1-State the prevalence of smoking nationally,regionally and globally 2-Discuss the mechanism by...

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1-State the prevalence of smoking nationally ,regionally and globally 2-Discuss the mechanism by which smoking can induce lung emphysema3-Discuss the morphological changes of chronic bronchitis and emphysema

SMOKING

MY OBJECTIVES :

WAAD ALOTAIBI 311200661

Prevalence in KSA

About 19 percent of American adults smoke these days, compared with about 42 percent in 1965.less prevalent in Canada, Mexico and Iceland.Overall, the prevalence of smoking has gone down worldwide over the past few decades.

PREVALENCE OF TOBACCO USE 2009Men was highest in the WHO Western Pacific Region, with 51% of men aged 15 and above smoking some form of tobacco. Women was highest in the WHO European Region at 22%.In all WHO regions except Europe, girls aged 13–15 years old are using tobacco at higher rates than women aged 15 and older.

The high rates among girls suggest potential substantial increases for women in the near future.

The rates at which adolescent boys use tobacco average around 18% globally

EMPHYSEMA

DEFINITION :is characterized by abnormal permanent enlargement of

airspaces distal to terminal bronchioles accompanied by

destruction of their walls without obvious fibrosis

TYPES OF EMPHYSEMA: is classified according to its anatomic distribution

within the lobule 1-centriacinar 2- panacinar 3- distal acinar

4- irregular

1-centriacinar : more common and severe in upper lobs particulary in apical segments and this type is most commonly seen as a consequence of cigarette smoking in people who do not have congenital

deficiency of alpha 1-antitrypsin.

PATHOGENESIS :-the genesis of two common forms of emphysema (centriacinar – panacinar )is not completely understood

-emphysema arising as a consequence of two critical imbalances :the protease-antiprotease imbalance and oxidant-antioxidant imbalance

- . the protease-antiprotease imbalance hypothesis is based on the observation that patients with genetic deficiency of antiprotease alpha1-antitrypsin have a markedly enhanced tendency to develop pulmonary emphysema which is compounded by smoking

-alpha1-antitrypsin,normaly present in serum ,tissue fluids, and macrophages ,is major inhibitor of proteases (elastase) secreted by neutrophils during inflammation

-thus ,emphysema is seen to result from destructive effect of high protease activity in subjects with low antiprotease activity

MORPHOLOGICAL CHANGES IN EMPHYSEMA

GROSS:1-panacinar emphysema : pale, voluminous lungs that often obscure the heart

when the anterior chest wall is removed at autopsy 2-centriacinar emphysema: are less impressive .the lungs are deeper pink and

lesser voluminous than panacinar

MICROSCOPIC:Thinning and destruction of alveolar walls ,with advanced disease adjacent alveoli become confluent creating large airspaces

Terminal and respiratory bronchioles may be deformed because of the loss of septa

Loss of elastic tissue in surrounding alveolar septa

Bullous emphysema with large apical and subpleural bulla

COMPLICATED BY:

• CHF(cor pulmonal)• Pulmonary hypertension• Respiratory acidosis• Hypoxia • Coma• Pneumothorax • Collapse • Polycythemia

.

CHRONIC BRONCHITIS DEFINITION:

-the diagnosis of chronic bronchitis is made on clinical grounds : persistent

productive cough for at least 3 consecutive months in at least 2

consecutive years

TYPES /CLASSIFICATION :1- simple chronic bronchitis : mucoid sputum ,no obstruction of airflow 2- chronic asthmatic hyper-responsive airways with intermittent bronchospasm and wheezing 3- chronic obstructive bronchitis chronic outflow obstruction , usually with evidence of associated emphysema

•GROSS:Mucosal lining of the larger airways is usually hyperemic and swollen by edema fluid It is covered by a layer of mucinous or mucopurulent secretions

The smaller bronchi and bronchioles may also be filled with similar secretions

MICROSCOPIC:Enlargement of the mucus-secreting glands in the trachea and larger bronchi

It is assessed by the ratio of the thickness of the submucosal gland layer to that of the bronchial wall (Reid index;normally 0.4)Inflammatory cells , largely mononuclear -+/- neutrophils.

MORPHOLOGICAL CHANGES IN CHRONIC BRONCHITIS

• Pulmonary hypertension• Cardiac failure• Recurrent infections • Respiratory failure • COPD• Atypical metaplasia and dysplasia of respiratory epithelium

leads to malignancy

COMPLICATED BY:

REFERENCES:-CDC website

-Robbins