respiratory_week_1_20190518190149 Flashcards
what are the 4 steps of external respiration
ventilation (gas exchange between atmosphere n alveoli)exchange between air in alveoli and blood coming into lungstransport in blood between tissues and lungsexchange between blood and tissues
boyle’s law
at any temperature the pressure exerted by gas varies inversely with volume of gas
what is the forces that link lungs to thorax
intra pleural fluid cohesivenessnegative intrapleural pressure - creates gradient
values of different pressures
atmospheric - 760mmHg/101pKaintra alveolar - 760mmHg/101pKa (less for air to flow)intrapleural - 756mmHg
what muscles are used in active process of inspiration and forceful inspiration
external intercostals lift ribs and move sternum accessory: sternocleidomastoid, scalenus and pectoral
why is the phrenic nerve important in inspiration and expiration and where is it located
passes motor information to diaphragm and receives sensory information from it cervical 3, 4 and 5
what causes the lungs to recoil in the passive process of expiration
elastic connective tissue and alveolar surface tension (attraction between water molecules produce force which resists lung stretching)
what are the muscles of active expiration (hyperventilation)
abdominal muscles and internal intercostals
what are signs of pneumothorax
shortness of breath, chest pain, hyper resonant percussion note and decreased/absent breath sounds
which forces keep alveoli open
transmural pressure gradient pulmonary surfactant (secreted by type II alveoli and lowers surface tension to prevent smaller alveoli collapsing)alveolar independence
What are the lung volumes and capacities?
SEE PICTURE ON DOCUMENT
what is the FEV1/FVC ratio
proportion of forced vital capacity that can be expired in first second normal is >70%
what is equation of airway resistance
F = ΔP/R
what does airway obstruction do to airway pressure
causes fall in airway pressure along airway downstream resulting in airway compression and rising pleural pressure
what causes decreased pulmonary compliance (greater change in pressure needed for change in volume - stiffer)
pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia, absence of surfactant
what causes increased pulmonary compliance
if elastic recoil of lungs is lost and age
what increases the work of breathing
decreased pulmonary compliance, increased airway resistance, decreased elastic recoil
what is anatomical dead space
inspired air which remains in airways where it is not available for gas exchange - makes it more advantageous to increase depth of breathing rather than rate
what is alveolar dead space
ventilated alveoli which are not adequately perfused with blood
what is physiological dead space
alveolar dead space + anatomical dead space
what is the effect of decreasing O2 on pulmonary and systemic arterioles
vasoconstriction of pulmonaryvasodilation of systemic
what is the partial pressure gradient and what is the equation
pressure exerted by one gas if it occupies full volumePaO2 = PiO2 (PaCO2/0.8)when calculating PiO2, water vapour must be accounted for
what does a big gradient between alveolar PO2 and arterial PO2 suggest
problem of gas exchange in lungs or a right to left shunt in heart
what is ficks law of diffusion
the amount of gas that moves across sheet of tissue is proportional to area of sheet but inversely proportional to thickness
what is henrys law
the amount of gas dissolved in a given type and volume of liquid (blood) at a constant temperature is proportional to partial pressure of the gas in equilibrium with liquid
what is the equation for the oxygen delivery index
DO2l = CaO2 x Cloxygen content of arterial blood x cardiac index
what is equation for oxygen content of arterial blood
1.34 x haemoglobin conc x %Hb saturated with O2
what does the steep part of lower sigmoid curve signify
peripheral tissues will get a lot of oxygen for a small drop in capillary PO2
what is the Bohr effect do to the sigmoid curve
shift to right due to increased release of O2 caused by: increase PCO2, increase H+, increase temp, increase 2,3-BPG
what is special about HbF
2 alpha and 2 gamma structure so interacts less with 2,3BPG so higher affinity for O2
how much CO2 transported in solution and how is this done
10% - done by Henrys Law
how much CO2 transported as carbonate and how is this done
60% - formed in blood by CO2 + H2O ⇌ H2CO2 ⇌ H+ + HCO3- enzyme is carbonic anhydrase which occurs in RBC
how much CO2 transported as carbamino compounds and how is this done
30% - formed by combination of CO2 with terminal amine groups in blood proteins (e.g. globulin of haemoglobin to give carbamino-haemoglobin) reduced Hb can bind more CO2 than HbO2
what is the Haldane effect
removal of O2 from Hb increases ability to pick up CO2 and H+ O2 shifts CO2 dissociation curve (upwards diagnonal straight line) to right
parasympathetic stimulation of post-ganglionic cholinergic fibres
bronchial contraction mediated by M3 ACh receptors on ASM cells which increases mucus secretion by M3 on gland/globlet cells
parasympathetic stimulation of non-cholinergic fibres
vascular relaxation mediated by nitric oxide and VIP
sympathetic stimulation response
bronchial smooth muscle relaxation via B2-adrenoceptors on ASM activated by adrenaline &vascular contraction mediated by a1-adrenoceptors on vascular smooth muscle cells
what is the mechanism of contraction of smooth muscle
phosphorylation of regulatory myosin light chain (MLC) in presence of intracellular Ca2+ and ATP
what is the mechanism of relaxation of smooth muscle
dephosphorylation of MLC by myosin phosphatase which has constitutive activity
how does extracellular signals, such as adrenaline, regulate MLC and myosin phosphatase
adrenaline stimulations phosphorylation and inhibition of MLC as well as phosphorylation and stimulation of myosin phosphatase - relaxation of bronchial smooth muscle
what are the steps of the development of chronic asthma
1) increased mass of smooth muscle2) accumulation of interstitial fluid 3) increased secretion of mucus4) epithelial damage - exposes sensory nerve endings5) sub epithelial fibrosis
what is thought to be the cause of asthma
immune imbalance between TH1 and TH2 lymphocytes - detailed steps on document
what are the three different kinds of short acting agonists (SABA)
salbutamol, albuterol and terbutaline
when are SABAs used
first line treatment for mind, intermittent asthma - relievers
what is the mechanism of SABAs
stimulate B2 adrenoceptors to increase mucus clearance and decrease mediator release from mast cellsside effects - tachycardia, cardiac dysrhythmia and hypokalaemia
what are the three different kinds of long acting agonists (LABA)
salmeterol (slow to act), formoterol and isoprenaline
when are LABAs used
in addition to glucocorticoidsused for persistent asthma patients or patients with chronic obstructive pulmonary diseasework up to 12 hours
what are the mechanism of LABA
same as SABA just longer acting
what are the two different kinds of CysLT1 bronchodilators
montelukast, zarfirlukast
when are CysLT1 bronchodilators used
in combination with others e.g. corticosteroidseffective against antigen induced (allergies) and exercised induced bronchospasm (2nd line treatment)
what is the mechanism of CysLT1 bronchodilators
antagonists - act competitively with CysLT1 receptor since CysLTs (LTC4, LTD4 and LTE4) cause smooth muscle contraction, mucus secretion and oedema
what are the five different kinds of muscarinic antagonists (anticholinergics)
ipratropium (short acting and non selective)tiotropium, glycopyronium, umeclidinium and aclidinium (long active and selective)
when are muscarinic antagonists used
high therapeutic ratio so used in COPD on own or LAMA/LABA dual (LAMA prevents contraction)
what is the mechanism of muscarinic antagonists
block post junctional M3 receptors in response to AChblock of M3 desirable but not M1/M2 because release of ACh can actually be increased by auto receptor antagonism
what are the two different types of bronchodilators / anti-inflammatory Xanthines
theophylline (oral maintenance) and aminophylline (IV acute attacks) found in coffee
when are Xanthines used
used to treat asthma and COPD - in combination with b2-adrenoceptor agonists and glucocorticoids
what is the mechanism of Xanthines
non selective phosphodiesterase inhibitor which increases cAMP (second messengers that relax smooth muscle and exert anti-inflammatory effect)adverse effects involving CNS, CVS, GI and kidneys due to interactions involving CYP450s
what are the four different kinds of glucocorticoids
beclometasone (chronic asthma), budesonide, fluticasone and prednisolone (severe or rapid deteriorating asthma)
when are glucocorticoids used
2nd line additives,regulates inflammatory and immunological responseineffective in relieving bronchospasm but do treat/prevent asthmaused as ICS/LABA combo in COPD - benefit to patients who develop severe exacerbationssometimes unresponsive in COPD due to chronic tobacco smoke
what is the mechanism of glucocorticoids
decrease formation of TH2 and causes apoptosis, prevent production of IgE, reduce number of cells and decrease Fcs expression, prevent allergen-induced influx into lung also recruit HDACs to switch off transcription of genes encoding inflammatory proteins
what is the one type of cromones
sodium cromogilcate
when is cromones used
second line drugs used prophylactically (to prevent) in treatment of allergic asthma in children reduces both phases of asthma attack but late phase requires frequent dosing inhaled steroid
what is the mechanism of cromones
mast cell stabiliser and includes weak anti-inflammatory effect
what is the two types of monoclonal antibody treatment
omalizumab and mepolizumab
when is monoclonal antibody treatment used
for patients with severe, persistent allergic asthma requires IV administration
what is the mechanism of monoclonal antibody treatment
omalizumab - directed against IgE - inhibits binding to IgE which inhibits TH2 response and associated mediator releaseMepolizumab - directed against IL-5 - blocks TH2 and used for severe refractors eosinophilia asthma (>4%)
what is the one type of PDE4 inhibitor
rofumilast
when is PDE4 inhibitor used
suppresses inflammation and emphysema in COPD oral treatment for severe COPD accompanied by chronic bronchitis
what is the mechanism of PDE4 inhibitor
PDE4 is prominent PDE expressed in neutrophils, T cells and macrophages to inhibition has inhibitory effects on inflammatory and immune cells
what is the components of triple inhalers that have recently been approved for moderate/severe COPD (not asthma or bronchospasm)
fluticasone, umeclidinum and vilanterol
how much oxygen given in acute asthma
at least 60% O2intubated ventilation if falling PaO2 continues
minimal symptoms and few exacerbations
SAMA/SABA
more symptoms and few exacerbations
LABA/LAMA
all range of symptoms with frequent exacerbations
ICS/LABA/LAMA (increased eosinophilia)or LABA/LAMA
acute COPD exacerbation treatment
nebuliser high dose salbutamol and ipratropium or oral prednisolone24-28% O2 titrated against PaO2/PaCO2
when is the only time COPD patient intubated
if reversible e.g. pneumonia
what happens at C6 vertebrate
larynx becomes trachea (palpated at jugular notch) and pharynx becomes oesophagus
the isthmus of the thyroid gland is anterior to what?
tracheal cartilages 2-4
what arteries supplies chest wall
bilateral posterior intercostal arteries
where is phrenic nerve found
in neck on anterior surface of scalenus anterior muscle and in thorax descending over lateral aspects of heart
what is lung lobe
area of lung that each of lobar bronchi supply with air (right has 3 - upper, middle, lower)
what is bronchopulmonary segment
area of lung lobe that each one of segmental bronchi supply with air (each lung has 10)
which muscles are between ribs and intercostal spaces
external intercostals internal intercostals innermost intercostals
what is the nerve supply of intercostal spaces
anterior rams of spinal nerve
what is the posterior blood supply of intercostal spaces
thoracic aorta and azygous vein
what is anterior blood supply of intercostal spaces
internal thoracic artery and internal thoracic vein
why is the right dome of diaphragm usually more superior
presence of liver
what does the muscular part of diaphragm attach to
sternum, lower 6 ribs & costal cartilage and L1-L3 inferiorly
what is the costodiaphragmatic recess and where is it located
most dependent part of the pleural cavity (inferior when upright) located between diaphragmatic parietal pleura and costal parietal pleura
what is the most inferior region laterally of pleural cavity
costophrenic angle
what causes blunting of angles and fluid level seen on CXR
abdominal fluid in pleural cavity draining into recess
where is lung apex auscultated
superior to medial 1/3rd of clavicle
where is middle lobe auscultated
between ribs 4 and 6 in mid-clavicular and mix auxiliary lines
where is lung base found
T11
where is sternal angle located
rib 2
where is horizontal fissure located
rib 4
where is oblique fissure located
rib 6 anteriorly rising to T3 vertebral level posteriorly
