Symposium 133 (New Findings on Pathogenesis and Progress in Management of Inflammatory Bowel Diseases, Part I) held in Berlin, Germany, June 10-11, 2003. Kluwer Academic Publishers, 2004.

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8

R, Mahida Y., ed. Immunological aspects of gastroenterology. Kluwer Academic Publishers, 2001.

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9

Juliusson, Sigurdur. Allergic inflammation in the nasal mucosa: A clinical, morphological and biochemical study in allergic rhinitis with special reference to mast cells. 1993.

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10

Reintjes, Staci, and Susie Peterson. Rhinosinusitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0012.

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Rhinosinusitis is inflammation of the nasal passages and paranasal sinuses, commonly caused by allergies or viral infection. Sinusitis occurs after the development of rhinitis or inflammation of the nasal passages. Rhinitis is most commonly caused by allergens, but it also can be to the result of an infectious or autoimmune process. For rhinitis to progress to rhinosinusitis, there must be obstruction within the ostiomeatal complex, which is the draining center for the maxillary, anterior ethmoid, and frontal sinuses. History and physical exam are more specific than imaging for diagnosis. Comp

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11

Medicode. Midface--Sinus & Nasal Mucosa (Coding Illustrated). Ingenix - Sta/Medicode, 1995.

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12

Nasal Polyposis. Munksgaard,Denmark, 1997.

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13

Klementsson, Håkan. Eosinophil granulocytes and nasal responsiveness: A study of allergic inflammatory reaction in the human nasal mucosa. 1991.

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14

(Editor), R. Duchmann, R. S. Blumberg (Editor), M. F. Neurath (Editor), J. Schölmerich (Editor), W. Strober (Editor), and M. Zeitz (Editor), eds. Mechanisms of Intestinal Inflammation: Implications for Therapeutic Intervention in IBD (Falk Symposium). Springer, 2004.

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15

Lang, Steffen. On the pathways of transport and metabolism of therapeutic peptides in the nasal mucosa. 1995.

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16

Experimental models of mucosal inflammation. CRC Press, 1996.

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17

Jankowski, Janusz A. Z. Inflammation and Gastrointestinal Cancers. Springer Berlin / Heidelberg, 2013.

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18

Cooke, Helen, Don W. Powell, Ron H. Stead, Mary H. Perdue, and Kim Barratt. Neuro-Immuno-Physiology of the Gastrointestinal Mucosa: Implications for Inflammatory Diseases (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1992.

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19

Scordino, David. Infectious Colitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0031.

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Infectious colitis is diarrhea with evidence of colonic inflammation by visualization (colonoscopy), history (blood or mucus in the stool), or laboratory evidence (high lactoferrin). Infectious colitis is associated with direct bacterial or indirect bacterial toxin invasion of the colonic mucosa, leading to toxicity, volume loss, hemorrhage, and colonic inflammation. The most important treatment is adequate hydration, but treatment also may include loperamide (useful in patients without fever or bloody stools) and antibiotics in individuals with evidence of colitis (although not for mild to mo

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20

Hartigan-O’Connor, Dennis J., and Christian Brander. Immunology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0005.

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The key factor in HIV pathogenesis is the decline in CD4+ T cells with resultant immunodeficiency and chronic inflammation. Depletion of CD4+ T cells from the gastrointestinal mucosa followed by microbial translocation and subsequent immune activation are components of disease progression in untreated patients. Symptomatic and occult opportunistic infections including cytomegalovirus contribute to chronic inflammation in persons infected with HIV. Antiretroviral therapy (ART) results in immune reconstitution, with increases in peripheral CD4+ T cell lymphocytes in most persons infected with HI

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21

Johnson, Nicholas J., and Judd E. Hollander. Management of cocaine poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0324.

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Cocaine is powerful central nervous system (CNS) stimulant derived from the coca plant. It affects the body via a number of mechanisms including blockade of fast sodium channels, increased catecholamine release, inhibition of catecholamine reuptake, and increased concentration of excitatory amino acid concentrations in the CNS. It is rapidly absorbed via the aerodigestive, respiratory, gastrointestinal, and genitourinary mucosa, and also may be injected. When injected intravenously or inhaled, cocaine is rapidly distributed throughout the body and CNS, with peak effects in 3–5 minutes. With na

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22

Keshav, Satish, and Alexandra Kent. Inflammatory bowel disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0203.

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Inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn’s disease (CD). Both conditions cause chronic relapsing inflammation in the gastrointestinal (GI) tract, but have different characteristics. UC causes diffuse mucosal inflammation limited to the colon, extending proximally from the anal verge, with the rectum involved in 95% of patients. UC is described in terms of the disease extent: proctitis (confined to the rectum), proctosigmoiditis (disease confined to the recto-sigmoid colon), distal disease (distal to the splenic flexure), and pan-colitis (the entire large i

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