Sisteminis rukymo ir rukymo metimo poveikis
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Sisteminis rukymo ir rukymo metimo poveikis

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Sisteminis rukymo ir rukymo metimo poveikis

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1. Sisteminis rukymo ir rukymo metimo poveikis Dr. Lina Jancaityte KMUK Kardiologijos klinika

2. Paskaitos u?daviniai Sisteminis rukymo poveikis Laboratoriniu rodikliu pokyciai rukant ir nerukant Rukymo ir metimo rukyti itaka ivairioms organu sistemoms

3. Ar ?inote, kad Rukymas i?lieka antroji did?ioji mirties prie?astis pasaulyje. 2030 m., i?liekant dabartinei situacijai, rukymas nu?udys iki 9 milijonu ?moniu. molecules per puff.7 This oxidative stress can be registered in several different ways, either by direct measurements of the oxidative burden (reactive oxygen species [ROS] production by peripheral blood cells) or by the effects of oxidative stress on target molecules (lipid peroxidation products and oxidized proteins), or as the responses to the oxidative stress (antioxidant capacity of plasma)8 [Table 1]. Only a few studies9?11 have used ROS production by blood cells extracted from the circulation of smokers. Perhaps more important than the presence of oxidative stress are the effects of this oxidative stress on a variety of vital target molecules. Numerous markers for oxidative damage have been proposed, including oxidation and nitration of proteins. For example, nitration of tyrosine residues of proteins leads to the production of 3-nitrotyrosine, which may be considered as a marker of nitric oxide (NO)-dependent oxidative damage. Indeed, NOmediated and peroxynitrite-mediated formation of 3-nitrotyrosine is elevated in plasma and platelets of chronic smokers.12,13 Furthermore, Pignatelli and coworkers14 reported significantly higher levels of nitrated and oxidized fibrinogen, transferrin, plasminogen, and ceruloplasmin in smokers than in nonsmokers. Free radicals from cigarette smoke also cause peroxidation of the polyunsaturated fatty acids of cell membranes that amplify oxidative stress during smoking. The F2-isoprostanes, prostaglandin-like compounds, are products of free radical-catalyzed lipid peroxidation of arachidonic acid. Several studies15? 17 have reported an increased level of isoprostane 8-iso-prostaglandin F2 (PGF2) formation in smokers. molecules per puff.7 This oxidative stress can be registered in several different ways, either by direct measurements of the oxidative burden (reactive oxygen species [ROS] production by peripheral blood cells) or by the effects of oxidative stress on target molecules (lipid peroxidation products and oxidized proteins), or as the responses to the oxidative stress (antioxidant capacity of plasma)8 [Table 1]. Only a few studies9?11 have used ROS production by blood cells extracted from the circulation of smokers. Perhaps more important than the presence of oxidative stress are the effects of this oxidative stress on a variety of vital target molecules. Numerous markers for oxidative damage have been proposed, including oxidation and nitration of proteins. For example, nitration of tyrosine residues of proteins leads to the production of 3-nitrotyrosine, which may be considered as a marker of nitric oxide (NO)-dependent oxidative damage. Indeed, NOmediated and peroxynitrite-mediated formation of 3-nitrotyrosine is elevated in plasma and platelets of chronic smokers.12,13 Furthermore, Pignatelli and coworkers14 reported significantly higher levels of nitrated and oxidized fibrinogen, transferrin, plasminogen, and ceruloplasmin in smokers than in nonsmokers. Free radicals from cigarette smoke also cause peroxidation of the polyunsaturated fatty acids of cell membranes that amplify oxidative stress during smoking. The F2-isoprostanes, prostaglandin-like compounds, are products of free radical-catalyzed lipid peroxidation of arachidonic acid. Several studies15? 17 have reported an increased level of isoprostane 8-iso-prostaglandin F2 (PGF2) formation in smokers.

4. Vienas ketvirtadalis visu mirciu tarp rukanciuju yra del i?emines ?irdies ligos, kitas ketvirtadalis ? del plauciu ve?io ir letines obstrukcines plauciu ligos, kita puse ? del neoplastiniu ir kvepavimo ligu. Lyginant rukanciuosius ir niekad nerukiusius asmenis, nustatyta, kad bendras mir?tamumas yra didesnis tarp rukanciuju 2.77 karto (95% 2.65-2.90).

5. Sisteminis rukymo poveikis Sisteminis u?degimas Sisteminis oksidacinis stresas Poveikis i vazomorine funkcija ir endotelio funkcija

6. Sisteminis u?degiminis rukymo poveikis U?degiminiu lasteliu aktyvavimas ir atpalaidavimas i cirkuliuojanti krauja, padidejes cirkuliuojanciu mediatoriu kiekis charakterizuoja sistemini u?degima. Sisteminis u?degiminis poveikis pasirei?kia hemopoetines sistemos stimuliavimu, butent leukocitu ir trombocitu patekima i? kaulu ciulpu i krauja. Ilgalaikis rukymas sukelia leukocitu (neutrofilu) kiekio padidejima kraujyje. Stebimas jaunu leukocitu formu padidejimas kraujyje. Inflammatory Mediators in Peripheral Blood of Smokers Activated inflammatory cells produce a great variety of inflammatory mediators in response to cigarette smoke, first of all, acute-phase proteins (APPs) and cytokines. Conditions that commonly lead to substantial changes in the plasma concentrations of APPs and cytokines include infection, trauma, surgery, burns, tissue infarction, various immunologically mediated inflammatory conditions, and cancer. In recent years, these inflammatory mediators have been studied as potential markers of subtle and persistent systemic alterations. Many studies have reported changes in levels of inflammatory mediators not only in the lungs but also in the circulation of healthy smokers. Several studies47?49 have reported strong associations between cigarette smoking and different APPs such as C-reactive protein (CRP) and fibrinogen (Table 2). Stebimas jaunu leukocitu formu padidejimas kraujyje. Inflammatory Mediators in Peripheral Blood of Smokers Activated inflammatory cells produce a great variety of inflammatory mediators in response to cigarette smoke, first of all, acute-phase proteins (APPs) and cytokines. Conditions that commonly lead to substantial changes in the plasma concentrations of APPs and cytokines include infection, trauma, surgery, burns, tissue infarction, various immunologically mediated inflammatory conditions, and cancer. In recent years, these inflammatory mediators have been studied as potential markers of subtle and persistent systemic alterations. Many studies have reported changes in levels of inflammatory mediators not only in the lungs but also in the circulation of healthy smokers. Several studies47?49 have reported strong associations between cigarette smoking and different APPs such as C-reactive protein (CRP) and fibrinogen (Table 2).

7. Cirkuliuojantys citokinai tokie, kaip IL 1 ir IL 6 stimuliuoja kaulu ciulpus, sukeldami plauciu u?degima. T limfocitai susije su plauciu ligu, ypac LOPL , vystymusi. Daug rukantiems asmenims stebimas CD4 lasteliu suma?ejimas (T-helperiai) ir CD8 lasteliu (T-lasteliu supresoriai) padidejimas.

8. Plauciu mikrocirkuliacija ir u?degimas

9. Rukymas ir endotelio funkcija Rukymas sutrikdo NO gamyba ? rukanciuju ji ?enkliai suma?eja. Rukantiesiems nustatomas MTL padidejimas. Pakitusios endotelio lasteles netenka savo fiziologines ypatybes nesijungti su cirkuliuojanciomis imuninemis lastelemis (monocitais,makrofagais, T limfocitais, trombocitais). Rukymo sukeltas endotelio pa?eidimas skatina ir ateromos formavimasi, kas yra ankstyvas aterogenezes po?ymis. However, this hypothesis has to be taken cautiously because not all smokers acquire one or more of these diseases. It clearly suggests the existence of other mechanisms influencing common disease development, and, beyond doubt, genetic susceptibility is one of them.86 Different approaches like case-control and whole-genome association studies, linkage analysis of extended pedigrees, and affected sibling pairs are used to dissect genetic component of complex traits. For genetically complex disease like cardiovascular diseases, common disease-common variant hypothesis has been put forward, which assumes that common disease susceptibility or resistance variants are expected to be few at each genetic locus, relatively common in the human population and enriched in the coding and regulatory sequence of genes.87 Despite the small effects of such genes individually, the magnitude of their attributable risk may be large because they are quite frequent in the population, making them of public health significance. However, there is a possibility that many rare variants, each with small contribution, underlie the susceptibility to common human disease.88 Nevertheless, it seems that complete model of complex disease initiation and progression is based on cooperation where these multiple genes are likely to operate through interactions with many environmental factors where smoking is only one but a very important variable. However, this hypothesis has to be taken cautiously because not all smokers acquire one or more of these diseases. It clearly suggests the existence of other mechanisms influencing common disease development, and, beyond doubt, genetic susceptibility is one of them.86 Different approaches like case-control and whole-genome association studies, linkage analysis of extended pedigrees, and affected sibling pairs are used to dissect genetic component of complex traits. For genetically complex disease like cardiovascular diseases, common disease-common variant hypothesis has been put forward, which assumes that common disease susceptibility or resistance variants are expected to be few at each genetic locus, relatively common in the human population and enriched in the coding and regulatory sequence of genes.87 Despite the small effects of such genes individually, the magnitude of their attributable risk may be large because they are quite frequent in the population, making them of public health significance. However, there is a possibility that many rare variants, each with small contribution, underlie the susceptibility to common human disease.88 Nevertheless, it seems that complete model of complex disease initiation and progression is based on cooperation where these multiple genes are likely to operate through interactions with many environmental factors where smoking is only one but a very important variable.

11. Laboratoriniai rodikliai

16. Rukymas ir navikai Navikai plauciu kasos stemples inkstu ?lapimo pusles skrand?io The relationship between smoking and certain cancers, such as lung, bladder, esophageal and pancreatic cancer has been established for many years, while the relationship between smoking and others, such as renal cancer, has only recently been solidified. A number of studies published over the last few years have sought to further elucidate the effects of smoking on these cancers. Specifically, the effect of cigarette dose and duration of smoking was studied, as well as the effects of smoking cessation and duration of cessation on the reduction of risk.The relationship between smoking and certain cancers, such as lung, bladder, esophageal and pancreatic cancer has been established for many years, while the relationship between smoking and others, such as renal cancer, has only recently been solidified. A number of studies published over the last few years have sought to further elucidate the effects of smoking on these cancers. Specifically, the effect of cigarette dose and duration of smoking was studied, as well as the effects of smoking cessation and duration of cessation on the reduction of risk.

17. Plauciu ve?io rizika Key Point Smoking increases the likelihood of developing lung cancer. Quitting smoking can lower this increased risk. Participants (noninstitutionalized civilians aged 25-74 years) in the First National Health and Nutrition Examination Survey (1971-1975) were followed up for a median duration of 17.9 years and analyzed by Mannino et al. Subjects (N=5402) were analyzed using a proportional hazards model to determine the effect of smoking on the development of lung cancer. The mean smoke exposure of current and ex-smokers was comparable. Current smokers? (defined as those smoking at the time of the initial survey) mean smoke exposure was 33.1 (SE: 0.7) pack/years, and the mean smoke exposure of ex-smokers was 33.3 (SE: 1.0) pack/years. Ex-smokers had quit 8.6 (SE: 0.3) years before the initial survey. Compared with a value of 1.0 for never smokers, the hazard ratio for development of lung cancer was 3.6 (95% CI, 1.7-7.8) for ex-smokers and 8.4 (95% CI, 4.4-16.0) for current smokers. Key Point Smoking increases the likelihood of developing lung cancer. Quitting smoking can lower this increased risk. Participants (noninstitutionalized civilians aged 25-74 years) in the First National Health and Nutrition Examination Survey (1971-1975) were followed up for a median duration of 17.9 years and analyzed by Mannino et al. Subjects (N=5402) were analyzed using a proportional hazards model to determine the effect of smoking on the development of lung cancer. The mean smoke exposure of current and ex-smokers was comparable. Current smokers? (defined as those smoking at the time of the initial survey) mean smoke exposure was 33.1 (SE: 0.7) pack/years, and the mean smoke exposure of ex-smokers was 33.3 (SE: 1.0) pack/years. Ex-smokers had quit 8.6 (SE: 0.3) years before the initial survey. Compared with a value of 1.0 for never smokers, the hazard ratio for development of lung cancer was 3.6 (95% CI, 1.7-7.8) for ex-smokers and 8.4 (95% CI, 4.4-16.0) for current smokers.

18. Plauciu ve?io rizika Key Point The risk of developing lung cancer rises with increasing cigarette consumption. Mannino et al also determined the relationship between the number of cigarettes smoked and the risk of developing lung cancer. Pack/year was calculated by multiplying the average number of cigarettes smoked daily by the number of years smoked and dividing by 20. The hazard ratio for development of lung cancer compared with a value of 1.0 for never smokers, was 2.9 for those who smoked <30 pack/years, 9.0 for those who smoked 30 to <60 pack/years, and 19.9 for those who smoked 60 or more pack/years.Key Point The risk of developing lung cancer rises with increasing cigarette consumption. Mannino et al also determined the relationship between the number of cigarettes smoked and the risk of developing lung cancer. Pack/year was calculated by multiplying the average number of cigarettes smoked daily by the number of years smoked and dividing by 20. The hazard ratio for development of lung cancer compared with a value of 1.0 for never smokers, was 2.9 for those who smoked <30 pack/years, 9.0 for those who smoked 30 to <60 pack/years, and 19.9 for those who smoked 60 or more pack/years.

19. Kasos ve?io rizika Key Point Smoking increases the risk of pancreatic cancer. Lin et al analyzed data from the Japan Collaborative Cohort Study for the Evaluation of Cancer Risk. The subjects, 99,527 Japanese citizens aged 40 to 79 years with known smoking status and no reported history of cancer, were followed up from the beginning of the study (1988-1990) through 1997. The RR of death from pancreatic cancer was determined after adjusting for age, body mass index, diabetes, and gallbladder disease. Compared with nonsmokers, male smokers had a RR of 1.6 (95% CI, 0.95-2.6), and female smokers had a RR of 1.7 (95% CI, 0.85-3.4). There was a trend (P=.59) toward a higher RR (3.3; 95% CI, 1.38-8.1) for male smokers who smoked more than 40 cigarettes per day.Key Point Smoking increases the risk of pancreatic cancer. Lin et al analyzed data from the Japan Collaborative Cohort Study for the Evaluation of Cancer Risk. The subjects, 99,527 Japanese citizens aged 40 to 79 years with known smoking status and no reported history of cancer, were followed up from the beginning of the study (1988-1990) through 1997. The RR of death from pancreatic cancer was determined after adjusting for age, body mass index, diabetes, and gallbladder disease. Compared with nonsmokers, male smokers had a RR of 1.6 (95% CI, 0.95-2.6), and female smokers had a RR of 1.7 (95% CI, 0.85-3.4). There was a trend (P=.59) toward a higher RR (3.3; 95% CI, 1.38-8.1) for male smokers who smoked more than 40 cigarettes per day.

20. Stemples ve?io rizika Rukantys 3 kartus da?niau serga plok?cialasteliniu stemples ve?iu. Buve rukoriai serga reciau nei esami rukoriai. Po 10 nerukymo metu buve rukoriai turi 2-kartus didesne ve?io rizika. Key Point Smoking increases the risk of developing esophageal cancer. Wu et al reported an approximate 3-fold increase in risk of esophageal cancer over that of nonsmokers (see next slide). Bosetti et al reviewed 20 studies investigating the effect of smoking cessation on increased risk. Many of the studies were in agreement that the risk of esophageal cancer is reduced after smoking cessation, but that there is a lasting effect of smoking on this risk, and even after 10 years or more, the risk of ex-smokers developing this cancer is twice as high as that for nonsmokers.Key Point Smoking increases the risk of developing esophageal cancer. Wu et al reported an approximate 3-fold increase in risk of esophageal cancer over that of nonsmokers (see next slide). Bosetti et al reviewed 20 studies investigating the effect of smoking cessation on increased risk. Many of the studies were in agreement that the risk of esophageal cancer is reduced after smoking cessation, but that there is a lasting effect of smoking on this risk, and even after 10 years or more, the risk of ex-smokers developing this cancer is twice as high as that for nonsmokers.

21. ?lapimo pusles ve?io rizika Rukymas yra viena da?niausiu prie?asciu. Rukymo prevencija suma?ina ve?io rizika vyrams 50% ir moterims 23%. Rukoriai beveik 3-kartus da?niau serga pusles ve?iu nei nerukantys. Key Point Smoking is one of the most important risk factors associated with bladder cancer. Bladder cancer is the ninth most frequent cancer in men worldwide (approximately 330,000 new cases per year), and one of the top 5 most frequent cancers in men in the United States. It is more common in men, but there are approximately 60,000 women diagnosed with bladder cancer per year worldwide. In a meta-analysis of 43 studies, Zeeger et al concluded that cigarette smokers have an approximately 3-fold greater risk of bladder cancer than nonsmokers. Summary ORs compared with nonsmokers were 3.33 (95% CI, 2.63-4.21) for smokers and 1.98 (95% CI, 1.72-2.29) for ex-smokers. Key Point Smoking is one of the most important risk factors associated with bladder cancer. Bladder cancer is the ninth most frequent cancer in men worldwide (approximately 330,000 new cases per year), and one of the top 5 most frequent cancers in men in the United States. It is more common in men, but there are approximately 60,000 women diagnosed with bladder cancer per year worldwide. In a meta-analysis of 43 studies, Zeeger et al concluded that cigarette smokers have an approximately 3-fold greater risk of bladder cancer than nonsmokers. Summary ORs compared with nonsmokers were 3.33 (95% CI, 2.63-4.21) for smokers and 1.98 (95% CI, 1.72-2.29) for ex-smokers.

22. Inkstu ve?io rizika Key Point Smoking increases the risk of renal cell carcinoma in both men and women in a dose-dependent manner. Hunt et al conducted a meta-analysis of 19 case-controlled and 5 cohort studies investigating the relationship between smoking and renal cell carcinoma. Smokers were divided into categories based on the extent of their smoking. All male smokers had an increased risk of developing renal cell carcinoma, and women who smoked more than 10 cigarettes/day (10-20 c/d: RR, 1.38; 95% CI, 0.9-2.11) also had an increased risk. The risk for both men and women was dose-dependent. Key Point Smoking increases the risk of renal cell carcinoma in both men and women in a dose-dependent manner. Hunt et al conducted a meta-analysis of 19 case-controlled and 5 cohort studies investigating the relationship between smoking and renal cell carcinoma. Smokers were divided into categories based on the extent of their smoking. All male smokers had an increased risk of developing renal cell carcinoma, and women who smoked more than 10 cigarettes/day (10-20 c/d: RR, 1.38; 95% CI, 0.9-2.11) also had an increased risk. The risk for both men and women was dose-dependent.

23. Rukymo poveikis endokrininei sistemai Osteoporoze Skydliaukes ligos Rezistencija insulinui/cukrinis diabetas In relatively recent years, smoking has been shown to increase the risk of various disorders of the endocrine system. The following section will present a number of studies that clarified the connection between smoking and these disorders.In relatively recent years, smoking has been shown to increase the risk of various disorders of the endocrine system. The following section will present a number of studies that clarified the connection between smoking and these disorders.

24. Kaulu tankis vyresnio am?iaus moterims Key Point Heavy smoking in older women causes a significant reduction in BMD compared with light or no smoking. Rapuri et al conducted an osteoporotic study in elderly women, including 390 nonsmokers, 33 light smokers (<1 pack/day), and 21 heavy smokers (=1 pack/day), aged 65-77 years, measuring bone density at a number of locations in the body. There was a significant decrease in BMD at the total femur (6%) and total body (4%) in heavy smokers, but not in light smokers. Other sites (lumbar spine, femoral neck) displayed a similar but not significant trend.Key Point Heavy smoking in older women causes a significant reduction in BMD compared with light or no smoking. Rapuri et al conducted an osteoporotic study in elderly women, including 390 nonsmokers, 33 light smokers (<1 pack/day), and 21 heavy smokers (=1 pack/day), aged 65-77 years, measuring bone density at a number of locations in the body. There was a significant decrease in BMD at the total femur (6%) and total body (4%) in heavy smokers, but not in light smokers. Other sites (lumbar spine, femoral neck) displayed a similar but not significant trend.

25. Rukymas ir skydliaukes disfunkcija Key Point Smoking increases the risk of developing thyroid disease in women. Vestergaard et al analyzed 617 patients with hyperthyroidism (Graves? disease) and 408 patients with autoimmune hypothyroidism in Denmark, an area with a high incidence of thyroid disease where smoking is frequent and iodine intake is relatively low. Each subject was age- and sex-matched to a control subject, and each was assessed on the basis of ever smoking and use of hormonal contraceptives or replacement. In each case, 88% to 89% of the subjects were women. Men and women were analyzed separately. Among the women, the patients were found to have a higher frequency of smoking than the controls. Using logistic regression to calculate the odds ratios, then calculating percent attributable risk, it was determined that smoking increases the chances of women developing all 3 of the conditions. The greatest effect of smoking was observed in Graves? disease, where the risk attributed to smoking was 45%. As in previous studies, smoking was not found to have an effect on thyroid disease in men.Key Point Smoking increases the risk of developing thyroid disease in women. Vestergaard et al analyzed 617 patients with hyperthyroidism (Graves? disease) and 408 patients with autoimmune hypothyroidism in Denmark, an area with a high incidence of thyroid disease where smoking is frequent and iodine intake is relatively low. Each subject was age- and sex-matched to a control subject, and each was assessed on the basis of ever smoking and use of hormonal contraceptives or replacement. In each case, 88% to 89% of the subjects were women. Men and women were analyzed separately. Among the women, the patients were found to have a higher frequency of smoking than the controls. Using logistic regression to calculate the odds ratios, then calculating percent attributable risk, it was determined that smoking increases the chances of women developing all 3 of the conditions. The greatest effect of smoking was observed in Graves? disease, where the risk attributed to smoking was 45%. As in previous studies, smoking was not found to have an effect on thyroid disease in men.

26. Rukymas ir cukrinis diabetas Tiriant moteris, sergancias cukriniu diabetu, nustatyta, kad lyginant su niekada nerukiusiomos mirties rizika metusioms rukyti yra 1.31 (95% CI, 1.11-1.55), rukancioms 1-14 cigareciu dienai - 1.43 (95% CI, 0.96-2.14), rukancioms 15-34 cigareciu dienai - 1.64 (95% CI, 1.24-2.17), rukancioms > 35 cigareciu dienai - 2.19 (95% CI, 1.32-3.65). Rukymas yra susijes su II tipo cukrinio diabeto atsiradimu ? pa?eid?iamas rezistenti?kumas insulinui, pakinta insulino sekrecija, toksinis poveikis kasai, padideja adrenalino kiekis.

27. Lyginant su niekada nerukiusiais II tipo cukrinio diabeto atsiradimas da?nesnis tarp daug rukanciuju (RR 1.61; 95%CI, 1.43-1.80), nedaug rukanciu (RR 1.29; 95% CI, 1.13-1.48), metusiu rukyti (RR 1.23; 95% CI, 1.14-1.33). Rukantiems ir sergantiems cukriniu diabetu asmenims da?niau stebimos mikrovaskulines komplikacijos tokios, kaip diabetine nefropatija, mikroalbuminurija, kurios gali buti gri?tamos metus rukyti.

28. II tipo cukrinio diabeto rizika Key Point Smoking can cause an elevated risk of type 2 diabetes in men. To assess whether there is a relationship between smoking and type 2 diabetes, Beziaud et al conducted a study in France of 27,777 volunteers (12,417 men and 15,360 women), aged 20-69 years. Smoking and alcohol consumption habits were determined, clinical parameters recorded, and glucose levels measured. Ex-smokers were defined as those who had stopped smoking at least a month before the examination. The risk of diabetes was calculated based on the subjects? glucose levels and expressed using odds ratios. Among men 20 to 69 years old, current smokers had an increased risk of diabetes (RR: 1.49; CI 1.13-1.96) compared with nonsmokers, and cessation of smoking did not significantly reduce this risk. Interestingly, the effect of smoking on the development of diabetes in women was not conclusive.Key Point Smoking can cause an elevated risk of type 2 diabetes in men. To assess whether there is a relationship between smoking and type 2 diabetes, Beziaud et al conducted a study in France of 27,777 volunteers (12,417 men and 15,360 women), aged 20-69 years. Smoking and alcohol consumption habits were determined, clinical parameters recorded, and glucose levels measured. Ex-smokers were defined as those who had stopped smoking at least a month before the examination. The risk of diabetes was calculated based on the subjects? glucose levels and expressed using odds ratios. Among men 20 to 69 years old, current smokers had an increased risk of diabetes (RR: 1.49; CI 1.13-1.96) compared with nonsmokers, and cessation of smoking did not significantly reduce this risk. Interestingly, the effect of smoking on the development of diabetes in women was not conclusive.

29. II tipo CD rizika metus rukyti Key Point Risk of diabetes decreases with increased duration of cessation. Wannamethee et al then studied the effects of smoking cessation on the increased risk of diabetes, finding that the risk of developing diabetes decreased with longer duration of cessation and returns to the nonsmoker level by 20 years after cessation. However, within the first 5 years, the risk actually increased even when adjusted for BMI. They determined that for those in this group, the length of time they had previously smoked was important. The increased risk was found only for those who had smoked for at least 30 years. The length of time smoked made no difference once a man had stopped smoking for more than 5 years.Key Point Risk of diabetes decreases with increased duration of cessation. Wannamethee et al then studied the effects of smoking cessation on the increased risk of diabetes, finding that the risk of developing diabetes decreased with longer duration of cessation and returns to the nonsmoker level by 20 years after cessation. However, within the first 5 years, the risk actually increased even when adjusted for BMI. They determined that for those in this group, the length of time they had previously smoked was important. The increased risk was found only for those who had smoked for at least 30 years. The length of time smoked made no difference once a man had stopped smoking for more than 5 years.

30. Rukymo neigiamas poveikis inkstu fukcijai Rukymas yra nefrotoksinis senesnio am?iaus pacientams, pacientams, sergantiems pirmine arterine hipertenzija, pacientams su beprasidedancia inkstu liga. Rukymas, sergantiems glomerulonefritu, policistiniu inkstu liga, skatina greitesni inkstu funkcijos nepakankamumo progresavima. Death-censored renal graft survival is decreased in smokers, indicating that smoking also damages the renal transplant. We performed a retrospective case-control study to assess whether smoking increases the risk to progress to ESRF in patients with IgA-glomerulonephritis or autosomal dominant polycystic kidney disease (23). Because of the small sample size and modest average tobacco consumption, the subgroup of women was excluded from further analysis. After adjustment for possible confounders, multivariate analysis revealed that the risk for ESRF was substantially higher in male smokers with no history of ACE inhibitor treatment (OR, 10.1 [2.3 to 45]; P 0.002). In contrast, the risk for smokers with a history of ACE inhibitor treatment was not significantly increased (OR, 1.4 [0.3 to 7.1]; P 0.65). Another case-control study confirmed that male patients who have glomerulonephritis and smoke are at increased risk of renal function impairment (24). In this study, the negative impact of smoking was particularly marked in elderly hypertensive men. Death-censored renal graft survival is decreased in smokers, indicating that smoking also damages the renal transplant. We performed a retrospective case-control study to assess whether smoking increases the risk to progress to ESRF in patients with IgA-glomerulonephritis or autosomal dominant polycystic kidney disease (23). Because of the small sample size and modest average tobacco consumption, the subgroup of women was excluded from further analysis. After adjustment for possible confounders, multivariate analysis revealed that the risk for ESRF was substantially higher in male smokers with no history of ACE inhibitor treatment (OR, 10.1 [2.3 to 45]; P 0.002). In contrast, the risk for smokers with a history of ACE inhibitor treatment was not significantly increased (OR, 1.4 [0.3 to 7.1]; P 0.65). Another case-control study confirmed that male patients who have glomerulonephritis and smoke are at increased risk of renal function impairment (24). In this study, the negative impact of smoking was particularly marked in elderly hypertensive men.

31. Rukymas pa?eid?ia inkstus, umiai pa?eisdamas hemodinamika padidina kraujo spaudima, padidina intraglomerulini spaudima, letai sutrikdo endotelio lasteliu funkcija.

32. Rukantiems asmenims da?niau stebima padidinta albumino ekskrecija ir mikroalbuminurija lyginant su nerukanciais asmenimis. Pacientams, surukantiems iki 20 cigareciu per diena ir surukantiems vir? 20 cigareciu dienai, stebimas skirtingas albumino koncentracijos ?lapime padidejimas (atitinkamai 1.33 ir 1.98) skirtingas mikroalbuminurijos da?nis (atitinkamai 1.92 ir 2.15). Atsirades inkstu funkcijos nepakankamumas pats savaime didina ?irdies ir kraujagysliu ligu rizika.Atsirades inkstu funkcijos nepakankamumas pats savaime didina ?irdies ir kraujagysliu ligu rizika.

33. Rukymas padidina rizika greitai progresuoti terminaliniam inkstu funkcijos nepakankamumui. Rukymo nutraukimas suma?ina inkstu nepakankamumo progresavima tiek pacientams su inkstu liga, tiek pacientams su transplantuotu inkstu. Rukanciuju, serganciu cukriniu diabetu ir turinciu transplantuota inksta, i?gyvenamumas yra labai ma?as. More recent studies using ambulatory BP measurement clearly document that smokers have higher BP than nonsmokers, i.e. an increase of approximately 3 to 12 mmHg in mean arterial pressure (MAP). This has been shown in several studies including healthy subjects, hypertensive subjects, patients with type 1 and type 2 diabetes, and patients with primary renal disease (for review, see reference 7).More recent studies using ambulatory BP measurement clearly document that smokers have higher BP than nonsmokers, i.e. an increase of approximately 3 to 12 mmHg in mean arterial pressure (MAP). This has been shown in several studies including healthy subjects, hypertensive subjects, patients with type 1 and type 2 diabetes, and patients with primary renal disease (for review, see reference 7).

34. Rukymas ir letines inkstu ligos rizika Key Point Smoking doubles the risk of chronic kidney disease (CKD). Cessation can greatly reduce this risk. Shankar et al conducted a study of 4926 people, aged 43 to 86 years, to determine what effect smoking (or alcohol consumption) has on kidney function. Smoking status was determined, serum creatinine measured, and glomerular filtration rate (GFR) calculated. In this study, CKD was defined as an estimated GFR of less than 60 mL/minute per 1.73 m2. Of the total participants, 324 had CKD, and of the total, 967 were smokers and 1737 were ex-smokers (defined in slide). Current smokers had double the risk of CKD than nonsmokers. Smoking cessation was able to return the odds to that of nonsmokers. When years since cessation were analyzed, the benefit was apparent in smokers who had stopped smoking for more than 5 years (odds ratio, 0.98; 95% CI, 0.51-1.90) as opposed to <5 years (odds ratio, 2.09; 95% CI, 1.14-3.83).Key Point Smoking doubles the risk of chronic kidney disease (CKD). Cessation can greatly reduce this risk. Shankar et al conducted a study of 4926 people, aged 43 to 86 years, to determine what effect smoking (or alcohol consumption) has on kidney function. Smoking status was determined, serum creatinine measured, and glomerular filtration rate (GFR) calculated. In this study, CKD was defined as an estimated GFR of less than 60 mL/minute per 1.73 m2. Of the total participants, 324 had CKD, and of the total, 967 were smokers and 1737 were ex-smokers (defined in slide). Current smokers had double the risk of CKD than nonsmokers. Smoking cessation was able to return the odds to that of nonsmokers. When years since cessation were analyzed, the benefit was apparent in smokers who had stopped smoking for more than 5 years (odds ratio, 0.98; 95% CI, 0.51-1.90) as opposed to <5 years (odds ratio, 2.09; 95% CI, 1.14-3.83).

35. Proteinurijos rizika rukantiems Key Point Current and ex-smokers have an increased risk of proteinuria. Halimi et al studied a sample from the general French population who had no known renal disease. Information about smoking habits was obtained from 27,777 people aged 20 to 69 years. Ex-smokers were defined as those who had quit smoking at least 1 month prior to the examination. The presence of proteinuria was determined by measurement from overnight urine samples; 1+ proteinuria was defined as 0.30 g/L and 2+ as 1 g/L. Unadjusted relative risk was determined to estimate the effect of smoking on proteinuria. Current and ex-smoking were associated with statistically similar increased risks of proteinuria (1+: approximately 2-fold; 2+: approximately 3-fold).Key Point Current and ex-smokers have an increased risk of proteinuria. Halimi et al studied a sample from the general French population who had no known renal disease. Information about smoking habits was obtained from 27,777 people aged 20 to 69 years. Ex-smokers were defined as those who had quit smoking at least 1 month prior to the examination. The presence of proteinuria was determined by measurement from overnight urine samples; 1+ proteinuria was defined as 0.30 g/L and 2+ as 1 g/L. Unadjusted relative risk was determined to estimate the effect of smoking on proteinuria. Current and ex-smoking were associated with statistically similar increased risks of proteinuria (1+: approximately 2-fold; 2+: approximately 3-fold).

36. Rukymas ir arterine hipertenzija Arterines hipertenzijos da?nis didesnis tarp rukanciuju nei tarp nerukanciuju (13.5 ir 8.8%; P=0.001). Hipertenzijos rizika yra didesne tarp rukanciuju nei tarp nerukanciuju (?S 1.31 [1.13 to 1.52]; P=0.001). Hipertenzijos rizika priklauso ir nuo per diena surukytu cigareciu skaiciaus (?S kiekvienoms 10 cigareciu 1.13 [1.05 to 1.21]; P=0.001) ir rukymo trukmes (?S, 0.99 [0.98 to 1.00]; P=0.01). Pacienti sergantys arterine hipertenzija ir turintys kairiojo skilvelio hpertrofija, surukantys 20 cigareciu per diena, rizika mikroambuminurijos yra 1.6 karto ir makroalbuminurijos rizika yra 3.7 didesne nei niekada nerukiusiuju. When body mass index was entered into the model, the risk of hypertension in former smokers was no longer significant; current smokers remained at risk for systolic hypertension, however. Some studies found an increase of BP only during daytime, which supports the observation that the effect of smoking on BP is short (lasting approximately 30 min) (7) There have also been case reports of an increase in BP as a result of smoking discontinuation.19 One potential explanation for increased BP as a result of quitting smoking may be the weight gain known to accompany quit attempts. Smoking appears to keep weight down, either through effects on the hypothalamus or through effects on the basal metabolic rate. Several studies have indicated that an approximate 5-kg weight gain often occurs with quitting smoking.24 A recent review25 of hypertension treatment suggests that maintaining the ideal body weight is effective in the prevention or management of hypertension. The same review states that BP is reduced by an average of 1.6/1.1 mm Hg for each 1 kg of weight loss. Pacienti sergantys arterine hipertenzija ir turintys kairiojo skilvelio hpertrofija, surukantys 20 cigareciu per diena, rizika mikroambuminurijos yra 1.6 karto ir makroalbuminurijos rizika yra 3.7 didesne nei niekada nerukiusiuju. When body mass index was entered into the model, the risk of hypertension in former smokers was no longer significant; current smokers remained at risk for systolic hypertension, however. Some studies found an increase of BP only during daytime, which supports the observation that the effect of smoking on BP is short (lasting approximately 30 min) (7) There have also been case reports of an increase in BP as a result of smoking discontinuation.19 One potential explanation for increased BP as a result of quitting smoking may be the weight gain known to accompany quit attempts. Smoking appears to keep weight down, either through effects on the hypothalamus or through effects on the basal metabolic rate. Several studies have indicated that an approximate 5-kg weight gain often occurs with quitting smoking.24 A recent review25 of hypertension treatment suggests that maintaining the ideal body weight is effective in the prevention or management of hypertension. The same review states that BP is reduced by an average of 1.6/1.1 mm Hg for each 1 kg of weight loss.

37. Rukymas ir ?irdies ligos Asmenims, gyvenantiems su rukanciuoju, I?L rizika yra 30% didesne nei gyvenusiu tarp nerukanciuju. Pacientu, serganciu I?L, jei metama rukyti, bendro mir?tamumo rizika suma?eja 36% (RR 0.64; 95% PI, 0.58-0.71). Esant arterinei hipertenzijai, padidintam cholesterolio kiekiui, rukymui, tikimybe umaus i?eminio sindromo padideja iki 8 kartu.

38. Klinikinis atvejis Ligone V. N. Gimusi 1971.05.15 (37 m.) Gyvenanti Kaune Gydyta KMUK I kardiologijos skyriuje nuo 2009.02.15 iki 2009.02.23.

39. Nusiskundimai Skausmas krutineje spaud?iancio pobud?io, stiprus, atsirandes ramybeje, u?trukes apie 1 val. laiko. Mineta simptomatika pirma karta gyvenime.

40. Rizikos veiksniai Rukymas: 20 cig./d. 15 m. Antsvoris Cukrinis diabetas II tipo, gydomas insulinu.

41. Objektyvus duomenys Bendra bukle sunki. Lie?uvis su apna?u. Krutines lastos skausmingumas pavir?inis. Alsavimas vezikulinis visame plauciu plote. ?irdies veikla ritmi?ka. ?SD 91 k/min. ?irdies tonai ai?kus. AKS 131/89 mmHg. Pilvo palpacija neskausminga. Peristaltika normali.

42. EKG (atvykus)

43. Laboratoriniai tyrimai leuk. 17,6-4,7x10/9, eritr. 4,46x10/12, Hb 145 g/l, tromb. 285x10/9, troponinas I - 0,19 mcg/l, glik. 6,74-13,15 mmol/l, Na 134 mmol/l, K 4,1 mmol/l, urea 5 mmol/l, kreatin. 59 mcmol/l, BCH 5,1 mmol/l, DTLCH 1,3 mmol/l, MTLCH 2,6 mmol/l, TG 1,53 mmol/l, GOT 165 U/l, GPT 97 U/l, CK 948 U/l, CRB 5,7 mg/l.

47. Gydymas R - II-III, D - Na, R (-) + CD; glycerol trinitras 0,5 mg/h i/v A?P, heparinas 5000 v.v. -> 1000 v.v./h i/v A?P; I kard. sk. ? aspirinas 100 mg x 1, klopidogrelis 75 mg x 1, nebivololis 2,5 mg x 1, ramiprilis 2,5 mg x 1, rosuvastatinas 10 mg x 1, KCl 1,5 g per os, humulin MIX 10 v.v. ryte ir 10 v.v. vakare, humalog 10 v.v. per pietus.

48. CHAMPIX skyrimas 1-3 dienos: 0,5 mg viena karta per para. 4-7 dienos: 0,5 mg du kartus per para. Nuo 8 dienos iki gydymo pabaigos: 1 mg du kartus per para. Pacientas turi pasirinkti data, kada mes rukyti. CHAMPIX reikia pradeti vartoti 1-2 savaites prie? ?ia data.

49. EKG (i?vykstant)

50. Rukymas ir dislipidemija Rukymas padidina MTL cholesterolio kieki kraujyje. Mesti rukyti ypac svarbu asmenims su padidintu MTL-Ch kiekiu kraujyje. Yra stiprus ry?ys tarp rukymo, trigliceridu kiekio ir DTL kiekio kraujyje. Ma?as DTL kiekis bei hipertrigliceridemija yra nepriklausomi I?L rizikos veiksniai. CHD and stroke was increased 3-fold, and CV mortality was markedly increased in subjects with the metabolic syndrome (P<0.001 for both outcomes). Perhaps not surprisingly, studies have indicated that the prevalence of smoking is higher in patients with the metabolic syndrome than in subjects without the metabolic syndrome.40 Another study41 established that cigarette smoking is independently associated with the metabolic syndrome. However, Masulli et al36 concluded that this association does not appear to be related to an insulin-resistance effect of smoking or an anti-insulin secretion effect of nicotine on pancreatic beta cells. In a further study, these authors concluded that the increase in the metabolic syndrome seen in smokers was largely driven by the higher prevalence of dyslipidemia.42 Regardless of the reasons for the association between smoking and the metabolic syndrome, studies have revealed that patients with the metabolic syndrome who quit smoking after an MI had a lower risk of further cardiac events (HR 0.485; 95% CI, 0.281-0.837) compared with those who continued to smoke. CHD and stroke was increased 3-fold, and CV mortality was markedly increased in subjects with the metabolic syndrome (P<0.001 for both outcomes). Perhaps not surprisingly, studies have indicated that the prevalence of smoking is higher in patients with the metabolic syndrome than in subjects without the metabolic syndrome.40 Another study41 established that cigarette smoking is independently associated with the metabolic syndrome. However, Masulli et al36 concluded that this association does not appear to be related to an insulin-resistance effect of smoking or an anti-insulin secretion effect of nicotine on pancreatic beta cells. In a further study, these authors concluded that the increase in the metabolic syndrome seen in smokers was largely driven by the higher prevalence of dyslipidemia.42 Regardless of the reasons for the association between smoking and the metabolic syndrome, studies have revealed that patients with the metabolic syndrome who quit smoking after an MI had a lower risk of further cardiac events (HR 0.485; 95% CI, 0.281-0.837) compared with those who continued to smoke.

51. Nikotinas stimuliuoja antinksciu ?ieve, del to i? adipocitu mobilizuojamos laivosios riebiosios rug?tys ir skatinama trigliceridu sinteze. Kita teorija ? rukantys turi ma?iau fermentu, skatinanciu DTL transportavima i? periferiniu audiniu, kas sukelia DTL suma?ejima plazmoje.

53. Rukymas ir odos ligos Budingi po?ymiai Odos pa?eidimai Plok?cialasteline adenoma ?aizdu gijimo sutrikimai In many cases, to the trained eye, smokers can be identified just by looking at their skin. The following slides illustrate some of the cutaneous manifestations of smoking, and demonstrate smoking?s effect on the development of squamous cell carcinoma. Data on the effect of smoking on wound healing will also be presented. In many cases, to the trained eye, smokers can be identified just by looking at their skin. The following slides illustrate some of the cutaneous manifestations of smoking, and demonstrate smoking?s effect on the development of squamous cell carcinoma. Data on the effect of smoking on wound healing will also be presented.

54. Odos po?ymiai Gerai matomos periorbitalines linijos Nuovargio po?ymiai Odos pilkumas Raudonos demes Smoker?s face Lines or wrinkles on the face, typically radiating at right angles from the upper and lower lips or corners of the eyes, deep lines on the cheeks, or numerous shallow lines on the cheeks and lower jaw A subtle gauntness of the facial features with prominence of the underlying bony contours An atrophic, gray appearance of the skin A plethoric, slightly orange, purple, and red complexionSmoker?s face Lines or wrinkles on the face, typically radiating at right angles from the upper and lower lips or corners of the eyes, deep lines on the cheeks, or numerous shallow lines on the cheeks and lower jaw A subtle gauntness of the facial features with prominence of the underlying bony contours An atrophic, gray appearance of the skin A plethoric, slightly orange, purple, and red complexion

55. Odos pa?eidimai Nagu geltonumas Nagu demarkacines linijos Smoker?s nail: yellow pigmentation of the nail plate in chronic smokers.Smoker?s nail: yellow pigmentation of the nail plate in chronic smokers.

56. Plok?cialastelinis ve?ys Rukantys turi 50% didesne ve?io rizika nei nerukantys Esami rukoriai turi didesne rizika nei mete rukyti. Key Point Smokers have a greater chance of developing cutaneous squamous cell carcinoma (SCC) than do nonsmokers. In a study of 107,900 white women, Grodstein et al showed that over an 8-year period, smokers were 50% more likely to develop cutaneous SCC than nonsmokers (RR, 1.5; 95% CI, 1.1-2.1). In a controlled study of people with various forms of carcinoma, De Hertog et al determined that current smokers were 3.3 times more likely (95% CI, 1.9-5.5) to develop SCC than nonsmokers, and that cessation of smoking reduced the RR to 1.9 (95% CI, 1.2-3.0).Key Point Smokers have a greater chance of developing cutaneous squamous cell carcinoma (SCC) than do nonsmokers. In a study of 107,900 white women, Grodstein et al showed that over an 8-year period, smokers were 50% more likely to develop cutaneous SCC than nonsmokers (RR, 1.5; 95% CI, 1.1-2.1). In a controlled study of people with various forms of carcinoma, De Hertog et al determined that current smokers were 3.3 times more likely (95% CI, 1.9-5.5) to develop SCC than nonsmokers, and that cessation of smoking reduced the RR to 1.9 (95% CI, 1.2-3.0).

57. ?aizdu gijimo sutrikimai Pablogeja odos kraujotaka Suma?eja imuninis atsakas, didesne infekcijos rizika. Didesne komplikaciju rizika pooperaciniame periode. U?trunka gijimo procesas. Key Point Smoking decreases the body?s ability to repair wounds. It has been known for 40 years that smoking decreases cutaneous blood flow, and this effect has been correlated with impaired wound healing. Dermal fibroblasts have been shown to undergo a significant decrease in activity upon nicotine exposure. In addition, smoking negatively affects mediators of the immune response, including decreasing interleukin (IL)-1 production, inhibition of early signals for B-cell transduction pathways, lowering natural killer cell cytotoxicity, and causing T-cell anergy. This, combined with the decreased cutaneous blood flow, has a significant effect on postsurgical healing, and surgeons often refuse to perform cosmetic surgery on patients who smoke and will not quit. Key Point Smoking decreases the body?s ability to repair wounds. It has been known for 40 years that smoking decreases cutaneous blood flow, and this effect has been correlated with impaired wound healing. Dermal fibroblasts have been shown to undergo a significant decrease in activity upon nicotine exposure. In addition, smoking negatively affects mediators of the immune response, including decreasing interleukin (IL)-1 production, inhibition of early signals for B-cell transduction pathways, lowering natural killer cell cytotoxicity, and causing T-cell anergy. This, combined with the decreased cutaneous blood flow, has a significant effect on postsurgical healing, and surgeons often refuse to perform cosmetic surgery on patients who smoke and will not quit.

58. Rukymas ir periodontines ligos Rukymas sutrikdo neutrofilu fukcija, pa?eid?ia u?degimini ir imunini atsaka i periodontinius patogenus. Rukymas susijes su periodontinemis ligomis tokiomis, kaip dantenu, alveolinio kaulo netekimo, infekcinemis-u?degiminemis ligomis.

59. Rukantys beveik 4 kartus nei niekada neruke serga periodontitu. Periodontologines ligos yra pasaulyje da?niausia dantu netekimo prie?astis. Key Point Smoking dramatically increases the risk of developing periodontitis. Cigarette smoking has been reported to increase the risk of periodontitis. Tomar et al conducted a statistical study to determine what proportion of periodontitis in the United States could be attributed to smoking (details on next slide). They concluded that current smokers are 4 times more likely to develop periodontitis than never smokers, and that 52.8% of periodontitis in the United States is attributable to smoking.Key Point Smoking dramatically increases the risk of developing periodontitis. Cigarette smoking has been reported to increase the risk of periodontitis. Tomar et al conducted a statistical study to determine what proportion of periodontitis in the United States could be attributed to smoking (details on next slide). They concluded that current smokers are 4 times more likely to develop periodontitis than never smokers, and that 52.8% of periodontitis in the United States is attributable to smoking.

60. Periodontito rizika Key Point Smoking increases the risk of periodontitis in a dose-dependent fashion. Tomar et al analyzed data from 12,329 participants in the Third National Health and Nutrition Examination Survey (NHANES III). Periodontitis was defined as the presence of one or more periodontal sites that had both a probing depth and loss of clinical attachment of =4 mm. Current smokers were defined as those who had smoked at least 100 cigarettes and currently smoked. ex-smokers had smoked at least 100 cigarettes and were not currently smoking. Bivariate analysis and multiple logistic regression was used to determine the link between smoking and periodontitis. Compared with never smokers, smokers? risk of periodontitis was increased in a dose-dependent manner over that of nonsmokers, up to almost 6-fold for the heaviest smokers. Cessation of smoking decreased the risk in a time-dependent fashion. After 11 years of not smoking, the risk was similar to that of a never smoker (not shown).Key Point Smoking increases the risk of periodontitis in a dose-dependent fashion. Tomar et al analyzed data from 12,329 participants in the Third National Health and Nutrition Examination Survey (NHANES III). Periodontitis was defined as the presence of one or more periodontal sites that had both a probing depth and loss of clinical attachment of =4 mm. Current smokers were defined as those who had smoked at least 100 cigarettes and currently smoked. ex-smokers had smoked at least 100 cigarettes and were not currently smoking. Bivariate analysis and multiple logistic regression was used to determine the link between smoking and periodontitis. Compared with never smokers, smokers? risk of periodontitis was increased in a dose-dependent manner over that of nonsmokers, up to almost 6-fold for the heaviest smokers. Cessation of smoking decreased the risk in a time-dependent fashion. After 11 years of not smoking, the risk was similar to that of a never smoker (not shown).

61. Burnos patologija Key Point Aside from periodontitis, smoking also causes a number of oral pathologies. These include: Brown hairy tongue is condition of defective desquamation of the filiform papillae that results from a number of precipitating factors. Precipitating factors for hairy tongue include poor oral hygiene, the use of medications (especially broad-spectrum antibiotics), tobacco use, coffee or tea drinking and therapeutic radiation of the head and the neck. Bacterial and fungal overgrowth play a role in the color of the tongue. Leukoplakia is a premalignant white plaque or lesion that cannot be wiped off with a gauze square and cannot be classified as any other disease. They can be white, white yellow, gray, or a mix of white and red. They can be smooth or wrinkled, and appear as cracks, fissures, or fingerlike projections. Nicotine stomatitis, also known as ?smoker?s palate? is a result of heat or trauma from pipes, cigars, or any type of smoked tobacco. Tissue on the palate turns gray. Necrotizing ulcerative gingivitis, also referred to as trench mouth, is an acute, progressive, painful infection with ulceration, swelling and sloughing off of dead tissue from the mouth and throat due to the spread of infection from the gums marked by ulceration and necrosis of the gum margin, destruction of the interdental papillae, and foul breath.Key Point Aside from periodontitis, smoking also causes a number of oral pathologies. These include: Brown hairy tongue is condition of defective desquamation of the filiform papillae that results from a number of precipitating factors. Precipitating factors for hairy tongue include poor oral hygiene, the use of medications (especially broad-spectrum antibiotics), tobacco use, coffee or tea drinking and therapeutic radiation of the head and the neck. Bacterial and fungal overgrowth play a role in the color of the tongue. Leukoplakia is a premalignant white plaque or lesion that cannot be wiped off with a gauze square and cannot be classified as any other disease. They can be white, white yellow, gray, or a mix of white and red. They can be smooth or wrinkled, and appear as cracks, fissures, or fingerlike projections. Nicotine stomatitis, also known as ?smoker?s palate? is a result of heat or trauma from pipes, cigars, or any type of smoked tobacco. Tissue on the palate turns gray. Necrotizing ulcerative gingivitis, also referred to as trench mouth, is an acute, progressive, painful infection with ulceration, swelling and sloughing off of dead tissue from the mouth and throat due to the spread of infection from the gums marked by ulceration and necrosis of the gum margin, destruction of the interdental papillae, and foul breath.

62. Plok?cialasteline karcinoma 70% burnos ve?io atveju susije su rukymu Simptomai: ?aizdos negyjancios Kaklo, gerkles patinimas I?liekancios baltos ar raudonos demes burnoje Sunkumas kramtant ar ryjant Svorio netekimas Prognoze 5-metu i?gyvenamumas ma?iau nei 50% Key Point Smoking is associated with the majority of cases of SCC. Oliver et al reviewed the files of 92 primary oral SCC patients from a 7-year period (1985-1992). Seventy-two (80%) of these patients were tobacco users. In another study (not shown), Lewin et al analyzed 605 SCC cases from the Swedish male population (aged 40-79 years) from the period of January 1988 to January 1991; 756 control subjects were randomly selected. Current smokers (those who smoked 1 year prior to interview) had a 6.5-fold RR of head and neck cancer (95% CI, 4.4-9.5) compared with never smokers. Ever smokers (men who had ever regularly smoked at least 7 grams of tobacco per week) had a 4-fold (95% CI, 2.8-5.7) greater risk.Key Point Smoking is associated with the majority of cases of SCC. Oliver et al reviewed the files of 92 primary oral SCC patients from a 7-year period (1985-1992). Seventy-two (80%) of these patients were tobacco users. In another study (not shown), Lewin et al analyzed 605 SCC cases from the Swedish male population (aged 40-79 years) from the period of January 1988 to January 1991; 756 control subjects were randomly selected. Current smokers (those who smoked 1 year prior to interview) had a 6.5-fold RR of head and neck cancer (95% CI, 4.4-9.5) compared with never smokers. Ever smokers (men who had ever regularly smoked at least 7 grams of tobacco per week) had a 4-fold (95% CI, 2.8-5.7) greater risk.

63. Apibendrinimas Sisteminis rukymo poveikis pasirei?kia u?degimu, oksidaciniu stresu ir endotelio disfunkcija. Metus rukyti rodikliai gali susinormalizuoti, skiriasi tik atsistatymo laikas. Rukymas gali itakoti ivairiu organu ligas.


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