RS Lecture 11 and 12 - Lung Infection and Lung Mechanics Flashcards Preview

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Flashcards in RS Lecture 11 and 12 - Lung Infection and Lung Mechanics Deck (58):

What are the mechanical defense mechanisms of the respiratory tract against infections?

URT filtration, mucociliary clearance, cough, surfactant, epithelial barrier


What are the local defense mechanisms of the respiratory tract against infections?

BALT -> IS within resp tract that samples Ag we inhale and produce Ab to neutralise it; sIgA, lysozyme, transferrin, antiproteinases, alveolar macrophages


What are the systemic defense mechanisms of the respiratory tract against infections?

Polymorphonuclear leucocytes, complement, immunoglobulins


Where do ciliated epithelium line?

All airways up to respiratory bronchioles, knitted together with tight junctions


What surrounds the cilia?

Periciliary fluid which is watery -> mucus floats on top of cilia and is more sticky and gel-like


What happens when an infectious particle is breathed in?

It sticks to the mucus on the top and the beating of underlying cilia drive mucus up to back of throat where it is swallowed/coughed up


How often does each cilium beat?

15 x per second -> to a metachromal rhythm


How do the cilia beat the mucus in one direction?

Coordinated -> backward movement is different to forward movement -> downward stroke engages with mucus to push it forward, then at the bottom of forward movement, cilium withdraws in curved fashion, withdrawn within periciliary fluid back to start to repeat movement


How are the cilia specialised to engage with the mucus?

Little claws on their tips


What is the structure of a cilia?

9+2 pattern -> 9 pairs of microtubule around outside which have dynein arms


What do the dynein arms contain?

ATPase, which provides energy for microtubules in the cilium to move up and down each other to make the cilia bend -> central microtubules used as an axis


What are the 2 most common acquired defects of the mucociliary system?

Cigarette smoking and viral infection


What happens when a virus invades you airways?

Cilia are destroyed, cold-like symptoms, tight junctions fall apart -> mucus become yellow-green colour


Why does mucus become yellow-green when infected?

Bacterial infection has capitalised on the weakness of resp epithelium brought about by virus


What happens after the virus has been cleared?

Cilia need time to regrow, with mucociliary system disabled for around 6wks, but cilia can grow back as compound cilia (useless)


What are some respiratory infection syndromes?

Acute (overwhelming) - due to very virulent bug or disorder of host defence. Recurrent-acute (slow to resolve) - bronchial, pneumonic, abnormalities in host defences present in people with recurrent acute illnesses. Daily purulent sputum only temporarily responding to AB - releasing yellow/green phlegm on a daily basis is also unusual, could be abnormality of host defences


What is dextrocardia and what does it suggest?

Heart pointing towards RHS, suggests there could be a ciliary abnormality -> 50% of people born without functioning cilia have dextrocardia


Why does dextrocardia occur in those without functioning cilia?

Because microtubules are used to guide the cells around during embryological development


What cilia defect can occur?

Dynein arm defect -> outer dynein arm isn't present, so cilia don't work


What are the levels of NO in normal and people with primary ciliary dyskinesia?

People with PCD have less NO than normal people -> have less nasal NOs


What are some bacteria that infect the airway?

Haemophilus influenzae is the most common cause of bronchitis and sinusitis


How is Haemophilus influenzae adapted for airway infection?

Hair-like fimbriae that act as anchors to get the bug to attach to the epithelial surface -> once on epithelium it begins to divide and form a colony


Where do bacteria stick onto in the airway?

Onto DAMAGED epithelium not where there are cilia


What are some bacterial strategies to avoid clearance from the airways?

Exoproducts, Enzymes -> break down local Ig. Exoproducts, Adherence, Avoiding immune surveillance.


How do exoproducts impair mucociliary clearance and affect WBCs?

Impair mucociliary clearance by slowing and disorganising ciliary beat, stimulate mucus production, affect ion transport and damage epithelium. Impair neutrophil, macrophage and lymphocyte function.


How does adherence help bacteria avoid clearance from airways?

Increased by epithelial damage and tight junction separation.


How do bacteria avoid immune surveillance in the airways?

Surface heterogeneity, biofilm formation, surrounding gel and endocytosis


What are the clinical features of pneumonia?

Cough, sputum, fever, dyspnoea, pleural pain (pain fibres on surface of lungs, so when lung solidifies and inflammation enters periphery, stabbing pleuritic chest pain occurs), headache


What is the most common cause of bacterial pneumonia and how is this bacteria adapted to be virulent?

Streptococcus pneumoniae -> has a polysaccharide capsule around it (negatively charged), so bug has difficulty binding to epithelium but makes it more virulent and is able to invade bloodstream and cause systemic invasion -> produces toxin that punches holes in cells and kills them (pneumolycin)


What is bronchiectasis?

Abnormal widening of bronchi or their branches, causing risk of infection


What is gas trapping and what causes it?

Inspiration requires muscles to function, and for expiration passive recoil from lung elasticity is enough, however if lung is diseased and has lost its elasticity, so as it collapses back, the airways close down and air gets trapped -> hence why people with diseased lungs have much higher residual volume


What is the histology of bronchiectatic airways?

Dilated airways strung together by scar tissue, with pooling of phelgm


What are the common complaints of patients with bronchiestasis?

Daily sputum production, recurrent respiratory infections, breathlessness (asthma and small airways disease), fatigue (severe tiredness and lethargy, difficulty concentrating)


How can removing the built up phlegm help patients?

People do physiotherapy every day to empty lungs and by getting rid of dirty phlegm, you remove the stimulus for the neutrophils to move in, reducing the inflammation


What are the 8 causes of bronchial sepsis?

Congenital, mechanical obstruction, inflammatory pneumonitis, fibrosis, postinfective, immunological, impaired mucociliary clearance, immune deficiency -> people with Marfan's syndrome can also have it


What is the vicious cycle of infection and inflammation and how is it caused?

If the infection becomes chronic then you also get chronic inflammation, which in itself can damage the body, due to impaired lung defences which the inflammation further damages lung defences causing more infection and inflammation


What is the most important cause of the damage from inflammation?

Protease-antiprotease balance


How does the protease-antiprotease balance cause damage?

Neutrophil enters airway and releases proteases to kill the bacteria that it phagocytosed, with a little bit of protease spilling during phagocytosis onto the surrounding tissues, usually anti-proteases are present in the airways to neutralise it but with chronic inflammation too many neutrophils release too much proteases, so it overwhelms the antiproteases, so free proteases sit in yellow-green sputum and cause damage


What do proteases do?

Break down the elastin, digesting structure of bronchial wall, eats away at the epithelial surface causing damage


Whats the difference between normal, obstructive and restrictive pulmonary diseases?

Obstructive has bigger RV due to trapped air or due increased resistance, so is more difficult to move air (decreased radius due to mucus); restrictive has smaller RV due to chest wall not being able to expand. TLC is bigger in obstructive, smaller in restrictive. VC decreases in both obstructive and restrictive.


What are the chronic and acute causes of obstructive PD?

Chronic: COPD, emphysema, bronchitis. Acute: asthma


What are the pulmonary and extrapulmonary causes of restrictive PD?

Pulm: Lung fibrosis, interstitial lung disease. Extrapulm: obesity, neuromuscular disease


What is the mechanism of ventilation?

Small change in pressure gives a relatively large change in volume -> middle of curve. Huge amount of energy needed to change the same amount of volume -> at the ends


How do the lungs interact at different points of the graph?

Tending towards y-axis can be done steadily with recoil force or actively (expiration) -> NO NET AIRFLOW right: just after tidal inspiration; left: apply just a little bit of expiratory force; middle: functional residual capacity


How much energy is needed for tidal inspiration and expiration?

Tidal inspiration needs muscular effort, so energy; but tidal expiration is a passive process


How do the mechanics of ventilation change for restrictive and obstructive PD?

Restrictive: VC is smaller, FRC is lower, sigmoid shape is flattened, so to reach either ends even greater pressure is needed. Obstructive: Curves are narrower, flatter and is pushed higher -> more compliant, so bigger forces = bigger changes to volume


How does the alveolar pressure change during tidal breathing?

Pressure applied, so its more negative in the alveoli, so air flows in -> at the end of inspiration there is no air flow, then remove inspiratory force, so chest and lung recoil, increasing alveolar pressure, so air flows from inside to outside of lung


What is compliance?

Tendency to distort under pressure -> COPD (floppy) -> compliance = change in volume/change in pressure


What is elastance?

The tendency to recoil to its original volume, elastance = change in pressure/change in volume


How does surface tension affect compliance in the lungs?

Filling lungs with fluid means they are more compliant -> small amount of surfactant lining the lungs and the air-water interface exhibits surface tension, but the fluid-water one doesn't


What is surface tension?

Water molecules in alveolus all interact but at the top layer, there is air one side so no mathcing force, so the top layer molecules are pulled down, causing tension across the top


How does the shape of the alveoli affect distribution of water?

Distribution of water is more dense around the outside and on the inside, the water molecules are all attracted across the alveolar space to water molecules on the opposite side -> if the alveoli were too small the forces would pull alveoli together and collapse them -> surfactant ensures the collapsing pressure is lower as it spreads around the water disrupting the distribution with its phospholipids


What is present in pulmonary surfactant?

80% polar phospholipids, 10% non-polar lipids, 10% protein


What is the role of surfactant?

Prevents collapse of small alveoli (as there is increased surfactant in smaller ones, so overall pressure is the same), increases compliance by reducing surface tension, reduces the 'work of breathing'


What is resistance?

Resistance is inversely proportional to radius^4 -> as the airways bifurcate so rapidly, the air doesn't really flow at the very peripherals, so resistance is very low at the peripherals of the lung


What is conductance?

Resistance decreases as lung volume increases, as the airways dilate upon inspiration -> exponential decrease; conductance increases as lung volume increases -> linear relationship


What is Poiseuille's law?

Viscosity of gas (which increases resistance) = n -> radius changes resistance the greatest


How does air flow in collapsible tubes?

Airway transmural pressure is a pulling force, keeping the airways open = preinspiration. Airway is patent during pre/mid/post inspiration. During forced expiration, there will be a massive increase in intrapleural pressure -> if pleural pressure exceeds the internal pressure of any collapsible tube, then airway might close making expiration difficult

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