resp diseases Flashcards
name some of the chemicals that contribute to toxicity in cigs and where they are deposited in the body
formaldehyde, ammonia, hydrogen cyanide, acetone, carbon monoxide
what are the organ systems that are are effected by smoking
nicotine - ns
carcinogens - cancers
ROS - cardiovasc, strokes
volatilised hydrocarbons - widespread damage
what is anthracosis
black pigments = macrophages that are phagocytosing carbon pigments, but die
what are the specific effects of smoking on neurological system
ntsm release - stimulus and relaxant dopamine = addiction serotonin = calming aCH = memory aCH + norepinephrine - sharpness beta-endorphins - decrease anxiety
effcts of smoking on cardiovascular effects
inc HR, blood pressure
widespread vessel-damage, causes vasoconstriction
accelerated atherosclerosis through endothelial injury
smoking impact on lung defence mechanisms
paralyses cilia = smokers cough to remove toxins
affected alveolar macrophages phag ability
reduced immune response = widespread inflammation
inc mucus secretions = inc infection risk egflu, pneumonia
what is COPD
Chronic bronchitis + emphysema
obstruction os airflow in pulmonary (bronchial tree)
progressive + inflammation
what are the risk factors for COPD
smoking, hereditary deficiecy of a1-antitrypsin, asthma, airway hyper-responsiveness
dscribe both chronic bronchitis and emphysema
CB = inc musuc + obstruction of small airways emphysema = enlarged air space + destruction of lung tissue
how is COPD diagnosed
forced expiratroy V in 1 second FEV1 = decrased bc of:
- inc resistance bc narrowed airway (CB)
- dec outflow pressure = loss of elastic recoil (emphysema)
what are the 5 elements of pathogenesis in copd and what do they cause
- infalmmation + fibrosis bronchial wall
- hypetrophy of submucosal glands
- hypersecretion mucus (1+2+3 = obstruct airway = mismatch between ventilation + perfusion)
- loss elastic lung fibre = impairs exp flow => air trapped + ariway collapse
- loss alveoli = loss SA
what clinical features impact copd
time of day (worse morning)
severity day
relative contributions of CB and emphysema
what are the early clinical features of COPD
insidiious-onset with progressive decline
fatigue, exercise intolerance, cough, dysponea, sputum production
rhonchi = prolonged low-frequency gurgles
late clinical copd paitents
hypoxaemia + hypercania
= vasoconstrict pulmonary arteries, pulmonary artery hypertension, RHS heart failre + pulmonary oedema
cyanosis bc vent/perf imbalance
describe copd treatmnet
DEPENDS ON STAGE
stop smoking
early diagnosis can halt progression
o2 therapy maintain 90% perfusion
immunisation against flu and pneumoccoal disease
bronchodilators = b2 adrenergic agonist
removal of distented lung tissue/lung transplant
what is emphysema
abnormal permanenet enlargement of teh airspace distal to terminal bronchioles
destruction of alveolar walls without fibrosis
inc airspace = hyperinfaltion, inc lung capacity, impaired ventilation
pathogenesis = protease/antiprotease theory (inherited deficiency)
dscribe protease/anti-protease theory
normallyl balanced prod + destruction
a2-antitrypsin = anti-protease protects lungs
in emphysema = toxins => ROS => dec a1-antitrypsin (or hereditary)
neut + alveolar macs release protease/elastase to destruct elastin/proteins
overall = dec anti-protease activity, destruction elastin = dec outflow pressure
clinical features of emphysema
pink puffers 60 yrs older dyspnear on exertion use accessory muscles like pursed lips lungs overinflated (barrel chest) weight loss minimal productive cough lack cyanosis
what is the definitino of chronic bronchitis
persistent cough with sputum prod for at least 3 months in 2 consecutive years
describe CB pathogenesis
cig damage = squamous metaplasia
airway obstruction = mucus plus
hypersecretion mucus in large airways from hypertrophy of submucosal glands
hypersecretion of mucus in small airways bc inc in goblet cells
acute +chronic inflam => fibrosis (further obstruction)
more predisposed to infections from pathogens
CB clinical presentation
blue bloaters cyanosis + oedema persistent cough + sputum hypoxia, hypercapnia dyspnea on exertion
what is the main type of malignant primary tumour and its characteristics and where it arises
bronchogenic carcinoma
poor 5yr survival
aggressive, highly metastatic
from bronchi epithelium
pale appearnace bc chronic inflam healing response
arise in/around lung (squamous cell carcinoma) or in peripphery = alveolar septal cells/ terminal bronchioles
what is the pattern of spready of lung cancer
penetrate bronchus wall
fungate into bronchioles
extend to pleural surface
spread to tracheal, bronchial + mediastinal nodes
metastasise => adrenal, liver, brain, bone
symptoms of lung cancers
non-specific = cough, weight loss, chest pain, dyspnea later = bronchial obstruction, pleural invasial and effusion, chest wall invasion + rib destruction, pericardial involvement -> pericarditis + cardiac tamponade
what are the 4 main types of small cell carcinoma
- small cell carcinoma = only smokers
- non-small cell: adenocarcinoma = common women + non-smokers
- non-small cell : squamous cell carcinoma = common men + smokers
- non-small cell: large cell carcinoma = highly anaplastic = poorly differentiated
describe microscopically small cell carcinoma
only smokers
highly malignant; ectopic hormone production
from neuroendocrine cells of bronchial epithelium
large number of cells, small in size little cytoplasm, lack structure
describe microscopically adenocarcinoma
women + nonsmokers
abnormal glandular appearance
dark nuclear appearance (dividing cells)
(looks like disorganised glands)
describe microscopically squamous cell carcinomas
common men + smokers areas of squamous metaplasa highly variable, slow growing, resectable keratin accumulation/pearls ark nuclei = dividing cells keratin pearls
describe microscopically large cell carcinoas
poor differ
describe microscopically large cell carcinoas
poor differentiation, unrecognisable combo of squamous and adenocarcinoma
anaplastic tumours with large polygonal cells with pleomorphic nuclei
may contain IC mucus
may be giant cells
may have clear/spindle shaped cells
