Respiratory System Flashcards
What does the kinetic theory of gases state?
That gases are particles moving around a space, that generate pressure by colliding with the walls of that space. Increased frequency and strength of those collisions, increases the pressure
What does Boyle’s law state?
That at a constant temperature, pressure is inversely proportional to volume
What does Charles’ law state?
Pressure is directly proportional to absolute temperature
What is the universal gas law?
Allows calculation of how volume will change as temperature and pressure change
Vol. x pressure = gas constant x temp (K)
What is partial pressure?
The fractional pressure of a gas in a maxture, normally at the same proportion as the fraction of volume of the gas in a mixture
What is vapour pressure?
The partial pressure that’s exerted by water molecules evaporating out and gas molecules dissolving into water
What is saturated vapour pressure?
Partial pressure when the rate of water molecules evaporating and gas molecules dissolving at the same time, is equal
What is meant by tension of a gas?
How readily the gas will leave a liquid
What is the mean pressure of pulmonary arteries, veins and capillaries?
Arteries - 12-15 mmHg
Capillaries 9-12 mmHg
Veins 5 mmHg
What is the optimal perfusion/ventilation ratio?
0.8
How can chronic hypoxic vasoconstriction lead to heart failure?
Increased vascular resistance from pulmonary vessels increases the afterload for the right ventricle - right ventricle failure
What is the distinguishing feature between components of the upper and lower respiratory tract
Lower respiratory tract components lie within the thorax
What are the components of the lower respiratory tract?
Trachea, bronchi (main, lobar, segmental, sub-segmental) bronchioles (main, terminal, respiratory), alveolar ducts and alveoli
What components of the respiratory system make up the conducting portion?
Nasal cavity, pharynx, larynx, trachea, primary bronchi, secondary bronchi, bronchioles and terminal bronchioles
Which components of the respiratory system make up the extra-pulmonary portion
nasal cavity pharynx larynx trachea primary bronchi
What are the functions of the nose?
Smell Respiration Filtration of dust Humidification of inspired air Elimination of secretions from paranasal sinuses and lacrimal ducts
Where are conchae found?
Lateral walls of nasal cavity, hanging inferomedially
What is the purpose of conchae?
To provide increased surface area for heat exchange
What bones are the conchae formed by?
Inferior concha by the Inferior Concha bone
Middle and superioe conchae by the medial processes of the ethmoid bone
What lies superoposterior to the superior concha?
The Sphenoethmoidal recess which receives opening of ethmoid sinus
Where do the paranasal sinuses drain into?
Frontal - middle nasal meatus
Ethmoid - Middle and superior meatus
Maxillary - middle nasal meatus
Sphenoid - superior meatus via sphenoethmoidal recess
Where does the pharynx extend from and to?
From cranial base to inferior cricoid cartilage anteriorly and inferior C6 vertebra posteriorly
What are the different portions of the pharynx and where do they run from and to?
Nasopharynx - from Cranial base to soft palate
Oropharynx - from soft palate to superior border of epiglottis
Laryngopharynx - from superior epiglottis to inferior cricoid cartilage
What are the borders of the larynx?
From laryngeal inlet to inferior border of cricoid cartilage
How does the middle ear connect to the respiratory system?
Anteromedially through the Eustachian tube to the nasopharynx
What is the purpose of venous plexuses in the non-olfactory regions of the nasal cavity?
Swell every 20-30 minutes so that airflow alternates side to side to prevent overdrying
What are olfactory cells?
Bipolar neurones with one dendrite that extends to epithelial surface to form a swelling with non-motile cilia extending from it. Internal dendrites join up to make an olfactory nerve
What epithelia lines vocal cords?
Stratified squamous non-keratinised
What is contained in each vocal cord?
Skeletal vocalis muscle
Vocal ligaments - large bundle of elastic fibres
What is the purpose of vocal cords in the respiratory system?
To help prevent foreign objects from reaching the lungs. They also close to build up pressure for the coughing reflex
What do clara cells secrete?
Surfactant lipoprotein and protein CC16
How is Protein CC16 useful clinically?
Used as marker.
High levels mean there’s been leakage across blood-air barrier
Low levels mean there’s lung damage
What type of cells are type 2 pneumocytes?
Simple cuboidal that secrete surfactant
What is a terminal bronchiole?
Bronchiole with now alveolar openings
What is an alveolar sac?
Composite air space, onto which many alveoli can open
What are the borders of the thoracic cage?
Anterior - sternum and costal cartilages Posterior - thoracic vertebrae Laterally - ribs and intercostal spaces Superiorly - thoracic inlet continuous with neck Inferiorly - diaphragm
What are the anterior articulations of the ribs?
Ribs 1-7 - sternum via costal cartilages
8-10 - costal cartilages
11,12 - end free in abdominal muscles
Which are the typical ribs?
Ribs 3-9
What do transverse costal facets of thoracic vertebra articulate with?
Articular facets of tubercle of ribs
What are the features that make the atypical ribs atypical
first - only 1 articular facet. Two transverse grooves separate by scalene tubercle, for passage of subclavian artery and vein
second - Rough area on superior surface - tuberosity of serratus anterior
10-12 - only 1 articular facet
11,12 - short with no neck or tubercle
What muscles are responsible for chest expansion in quiet respiration?
External intercostals (30%) Diaphragm (70%)
Where are the openings of the diaphragm?
Entrance of vena cava at level of T8
Entrance of oesophagus at level of T10
Aortic hiatus at level of T12
What are the three sections of the diaphragm and where do they derive from?
Costal from internal surfaces of ribs 7 to 12
Sternal from posterior aspect of xiphoid process
Lumbar from L1-L3 and medial and lateral arcuate ligaments
Where do the intercostal vessels run?
Along inferior border in intercostal groove in order of vein, artery and nerve
Where do the intercostal veins drain into?
Anterior veins drain into internal thoracic then subclavian.
Right and left posterior drain into azygous and hemizygous veins respectively, then superior vena cava
What kind of lobes does each lung have?
Right has superior middle and inferior, formed by horizontal and oblique fissures.
Left has superior and inferior, formed by oblique fissure
Where does the trachea start and end?
Starts at inferior cricoid cartilage. Ends at level of sternal angle
How many pulmonary artery and veins are there?
1 artery per lung and 2 veins per lung
Where do bronchial arteries arise from?
2 on the left come directly from thoracic aorta
1 on the right comes from thoracic aorta via the 3rd intercostal artery
What do the bronchial veins drain?
Superficial drain visceral pleura and bronchi in hilum in azygous and accessory hemiazygous veins
Deep drain all the other bronchi into main pulmonary vein
What muscles are involved in quiet respiration?
External intercostals and diaphragm for quiet inspiration
What muscles are involved in forced inspiration?
Diaphragm, scalene, pectoralis major, sternocleidomastoid, serratus anterior, external intercostals
What muscles are involved in forced expiration?
Abdominal muscles, internal intercostals, innermost intercostals
What does alveolar gas have to diffuse through during exchange?
Alveolar epithelial cell Interstitial fluid Capillary endothelial cell Plasma RBC membrane
Why is oxygen exchange affected more than carbon dioxide in problems affecting diffusion?
As CO2 is more soluble than oxygen so it diffuses 21 times as fast as oxygen so oxygen diffusion is limiting, not carbon dioxide so oxygen exchange is affected first
What are the partial pressures of oxygen and carbon dioxide in alveolar gas?
oxygen - 13.3 kPa
Carbon dioxide - 5.3 kPa
How is atmospheric air related to air exchanged with blood?
Brought close to alveolar gas by ventilation where increase in volume of respiratory and terminal bronchioles in inspiration decreases pressure, so air is brought downwards through airways. Then, atmospheric air exchanges with alveolar gas through diffusion in terminal and respiratory bronchioles
What is residual volume?
Volume left in the lungs at maximal expiration
What is vital capacity?
The biggest breath that can be taken from maximal expiration to maximal inspiration
What is the functional residual capacity?
The volume left in the lungs at resting expiratory level
What is the inspiratory capacity?
The biggest breath that can be taken from resting expiratory level
What is serial dead space?
aka anatomical dead space.
It’s the volume of the airways that aren’t involved in gas exchange.
Measured by nitrogen washout test
What is physiological dead space?
All the dead space of lungs. Calculated by adding serial dead space and alveolar dead space (aka distributive dead space)
Avleolar DS is the volume of lungs that are adapted to take part in gas exchange but don’t either due to damage or poor blood supply.
Physiological dead space can be determined by measuring dilution of alveolar air by dead space air by measuring pCO2
How is alveolar ventilation rate calculated?
Pulmonary ventilation rate (tidal volume x resp rate) MINUS dead space ventilation rate (dead space volume x resp rate)
How is compliance measured?
Volume change per unit of pressure change
How is specific compliance measured?
Volume change per unit pressure change/starting volume of lungs
How does surfactant help keep small alveoli intact?
Normally, laplace’s law is applied and so alveoli with larger radius have lower pressure than small alveoli, therefore if interconnected, air will flow from high pressure to low pressure and small alveoli will collapse into large alveoli.
However, with surfactant, as surface area increases, its effects lessen so surface tension is higher so pressure in large alveoli remains high
What does laplace’s law state?
Pressure = (2 x surface tension)/Radius
What is poiseulle’s law?
Resistance = pressure/rate of flow
Resistance = (8 x air viscosity x tube length)/ pi x (radius)^4
What is FVC?
Forced vital capacity - volume that can be expired from full lungs
What is FEV1?
Forced Expiratory Volume in 1 second - volume expired in first second of expiration, from full lungs
What is a restrictive deficit?
Where lungs are hard to fill that may be due to stiffness or reduced inspiratory effort (muscle weakness, deformity) but still easy to empty. Gives a reduced FVC but FEV1 is more than 70% of FVC as proportionally, lungs can empty normally
What is an obstructive deficit?
When small airways are overly narrowed in expiration so it’s hard to force air out through them. Gives a low FEV1 but normal FVC
How do flow volume loops work?
Plot Flow rate against either volume expired or volume of lungs.
Use vitalograph trace of volume against flow rate.
Flow rapidly increases as there’s low resistance initially in expiration then as airways narrow and resistance increases, Volume expired increases but flow rate decreases until flow rate = 0 and volume of lungs = residual volume/ volume expired = total lung capacity
Total volume expired = vital capacity
How does the helium dilution test work?
After normal expiration, where patient’s lungs are at FRC, patient’s connected to a system with know concentration of helium and known volume of gas. Patient then breathes normally until an equilibrium is reached and the new concentration of helium in container is calculated. As amount = C x V and amount has to have stayed constant as helium is inert and system is closed, orignal C x V = New C x V in whole system. This V2 is equal to original volume + FRC. As all other 3 variables are know, V2 can then be calculated and from that FRC can be calculated.
Residual volume can then be found as Residual volume = FRC - Expiratory Reserve Volume, that’s found by spirometry
How does the transfer factor test work?
Patient makes full expiration then rapid full inspiration containing air mixture containing a very small fraction of Carbon monoxide. Breath is held for 10 seconds then concentration of CO is taken mid-exhalation. The difference in levels of CO then gives rate of transfer of CO in ml/min/kPa so diffusion capacity of lungs is calculated as diffusion capactiy is the only limiting factor due to CO’s extremely high capacity to Hb
What is the solubility coefficient of oxygen?
0.01mmol/L/kPa at 37degrees
What diseases can give a low transfer factor result?
Diseases which destroy alveolar membrane eg emphysema
Diseases which increase length of blood-gas barrier eg interstitial lung disease or pulmonary oedema
What effect do pCO2 and HCO3- conc have on pH?
High HCO3- moves reaction between HCO3- and H+ in direction of CO2 formation so there’s less H+ so pH rises
High pCO2 pushes reaction in direction of HCO3- formation so there’s more H+ so pH falls
When are carbamino compounds formed?
When CO2 reacts with protein part of haemoglobin
What is the henderson hasselbach equation?
pH= 6.1 + Log( HCO3-conc/ (pCO2 x 0.23) )
What are the normal pCO2 and CO2 content in arterial and venous blood?
Arterial - pCO2 = 5.3 kPa and content = 21.31 mmol/l
Venous - pCO2 = 6.0 kPa and content = 23.21 mmol/l
What percentage of transported CO2 is transported in its various forms?
Dissolved CO2 - 8%
Carbamino compund - 12%
as HCO3- - 80%
How does hyperventilation affect pH?
Lowers pCO2. sing Henderson Hesselbach equation, lower pCO2 increases pH.
What are the general effects of hypoxia?
Causes Hypercapnia so respiratory acidosis and pH can fall below 7. This means that enzymes can become lethally denatured
How is calcium concentration affected by hyperventilation?
Hyperventilation causes respiratory alkalosis. Calcium is only soluble in acid so in a higher pH, it can’t stay in the blood. This makes nerves hyper excitable so can cause tetany
What is compensated respiratory acidosis?
Acidosis persists so kidneys respond by decreasing secretion of HCO3- to try and increase pH
What is compensated metabolic acidosis?
Acidosis persists so body compensates by increasing ventilation to reduce pCO2 and restore CO2:HCO3- to normal
What detects falls in inspired pO2?
Peripheral chemoreceptors in aortic and carotid bodies. Only stimulated by large changes and so they increase respiratory rate and tidal volume and heart rate and divert blood to brain and kidneys
What are changes in pCO2 detected by?
Peripheral chemoreceptors but these are insensitive.
Central chemoreceptors in medulla. These rapidly alter ventilation and react to changes in the pH of the cerebrospinal fluid
What controls the HCO3- conc. of the CSF?
Choroid plexus cells which alter HCO3- levels in persisting changes and so can reset ‘normal’ HCO3- level
What is the difference between type 1 and 2 respiratory failure?
Type 2 has low levels of oxygen and high CO2 but type 1 has low oxygen and normal/low CO2
What are the 5 factors needed to maintain arterial pO2 in the normal range?
pO2 in inspired air Alveolar ventilation Normal alveolar capillary membrane Ventilation perfusion matching All of right ventricular output passes through gas exchanging alveoli
What can cause low pO2 in inspired air?
Normally in people living at high altitudes so everything else is normal
What can cause hypoventilation?
Neuromuscular problems such as respiratory depression in opiate overdose, muscle weakness or head injury.
Chest wall problems such as kyphosis, scoliosis, morbid obesity, trauma, pneumothorax
DDifficulty ventilating lungs due to airway obstruction, COPD, severe asthma or severe fibrosis
What can cause an impairment in gas diffusion?
Increased path length, eg in pulmonary oedema
Structural changes such as fibrosis
Reduced availability for diffusion such as in emphysema
What can cause a ventilation-perfusion mismatch?
Reduced ventilation to some alveoli such as in lobar pneumonia
Reduced perfusion of some alveoli such as in pulmonary embolism
What kind of airflow obstruction is there in asthma?
Widespread
Variable
Reversible either spontaneously or with treatment
What are the most common symptoms of asthma?
A high pitched, expiratory, polyphonic wheeze
A dry, nocturnal cough that’s exercise induced
Breathlessness on exertion
Chest tightness
Variable airflow obstruction
What signs may be found on examination?
Hyperexpansion of chest
Indrawing of costal cartilages in children
Maybe be history or asthma/eczema
Hyperresonant on percussion
What tests are done to help diagnose asthma?
Flow-volume loop - will show scalloping, reduced PEFR, reduced FEV1:FVC and >12% improvement on salbutamol.
Skin prick allergy testing for atopic asthma
Chest X-ray to rule out differential diagnooses
What happens in the Immediate response phase of an asthma attack?
Macrophages present antigens to t lymphocytes which activates T cells, especially Th2, which release cytokines, attracting mast cells and eosinophils. Th2 cells also activate B cells which produce IgE antibodies.
IgE antibodies interact with the antigen, causing mast cell degranulation and release of mediators, including histamine and prostaglandins. This causes bronchoconstriction
What happens in the late phase response of asthma?
There’s infoltration of full spectrum of inflammatory cells, causing airway inflammation. Eosinophils release leukotriene C4 which are toxic to epithelial cells so cause shedding.
What causes reduction of airway calibre in asthma?
Mucosal oedema due to vascular leak
Thickening of bronchial wall due to inflammatory cell inflammation
Oversecretion of mucus
Shedded epithelia being incorporated into mucus, increasing thickness
Smooth muscle contraction
What remodelling is found in poorly controlled asthma?
Hyperplasia of smooth muscle
Damage to epithelia
Thickening of basement membrane due to collagen deposition
What drugs can precipitate an asthma attack?
Beta blockers
NSAIDs
What steps are taken in management of asthma?
Education
Primary prevention - quit smoking, lose weight, avoid exposure to triggers
Pharmacological - Beta agonists eg salbutamol for in exacerbations
Corticosteroids as preventative anti-inflammatory
What are the signs of a severe asthma attack?
Unable to complete sentences
Respiratory rate > 25 per min
Pulse >110bpm
PEFR <50% of predicted value
What are the signs of a life threatening asthma attack?
PEFR <33% of predicted Silent chest (wheeze sound of improvement) Cyanosis Feeble respiratory rate Bradycardia hpotension Exhaustion/confusion/coma Normal/ high pCO2 with low pO2 Low pH
What factors decrease reabsorption of pleural fluid?
Blockage of lymphatics
Increase in systemic venous pressure
What are the most common symptoms and signs of interstitial lung disease?
Dyspnoea (often progressive) Dry cough Exercise intolerance Tachypnoea Tachycardia Respiratory crackles Signs of right heart failure
What treatments can cause Interstitial lung disease?
Radiation Methotrexate Nitrofurantoin Chemotherapy Amiodarone
What is cryptogenic fibrosing alveolitis?
Ideopathic interstitial lung disease.
Increase in number of activated neutrophils which attract neutrophils and eosinophils so immune response causes tissue damage and fibrosis. Common sign is finger and toe clubbing as well as normal ILD symptoms
What is extrinsic allergic alveolitis?
Where inhalation of organic material triggers an allergic response in alveoli and bronchioles.
Can be acute with rapid progression where alveoli are infiltrated with inflammatory cells e.g. famer’s lung
Or chronic with granuloma formation and progressive fibrosis e.g. in bird fancier’s lung
How is pulmonary sarcoidosis staged?
Using chest x ray.
0 - normal CXR
1 - signs of Bilateral Hilar Lymphadenopathy
2 - BHL + peripheral pulmonary infiltrates
3 - peripheral pulmonary infiltrates only
4 - Progressive fibrosis with bulla formation and pleural involvement
What is paraneoplastic syndrome?
Symptoms/syndrome/disease caused by presence of cancer in the body but not due to local presence of cancer cells. Mediated by either immune response to tumour of by release of humoral components by tumour cells
What are the different histological types of lung cancer?
Small cell carcinoma
Non-small cell carcinoma - squmous, adeno, large cell
What does prognosis of lung cancer depend on?
Stage Cell type comorbidities Performance status of patient Biochemical markers
Explain the TNM staging of lung cancer
T = tumour size
T1 - Small and contained
T2 - larger, grown into main bronchus, visceral pleura or caused lobar collapse
T3 - Larger. Invading chest wall/ diaphragm/ pericardium. More than 1 nodule in same lung.
T4 - Nodules in more than one lobe of the same lung. Invading heart, major blood vessels, laryngeal nerve etc
N = regional lymph node involvement.
N0 - no lymph nodes involved
N1 - Most proximal lymph nodes affected
N2 - Lymph nodes of proximal mediastinum affected
N3 - Lymph nodes of distal mediastinum or supraclavicular nodes affected
M = Metastases
M0 - no distal cancer spread
M1 - Lung cancer cells in distal locations
How do SCC and NSCC respond to treatment (cancer)
20 % of NSCC are operable and of those operated on, 50% survive 5 years. Radical radiotherapy may be used if tumour is operable but patient’s unfit for surgery.
SCC responds to combination therapy but 75% have metastases on presentation and death from cerbral metastases is common
How do primary lung tumours present?
First with a cough that is ignored then depending on disease progression, may be dyspnoea, haemoptysis, monophonic wheeze, chest pain weight loss, lethargy and nerve compression
What biopsy techniques are used for lung cancer?
Bronchoscopy
Surgical
needle
How does TB present normally?
Tiredness/malaise Cough Low grade or hectic fever Weight loss and anorexia Night sweats if a pleural effusion then Dysponoea Haemoptysis Pallor Palpable cervical lymph nodes
How does miliary TB show up, radiologically?
With multiple little ‘seeds’
May also be microabscesses in liver and spleen
How does a host respond to TB?
Macrophages carry out phagocytosis but can’t complete as lipids in cell wall of MTB prevent formation of phagolysosome.
Frustrated phagocytosis leads to formation of granulomas with caseating center, as well as stimulates more better equipped macrophages.
Neutrophils, chemokines and cytokines are released which cause inflammatory infiltrate into the lung. Macrophages present MTB to T lymphocytes and caseating centers are calcified but still contain the bacterium.
What is Ghons’ focus?
Initial focus of TB infection. From here bacilli can drain into hilar lymph nodes (focus+nodes = primary focus)
What happens in post primary TB?
MTB proliferates in caseating center, causing liquefaction so a cavity forms. Fibrous tissue forms to try and contain the lesion but normally isn’t successful. Caseous material can then spread into blood vessels or bronchial tree.
There is inflammatory exudate into alveoli and if MTB spreads into the pleura or if there’s a hypersensitivity reaction then there may be pleural effusion
How is TB treated?
Multi-drug therapy to try and reduce drug resistance.
Initial phase lasting 2 months of isoniazide, rifampicin, ethambutal and pyrazinamide
Continuation phase of 4 months or 12 months if CNS involvement, of rifampicin and isoniazide
In a respiratory history, how do you calculate pack-years?
Number of packs a day x number of years
