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Medicine Notes Cardiorespiratory Fitness Notes

Effects Of Smoking Copd Notes

Updated Effects Of Smoking Copd Notes

Cardiorespiratory Fitness Notes

Cardiorespiratory Fitness

Approximately 173 pages

These notes offer you pretty much everything you could need to know for the Heart, Lungs & Blood module. They are designed around the Manchester PBL system, but aren't specific to it. The main topics of the PBL cases were: pneumothorax, asthma, COPD, heart failure, myocardial infarction, anaemia, DVT & PE, and blood loss. These topics are covered, as well as all of the normal physiology and behavioural & social aspects....

The following is a more accessible plain text extract of the PDF sample above, taken from our Cardiorespiratory Fitness Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Semester 2

Case 3: Turning Blue

• What are the dangers of smoking?

[1] General effects: Lung cancer, COPD, carcinoma of the oesophagus, ischaemic heart disease, peripheral vascular disease, bladder cancer, an increase in abnormal spermatozoa, and memory problems.

Maternal smoking: A decrease in birth weight of the infant, an increase in foetal and neonatal mortality, and an increase in asthma.

Passive smoking: Risk of asthma, pneumonia and bronchitis in infants of smokers, an increase in cough and breathlessness in smokers and non-smokers with COPD and asthma, and increased cancer risk.

• What are the effects of smoking on the respiratory system?

[1, 2, 3, 4] Cigarette smoke contains polycyclic aromatic hydrocarbons & nitrosamines, which are potent carcinogens & mutagens in animals. It causes release of proteolytic enzymes from neutrophils granulocytes & macrophages. This attracts leukocytes, which release proteases, including elastase, which destroys elastin, and leads to lung damage. This process is usually inhibited by α1-antitrypsin, but this itself is inhibited by oxygen radicals released by leukocytes.

Pulmonary epithelial permeability increases & correlates with the concentration of carboxyhaemoglobin in the blood. This increased permeability possibly allows easier access to carcinogens.

A low-grade systemic inflammatory response is evident in smokers, involving mediators such as; elevated levels of C-reactive protein (CRP), fibrinogen, IL-6, & increased counts of WBC.

There is also a reduction in endogenous nitric oxide production, which plays a role in regulation of pulmonary vasomotor tone. NO causes increased levels of cGMP in lung smooth muscle, which controls K+ and Ca2+ channels, controlling vasodilation.

Effects on mouth, larynx, & pharynx

These areas suffer continual irritation from smoking, & tobacco users my develop hoarseness, coughing & wheezing due to inflammation. Smoking is linked to cancers of the mouth, larynx, & pharynx.

Effects on bronchi

The smoke acts on the cilia & damages them so that they no longer function. Excess mucus & foreign matter build up in the bronchial space. Symptoms of chronic bronchitis arise to compensate for this. A frequent cough & expulsion of phlegm indicate this first stage of COPD.

Effects on lungs

The alveoli suffer from cigarette smoking, eventually breaking down & losing their effectiveness in gas exchange. It causes apoptosis of alveolar epithelial cells, which may be due to an interaction between aldehydes & oxidants present in cigarette smoke or formed in cigarette smoke-exposed cells. Cigarette smoke also suppresses proliferation, attenuates attachment and augments detachment of the alveolar epithelial cells. It can also suppress surfactant secretion & collagen production.

Effects on pulmonary blood vessels

Tobacco use causes atherosclerosis. When the pulmonary vessels are affected, high blood pressure results, which causes pulmonary hypertension. This can lead to arrhythmia, heart failure, DVT, and pulmonary embolism.

• What is COPD?

[1, 2] Chronic obstructive pulmonary disease is the occurrence of chronic bronchitis & emphysema in the same patient, who is almost always a smoker. Prior to 1979, patients with these conditions were often classified by: symptoms (e.g. chronic bronchitis, chronic asthma), pathological changes (e.g. emphysema), and physiological correlates (pink puffers & blue bloaters).

Pink Puffers Blue Bloaters
Body Size Thin Obese
Chest Hyperinflation Marked Present
Predominant Disease Emphysema Chronic bronchitis
Post-mortem Finding Panacinar emphysema Centrilobular emphysema
Cor Pulmonale Absent Present
Secondary Polycythaemia Absent Present
Cyanose Absent Centrally
Blood Gases Low PaCO2 Raised PaCO2

This presents 2 ends of a spectrum of illness & most patients fall between the two.

It was a recognition that emphysema & chronic bronchitis overlapped & often coincided which led to the need for the new term ‘COPD’. COPD is a disease state characterised by airflow limitation that isn’t fully reversible. Airflow limitation is usually both progressive & associated with an abnormal inflammatory response of the lungs to noxious particles or gases.

Epidemiology & Aetiology

It is caused by long-term exposure to toxic particles & gases. >90% of cases are caused by cigarette smoking in developed countries. However, only 10-20% of heavy smokers (30 cigarettes per day) develop COPD – some individuals are more susceptible. The risk to someone who smokes 30-a-day is 20 times that of a non-smoker.

Climate & air pollution are less important. However, there’s a great increase in COPD mortality during periods of heavy atmospheric pollution.

Urbanisation, social class, & occupation may also play a part in aetiology, but are difficult to separate from effects of smoking.

In the UK, COPD causes about 18million lost working days for men & about 2.1million lost working days for women per year. It accounts for 7% of sickness absences.

According to WHO, 65million people have moderate to severe COPD. >3million people died of COPD in 2005. It accounted for about 5% of all deaths globally. It is estimated that by 2020 it’ll become the 3rd most common cause of death.

Pathophysiology

Bronchitis Characteristics: The most consistent finding is hypertrophy & increase in number of mucus-secreting goblet cells of the bronchial tree, evenly distributed throughout the lung but mainly seen in larger bronchi. Initially in disease before development of breathlessness, small airways are particularly affected. The initial inflammation is reversible. In more advanced cases, the bronchi become obviously inflamed, and there is pus in the lumen. In severe disease, acute & chronic inflammatory cells & lymphoid follicles infiltrate on the walls of the bronchi & bronchioles. However, it is...

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