Respiratory Conditions Flashcards

Question

EFFECTS OF AGEING- in terms of lung

Answer 1

- Reduced respiratory surface area - increased alveolar size - reduced elasticity of lung tissue - dysregulation of fibroblast function - mitochondrial dysfunction

Answer 2

It is an obstructive disorder- meaning that patients who have this find it easy to inflate lungs but difficult to expel, so the lungs tend to hyper inflate. It is caused by a mutation of the CFTP gene on chromosome 7, where delta F508 amino acid is deleted in the genetic sequence. CFTR is a chloride ion transporter, so variants in this can cause defects in the whole transportation process: an epithelial cell pumps out a chloride ion into its surface using ATP, but this cannot happen when there is a CFTR variant. The cellular defects caused by variants include defects in protein production and processing, as well as defects in the function and regulation of the pump. Airway obstruction is a key issue in cystic fibrosis, as well as defects in antimicrobial defences. There is reduces chloride secretion, which causes increased sodium reabsorption into epithelial cells, and water also follows the sodium. Mucus in the lung becomes more sticky and dehydrated, so it sticks to the surface of the lungs. This causes a change in the pH of the bronchial epithelia- creating a defect in antimicrobial defences. In the respiratory system, mucus can plug bronchioles, which can then cause the alveoli to collapse- this seriously affects ventilation perfusion coupling and gas transfer. This can then cause a lung abscess if there are large areas of the lung that have collapsed. Cystic fibrosis can also cause bronchiectasis, which is a widening of the airway due to mucus restricting the amount of air that can pass. The mucus can cause bacterial infection, leading to inflammation and airway destruction, creating scarring of the airway wall- which thickens it. Aside from the lungs, cystic fibrosis affects multiple other systems. It can cause abnormal sweat production, chronic inflammation of the pancreas, and autoimmune damage to the biliary system in the liver due to blockage. It can also obstruct the vas deferens in men, which leads to sterility. Cystic fibrosis can cause pathological complications in the lung, such as chronic airway infection, pulmonary fibrosis, and chronic respiratory failure. It can also cause cysts that rupture, creating widespread tissue destruction.

Answer 3

It is an obstructive disorder mainly associated with adult behaviours such as smoking and living in a polluted environment, but childhood risk factors can also be significant such as childhood asthma, severe respiratory conditions before 5 years old, and maternal smoking. the obstruction comes from mucus plugging, inflammation, and a loss of tissue to hold the airways open. Chronic bronchitis and emphysema together cause the airway obstruction seen in COPD. emphysema is basically the structural changes of the lung, and chronic bronchitis shows clinical features, like the cough involved- and both are due to smoking. emphysema is an enlargement of the airspeces of the lung due to a loss of tissue (alveoli in particular). chronic bronchitis causes goblet cells to produce an excess amount of mucus in an attempt to move smoke out of the lungs, but smoke damages cillia so the mucocilliary escalator cannot move the mucus. this blocks the airway. this therefore stops air from being able to leave the lungs as well, coz it gets trapped, and can cause hyperinflation of the lung

Answer 4

Where there is permanent destruction and enlargement of the alveoli airspaces. This means that there is a loss of elastic recoil and a reduced surface area in the alveoli where gas exchange can happen. Macrophages and neutrophils phagocytose smoke perticles/chemicals that have been inhaled deep into the alveoli of the lungs. This changes their behaviour to become defensive, so they release serine elastase is released. This is an enzyme that breaks down elastic tissue by destroying the elastin. However, this occurs uncontrollably. This is because when macrophages and neutrophils phagocytose the smoke, they release reactive oxygen species, which, as well as the smoke itself, inactivate alpha1-antitripsin. This is produced in the liver and homeostatically controls how much serine elastase is released. So, this uncontrolled destruction of elastin in tissue is the cause of emphysema. some peopel have a deficiancy in alpha1-antitripsin, so they are at risk of early onset emphysema.

Answer 5

it is inflammation of the bronchi. basically, the production of excess mucus and loss of cillia create an inflammatory response. when smoke is inhalade, goblet cells produce an excess amount of mucus to try to get rid of it. however, we cant clear this excess mucus coz smoke damages cillia, so the mucocilliary escalator is not fully functioning. this causes pits of mucosa as it widens mucus ducts. to clear the pits, patients cough. the loss of cillia over time due to smoke exposure causes disorganised growth of stem cells, as colomner cells turn into squamous cells, further reinforcing the lack of cillia. This causes an inflammatory response. We get a generalised edema (swelling) of the lumen of the bronchiole. this, with the excess mucus fully blocks the bronchiole. and this with likely get infected with bacteria. Macrophages are recruited to reinforce the inflammatory response. in long term inflammation, fibroblasts are also recruited- they lay down large fibres in the tissue, which affects the flexibility of the bronchioles. This affects the bodys ability to vasoconstrict and vasodilate. all of this can cause hypoxemia and hypercapnia, as it prevents gas transfer. to prevent cyanosis from happening, vasocnstriction happens at the sites of blocked bronchioles to try to shunt the blood into areas where the bronchioles arent blocked. but, this can cause the pulmonary circulatory system to have more resistance against the heart beating, so its harder to pump blood to the lungs, so there is heart failure to this side of the heart.

Answer 6

1. Character of the air being breathed (cold/ pollutants/ smoking eg passive) 2. Acid reflux – where the acid in the stomach leaks out into the lower eosophagus 3. Post nasal drip – where someone sniffs to keep their runny nose in- it can go into the trachea 4. Stress and anxiety 5. Genetic linkage 6. Drug induced

Answer 7

This is also called interstitial lung disease, and it is a restrictive disorder, meaning that there is reduced ability to inflate the lungs. This is because excess bands of collagen are formed in the interstitial space between the alveoli, as well as inappropriate fibres being laid by fibroblasts. This is how scar tissue forms, and it compromises the elasticity of the lungs- so it restricts the lungs’ ability to increase its volume. The bronchioles tend to be wider due to extensive elastic recoil, which is reinforced by heavy bands of collagen in the connective tissue. If inflammation in the interstitial space becomes chronic, fibroblasts can invade the alveoli, which can section areas off and cause a collapse. These collapsed areas have high risk for infection. Symptoms include: dry cough, reduced chest movement, wheezing sounds from the chest, difficulty breathing.

Answer 8

Normal bronchioles are surrounded by elastic tissue, with a nice amount of alveoli holding the bronchiole open.

Answer 9

It is 2 phase process… In the immediate phase, an allergen in inhaled and enters the bronchioles. This activates mast cells to express immunoglobins, which recognises the allergy trigger. The individual is sensitised to the activation of the mast cells, which will degranulate with T-helper cells, and inflammatory mediators (eg mast cells) are released. This triggers bronchoconstriction, vascular permeability, and mucus production. Bronchoconstriction means that the bronchiole lumen is reduces due to smooth muscle contracting. Vascular permeability causes the edema of the tissues. Finally, mucus production further compromises the physical space available in the lumen. These are key features in developing an inflammatory response. In the delayed response, eosinophils and other inflammatory cells start to release factors which reduce ciliary function and can lead to epithelial damage due to the degradation of ciliated cells. This damage activates sensory nerve endings, which leads to a positive feedback loop that needs to be disrupted by medication. This is because the activation of nerve endings causes the NS to stimulate mucus secretion and bronchoconstriction, which further damages the tissue and activates more sensory nerve endings