Week 8 - COPD overveiw Flashcards
what is COPD?
chronic obstructive pulmonary disease
characterised by respiritory symptoms and airflow limittions due to airway/alveoli abnomralities
what are the cartacteristics of COPD
chornic and recurrent obstruction of airways and airflow
obstruction is usually progressive and is accompined by inflamatory responses
will usually encompase variations of combined bronchitis and emphysema with or with pout asthma?
what are the clinical features differentiating asthma and COPD?
Asthma - airway hyperactivity
bronchodilator repsone
corticosteriod response
COPD- no airway hyperactivity
poor bronchodilator response
poor corticosteriod response
what are the differences between asthma and COPD in relation to inflamatory cells?
Asthma- mast cells, eosinophils, macrophages +
COPD- neutrophils
macrophages ++
what are the differences between asthma and COPD in terms of inflamatory effects?
asthma- all airways, epithelial shedding. no parechymal involvments, mucous secertions +, fibrosis +, oxidative stress +
COPD- peripheral airways, epithelaia metaplasia, paranchymal envolvment, mucous secresion +++, fibrosis ++, oxadative stress +++
what are some differences youd see in chronic broncitis vs emphysema?
B - obese and cynotic, chronic porductive cough, roonchi and weezes on asultation
E - older and thinner, quiet chest, esevre dysponea, perminate enlargment of terminal bronchiols
what are the risk factors for COPD?
smoking - 80-90% smokers risk COPD development
asthmatics who smoke
resp infections during childhood
occupational exposere
exposure to air pollutions
age >40
possible genetics
what is the basic pathphys of bronchitis?
inflamatory response
increased mucous roduction
proloned inflamation - damage to cilia and bodys ability to secrete mucous decreased
narrowed and clogged bronchi
increased thickness bronchial walls
airway obstructin
what happens in the disease progression of bronchitits?
smoking - destroys cilia - decrease motility and increased coughing
inflamation - airway thickening (hyperplasia) - stratified sqaumous epithelium
globlet cell hypersecretion - increased mucous - increased sputum
accumulation bacteria - episodic bronchitis and chronic inflamtion
what is the basic pathophysiology of emphasyma?
inflamatory trigger
inflmatory response-neutrophils and macrophages secre protease
protease - reduced feedback due to smoking or genetics
increased protease action destruction alveoli elastin
reduced surface are for gas exchage - decreased external respiration
decreas elastic recoil causing hyperinflation
gas trapping and increased intra-thoracic pressure
what is emphysema?
focal destruction of terminal bronchiols and alveoli due to lost elestin that is replaced with collogen
what does emphasyma result in?
o compensate
hypoxia
hypoxemia
flatterned diapghram - increased WOB t
what does chronic bronachitis result in?
gas trapping, hypoxia, hypoxemia and hypercapnia
what are the systemic effects of COPD?
cachexia - skeletal muscle wastage related to inflmation and decreased activity
increased risk of CV disease
pulmonary hypertension
what causes an increase in pulmonary hypertension n COPD?
alveoloar hypoxia - pulmnary vasoconstiction
PH causes RVHm dysfunction and righ sided heart failure
