definitions

blood flow to the heart is cut off due to a blockage in the coronary artery

irreversible dilation of the bronchi due to structural airway injury.

caused my mutations to the CFTR gene. Causing abnormalities to salt and fluid clearance across the epithelium

inflammatory exudate within the alveolar space

excess fluid in the pleural space

air in the pleural space between the visceral and parietal pleura

expectoration (sputum) on most days for 3/12 for 2 years

enlargement of air spaces and destruction of alveolar walls

inflammation of the bronchi and lungs

lung disorder that produces similar inflammatory and fibrotic changes in the interstitum or intra-alveolar septa of the lung

Thin atrophied airway walls, and loss of alveolar walls and capillary beds

Mucous gland hypertrophy & goblet cell hyperplasia → ↑ mucus production. Ciliary dysfunction → impaired clearance of mucus. Chronic inflammation in small airways → * Narrowing of lumen * Cellular infiltrates (inflammatory cells), * Oedema of airway walls.

Loss of negative intrapleural pressure causes the lung to collapse inwards.

Fluid compresses the lung underneath and restricts expansion.

Alveolar spaces are filled partially or completely with fluid and blood cells (infectious debris & exudate)

Defective CFTR protein causes impaired chloride secretion and increased sodium absorption. Leads to dehydrated, thick mucus on epithelial surfaces. Lungs’ airway obstruction leads to infections, inflammation and bronchiectasis.

Loss of cilia, mucous gland hyperplasia, airway wall destruction, and permanent dilation of the bronchi

Inflammation and fibrosis develops in the interstitial and alveolar tissues. This makes the lungs stiffer (↓ compliance) → harder to expand with each breath. The alveolar–capillary membrane thickens, impairing diffusion of gases, especially oxygen.

Alveolar spaces are filled partially or completely with fluid and blood cells (infectious debris & exudate)

• a plaque in the heart artery breaks open forming a thrombus • this blocks O2 from reaching part of the heart muscle • without O2 the muscle gets injured and starts to die (necrosis) starting in the inner layer and going out • dead tissue is replaced by scar tissue

ANGINA: - Chest pain that’s triggered by exercise and stress - pain eases with rest -temporary decreased blood flow - no permanent heart damage MYOCARDIAL INFACTION: - chest pain is more severe and long-lasting - pain doesn’t go away - leads to permanent damage (death of the heart muscle)

Non-ST elevation myocardial infarction

ST Elevated myocardial infarction

complete artery blockage causing necrosis, characterized by elevated Troponins