RCM Week 1 (asthma) Flashcards
What are intercostal muscles
Located in intercostal spaces between ribs
3 layers of muscles: external, internal and innermost. Important in respiration and keeping ICS rigid
What is the pleura of the lungs
- each lung is enclosed with a serous pleural sac
- the sac is of 2 continuous membranes- the visceral and parietal pleura
- visceral pleura - covers the lungs
- parietal pleura lines pulmonary cavities
Why may you have to insert a needle into an intercostal space
To drain or sample fluid (pleural fluid, blood or pus) from the pleural cavity or to anaesthetise an intercostal nerve
How do you avoid damaging neurovascular bundles when inserting a needle into an intercostal space
Insert the needle close to the upper border of the lower rib
What is the difference between the superior thoracic aperture and the inferior thoracic aperture
Superior : opening for structures to enter / leave the neck / thorax
Inferior: opening at lower part of thoracic cavity (closed by diaphragm)
What is thoracic outlet syndrome
Important arteries and nerves pass through, into neck and upper limb. Compression of these such as against the clavicle or 1st rib can lead to a range of problems
Attachments, actions and nerve supply of the pectoralis major
Attachments: clavicle are head from medial half of clavicle; sternocostal head from sternum and upper 6 costal cartilages. All fibres converge on the intertubercular groove of humerus
Actions: adductor and medial rotator of arm at shoulder joint. Can act also as a flexor (when arm extended) and as extensor (when arm flexed). If pectoral girdle is ‘fixed’ it can also act as an accessory muscle of respiration
Nerve supply: medial and lateral pectoral nerves
Attachments, actions and nerve supply of the pectoralis minor
Attachments: coracoid process of scapula; ribs 3-5 near their cartilages
Actions: depressor of scapula (and hence shoulder) and protractor of scapula. Of pectoral girdle is ‘fixed’ it can also act as an accessory muscle of respiration
Nerve supply: medial pectoral nerve (mainly C8, T1)
Describe the location of the breast
Extends from ribs 2-6 and from the lateral margin of the sternum to the midaxillary line. An axillary tail runs superiorly and laterally towards the axilla
Describe the structure of the breast
A modified sebaceous gland with 15-20 lobes sending lactiferous ducts to the nipple. Lobes comprise glands and adipose tissue separated by fibrous septa (suspension ligaments) the breast is separated from the deeper pectoral mm by a retromammary space
Why is lymphatic drainage of considerable clinical importance
Because of the frequency of breast cancer and its spread to other parts of the body by lymph and blood vessels
What is the mediastinum
The central part of the thoracic cavity that lies between the pleural cavities. Contains the heart and pericardium, great vessels, oesophagus, trachea, thymus, lymph nodes, various nerves and other blood vessels
What are the boundaries of the mediastinum
Anteriorly: sternum
Posteriorly: thoracic vertebral column
Superiorly: thoracic inlet and root of the neck
Inferiorly: diaphragm
Describe the divisions of the mediastinum
Divided into superior and inferior parts by the plane of the sternal angle.
The superior is subdivided into anterior, intermediate and posterior
- the superior mediastinum lies behind the manubrium sterni
- the inferior mediastinum lies behind the body and xiphoid process of the sternum (between the plane of the sternal angle and the diaphragm)
What are the contents of the superior mediastinum
Thymus (lymphoid organ); great veins (SVC, brachiocephalic vv); phrenic nerves; arch of aorta and branches; origins of internal thoracic arteries; pulmonary aa and vv; vagus nn; recurrent laryngeal branches; trachea (lower half) and bifurcation into main bronchi; oesophagus; thoracic duct
Describe the structure of the inferior mediastinum
- divided into anterior, middle and posterior regions
- anterior: internal thoracic aa and vv (and anterior intercostal branches); thymus; sternopericardial ligaments
Middle: heart and pericardium; phrenic nn and pericardiophrenic aa and vv; IVC (diaphragm to right atrium)
Posterior: descending aorta and branches; azygous vv; oesophagus; thoracic duct; sympathetic trunks (and branches)
Explain the process of breathing
Muscles of respiration contract to expand thoracic cavity (mainly diaphragm). This increases thoracic volume / decreases intra-thoracic pressure. Air is drawn into the lungs from outside (where pressure is greater)
Air passes into terminal bronchioles / alveoli to oxygenate blood
Diaphragm relaxes, lungs recoil, thoracic volume decreases, intrathoracic pressure increases and air is expelled
Describe the diaphragm
Most important muscle in respiration - dome shaped muscular partition - separates the thorax and abdomen - innervated by phrenic nerve - C3-5 Anteriorly attaches into the xiphoid process and costal margin Laterally attaches to ribs 6-12 Posteriorly attached to T12 vertebra
Describe the role of the intercostal muscles
- assist in inspiration and expiration
- have obliquely angled fibres from rib to rib
- the contraction of external and internal fibres raises each rib toward the rib above to raise the rib cage
- innermost and internal depresses each rib to the rib below to lower the rib cage
What is pleura
Serous membrane divided into parietal and visceral layers; surround the lungs; contain the pleural cavities; separated by serous fluid
What is the difference between parietal and visceral pleura
Parietal: outer; lines thoracic cavity
Visceral: inner; covers lung following lung fissures
Define asthma
Reversible increases in airway resistance, involving bronchoconstriction and inflammation
Reversible decreases in the FEV1 : FVC
Variations in PEF which improve with a B2 agonist
What is asthma provoked by
Genetic predisposition
- allergens
- cold air
- viral infections
- smoking
- exercise
Clinical features of asthma
Wheezing Breathlessness Tight chest Cough (worse at night / exercise) (Nocturnal in children)
Decreases in FEV1, reversed by a B2 agonist
How do B2 agonists help treat asthma
- increase FEV1
- act on B2-adrenoceptors on smooth muscle to increase cAMP
- reduce parasympathetic activity
- given by inhalation
- prolonged use may lead to receptor down-regulation
- long acting beta agonists (LABA) eg salmeterol given for long term prevention and long term control
How do xanthines treat asthma
- bronchodilators, not as good as beta-adrenoceptor agonists (2nd line use)
- oral or iv aminophylline in emergency
- adenosine receptor antagonist
How can steroids be used to treat asthma
Given with B2 agonists - reduce receptor down-regulation
Side effects:
- throat infections, hoarseness (inhalation)
- adrenal suppression (oral)
How do leukotriene receptor antagonists treat asthma
Eg montelukast
- increased role as add on therapy
- preventative and bronchodilators
- antagonise actions of LTs
How does omalizumab treat asthma
A role in difficult to treat asthma
Monoclonal antibody which is directed against free IgE, but not bound IgE
Prevents IgE from binding to immune cells and which leads to allergen- induced mediator release in allergic asthma
How do airways cope with changing pressure
They are kept open by either bony or cartilaginous scaffolds.
Turbinate bones in the nasal cavity form narrow passageways that create turbulence, driving air in and out of sinuses
How is temperature adjustment and moisturising enhanced in nasal cavity
Large venous plexus in the sub mucosa. Large particles are prevented from entry by vibrissae (hairs at entry to nasal cavity)
Smaller particles are trapped by mucus which covers the lining all the way to the terminal bronchioles
What are the 3 components of the lower respiratory system
1) airways: progressively smaller tubes ending in blind ending sacs- conducts air to the sites for gaseous exchange and defence mechanisms
2) alveoli : sites for gaseous exchange
3) supported by connective tissue (interstitium)
Components of the airway system
- trachea
- 2 main bronchi
- 2 left lobar bronchi and 3 right lobar bronchi
- segmental bronchi
- bronchioles (terminal and respiratory)
5 layers of the airway
- respiratory epithelium: pseudostratified columnar ciliated + BM
- lamina propria: containing connective tissue, blood and lymph
- band of fibroelastic tissue at the base of the LP. This becomes more prominent and more muscular (smooth muscle) as the tubes get smaller to replace cartilage
- submucosa : seromucus glands, smooth muscle / elastin fibres
- cartilage: hyaline cartilage - c shaped in trachea and less prominent as the tubes get smaller
Describe the components of respiratory epithelium
- pseudostratified columnar ciliated epithelium (cilia beat rhythmically)
- basal cells (stem cells)
- goblet cells (produce mucus)
- neuroendocrine cells
- club cells (terminal bronchioles only)
All these give the pseudostratified appearance
What is metaplasia
Change in type of cell - reprogramming of stem cells
- survival mechanism in response to injury eg smoking
- specialised function is lost
- can predispose to cancer: squamous carcinoma
Describe structure of trachea
Anterior C shaped plates of cartilage with posterior smooth muscle. Mucous glands. Trachealis muscle (fibroelastic tissue) controls diameter
Describe structure of the bronchi
Discontinuous foci of cartilage ie cartilage plates, more prominent smooth muscle layer. Mucous glands
Describe the structure of the bronchioles
No cartilage of submucosal mucous glands, no goblet cells, Clara cells secreting proteinaceous fluid. Ciliated epithelium terminal = last conducting airway
Respiratory = cubodial ciliated epithelium and lots of openings into alveoli
Describe the structure of the alveolar duct
Flat epithelium, no glands, no cilia
Describe the structure of the alveoli
Type I and II pneumocytes
What are the 2 types of alveoli epithelium
Type I pneumocytes: flattened squamous epithelial cells with the cytoplasm to allow gaseous diffusion. BM is fused with capillary BM
Type II pneumocytes: rounded cells with prominent secretory granules for production and secretion of surfactant
What is surfactant
A detergent equivalent that reduces surface tension produced by club cells.
In a space of such a small diameter as an alveolus, any water on the alveolar surface would exert strong capillary forces, inhibiting the expansion of the lung
Why are lungs vulnerable to infection
Due to constant exposure to the external environment
- constant inhalation of nasopharyngeal flora
Lung parenchyma remains sterile by coughing, sneezing and lung defence mechanisms
What are the host defence mechanisms of the upper airways (nasopharynx and oropharynx)
Nasal hair Turbinates Mucociliary apparatus Immunoglobulin A (IgA) secretion Saliva Sloughing of epithelial cells Local complement production Interference from resident flora
What are the host defence mechanisms of the conducting airways (trachea and bronchi)
Cough, epiglottis reflexes, sharp-angled branching of airways, mucocilary apparatus, immunoglobulin production (IgG, IgM, IgA)
What are the host defence mechanisms of the lower respiratory tract (terminal airways, alveoli)
Alveolar lining fluid (surfactant, Ig, complement, fibronectin)
- cytokines (interleukin 1, tumour necrosis factor)
- alveolar macrophages
- neutrophils
- cell mediated immunity
Lung defence mechanisms
Organisms are trapped in the mucous and removed via the mucociliary elevator
Those that enter the distal respiratory tree are phagocytosed by resident alveolar macrophages
Organisms including those ingested by phagocytes, may reach the draining lymph nodes to initiate immune responses
Further defence mechanisms that operate after development of adaptive immunity
Upper respiratory tract: secreted IgA blocks attachment to epithelium
Lower respiratory tract: serum antibodies (IgM, IgG) are present in the alveolar lining fluid (activate complement + IgG is opsonic)
T cell immunity
Examples of obstructive diseases of the lungs
COPD Bronchitis Emphysema Asthma Bronchiectasis Cystic fibrosis
Examples of restrictive diseases of the lungs
Fibrosis
Pneumoconiosis (asbestosis, silicosis, coal workers disease)
What does the ratio of FEV1 / FVC as % show
The proportion of total volume of air that can be expired in the first second of expiration
How is FEV1 and FVC affected in obstructive disease and restrictive disease
In obstructive disease: FEV1 is reduced, FVC is normal : ratio is reduced
Normal >80%; COPD <70%
In restrictive disease FVC is reduced but FEV1 / FVC ratio is maintained
What is interstitial fibrosis
Persistent alveolitis: inflammation of alveolar walls and spaces: activation of pulmonary macrophages: attract and stimulate fibroblasts
Damage to pneumocytes by macrophages and neutrophils cause proliferation of type II pneumocytes. These attract macrophages and secrete stimulators factors for fibroblasts
What is pulmonary fibrosis
Scarring of the lung tissue - stretchiness of lung is compromised which has an effect on lung capacity
What is tidal volume
Volume of air entering and leaving the lung with each normal breath
What is inspiratory reserve volume (IRV)
Extra volume of air inspired above the normal tidal volume with full force
What is expiratory reserve volume (ERV)
Extra volume of air expired by forceful expiration at the end of normal tidal expiration
What is vital capacity (VC)
Maximum amount of air expelled from the lungs after first filling the lungs to a maximum then expiring to a maximum (TV + IRV + ERV)
What is residual volume (RV)
Volume of air remaining in the lungs after the most forceful expiration
What is functional residual capacity (FRC)
Amount of air that remains in the lungs at the end of normal expiration (ERV + RV)
What is total lung capacity (TLC)
The maximum volume of air the lungs can hold (VC + RV)
What is nitrogen washout in a lung function test
Patient inspires 100% O2
Expires into the spirometer system
Procedure repeated until N2 in lungs is replaced with O2
FRC calculated from exhaled N2 and estimated alveolar N2
Effects of obstructive deficits
Eg asthma, COPD
- FEV1 will be reduced but FVC will be relatively normal
- a low FEV1/FVC will be recorded
What is the fibrous pericardium and the serous pericardium
Fibrous pericardium: tough and not distensible; attached to diaphragm by pericardiophrenic ligaments; blends into adventitia of great vessels
Serous pericardium: comprises visceral layer (epicardium) and parietal layer (lining fibrous pericardium); potential space (pericardial cavity) between them
4 surfaces of the heart and pericardium
1) anterior or sternocostal: formed mostly of right (with a bit of left) ventricle
2) inferior or diaphragmatic: mostly L (with a bit of R) ventricle
3) posterior or base: mostly L and bit of R atrium and pulmonary vv
4) pulmonary: mostly L ventricle in cardiac notch of L lung
What is the apex of the heart
L ventricle usually posterior to L ics5 in adults
Location of ‘apex beat’
4 borders of the heart and pericardium
1) superior: from L costal cartilage 2 to R costal cartilage 3
2) right: convex to R; from R cc3 to R cc6; mainly R atrium with SVC and IVC
3) inferior: lies on diaphragm central tendon; from R cc6 to L intercostal space 5; mainly R ventricle and part of L ventricle
4) left: convex to L; from L ics5 and back to L cc2; mainly L ventricle and maybe some L atrium
What are the valve positions
All valves are retrosternal in position and close to the midline
Remember PAMT 3344
- pulmonary (P): medial to L cc3
- aortic (A): medial to L ics3
- bicuspid or mitral(M): medial to L cc4
- tricuspid(T): medial to R ics4
What are the valve auscultation sites (sites where you hear the lub-dup sound through the stethoscope)
1) pulmonary: L ics2 near sternal edge; dup sound
2) aortic: L ics2 near sternal edge; ‘dup’ sound
3) aortic: R ics2 near sternal edge; ‘dup’ sound
4) bicuspid or mitral: L ics5 at midclavicular line; ‘lub’ sound
5) tricuspid: L ics5/6 near lower sternal edge; ‘lub’ sound
What is the pleura
A serous membrane divided into parietal (outer) and visceral (inner) layers which surround the lungs and contain the pleural cavities; layers also separated by small amounts of serous fluid
What is the difference between parietal pleura and visceral pleura
Parietal: lines thoracic cavity lateral to mediastinum; supplied by intercostal and phrenic nn; sensitive to pain
Visceral : covers lung and follows lung fissures; supplied by autonomic nn
Describe the different surfaces of the lungs
Mediastinal: flat, faces mediastinum and has impressions of mediastinal structures; contains the hilum and pulmonary ligament
Diaphragmatic: concave and faces domes of diaphragm
Costal: convex and faces ribs
Cervical: extends into neck, 2-3cm above medial third of clavicle, as apex, dome or cupola
What are pleural reflections
The abrupt lines along which the pleura change direction (reflect) from one wall of the pleura cavity to another
Occur where the costal pleura becomes continuous with the mediastinal pleura anteriorly and posteriorly and with the diaphragmatic pleura inferiorly
Summary of the surface anatomy of the visceral pleura
Reflections closest at plane of sternal angle (rib 2)
Parallel down to rib 4
L indented (cardiac notch) but R continues to cc6
Cross rib 8 at midaxillary line
Cross rib 10 at lateral border of erector spinae
Summary of the surface anatomy of the parietal pleura
Close behind sternal angle (rib 2)
Parallel down to rib 4
L indented (cardiac notch) but R continues to cc6
Rib 8 at midclavicular line
Rib 10 at midaxillary line
Rib 12 at lateral border of erector spinae
Describe the right lung
Has 3 lobes (superior, middle and inferior) separated by the oblique and horizontal fissures
Oblique fissure from T2 vertebra posteriorly to rib 6 anteriorly
Horizontal fissure from rib 4 to oblique fissure
Superior and middle lobes mainly anterior
Inferior lobe mainly posterior
Describe the left lung
Has 2 lobes (superior and inferior) separated by oblique fissures
Oblique fissure from T2 vertebra posteriorly to rib 6 anteriorly
Superior lobe mainly anterior and has lingula
Inferior lobe mainly posterior
What are the 4 types of hypersensitivity reactions
1) type 1- IgE antibodies and mast cell degranulation mediator release (atopic allergy)
2) mediated by antibodies (IgG)- bind to killer cells or activate complement and bind to target cells causing cell damage
3) type 3- mediated by antibodies (IgG, IgA, IgM) immune complex hypersensitivity
4) type 4- delayed hypersensitivity (days / weeks) T cells activate macrophages to clear foreign material - tissue damage
What are mast cells
Found in all tissues - generate rapid inflammatory response
Activated by complement when pathogen comes into body causes cell to release inflammatory mediators
What is the role of IgE antibodies in type I hypersensitivity (atopic allergy)
Recognise other allergens
What is the first stage of type I hypersensitivity
Sensitisation
CD4 helper T cells are activated
B cells change the type of antibody they produce to form IgE antibodies which can sit on the surface of the mast cell
This is why you are only allergic to things that you have an IgE antibody that can bind to
What is stage 2 of type I hypersensitivity
Elicitation (second and subsequent exposure to the same allergen)
IgE antibodies that recognise specific allergen are sitting on surface of mast cell
Mast cell degranulates and releases pre formed and newly formed mediators
What is systemic anaphylaxis (IgE mediated allergic reaction)
An allergy to things like drugs, serum, venoms and peanuts
Intravenous route (either directly or following oral absorption into food)
Response: edema, increased vascular permeability, tracheal occlusion, circulatory collapse, death
What is acute urticaria (IgE mediated allergic reaction)
Allergens: insect bites or allergy testing
Route: subcutaenous
Response: local increase in blood flow and vascular permeability
What is allergic rhinitis ‘ hay fever (IgE mediated allergic reaction)
Allergens: pollens, dust mites
Route: inhalation
Response: edema of nasal mucosa, imitation of nasal mucosa
What is asthma (IgE mediated allergic reaction)
Allergens: danders, pollens, dust mite
Route: inhalation
Response: bronchial constriction, increased mucus production , airway inflammation
What is food allergy (IgE mediated allergic reactions)
Allergens: tree nuts, peanuts, shellfish, milk, eggs, fish
Route: oral
Response: vomiting, diarrhoea, pruritis (itching), hives, anaphylaxis (rare)
In development of the trachea what does the endoderm and splanchnic mesoderm give rise to
Splanchnic mesoderm- gives rise to cartilage, connective tissue and muscles
Endoderm- gives rise to epithelium and glands of trachea and pulmonary epithelium
4 stages of lung maturation
Pseudoglandular stage
Canalicular period
Terminal sac period
Alveolar period
What is the pseudogladnular stage of lung maturation
At 5-16 weeks
- terminal bronchioles form
- by the end of this period all major components of lung have formed except those required for gas exchange
What is the canalicular period of lung maturation
16-26 weeks
- lumens of the bronchi and terminal bronchioles enlarge
- tissues become vascularised
- by 24 weeks, each terminal bronchiole has formed 2 or more respiratory bronchioles
- towards the end of this period the first terminal sacs form at the end of the respiratory bronchioles
What is the terminal sac period of lung maturation
26 weeks - birth
- many terminal sacs form - the primordial alveoli
- epithelial cells of the terminal sacs become flat and thin - type 1 alveolar epithelial cells
- capillaries come into close contact with the flat epithelial cells and start to bulge into the primordial alveoli. This close contact, at the blood air barrier will allow gas exchange
- secretory, rounded epithelial cells start to form- are type II alveolar cells. Form in between the flat type I alveolar cells
What are type II alveolar epithelial cells
Rounded secretory epithelial cells lining alveolar sacs
- formed from the end of the 6th month
- produce surfactant
What is surfactant
Produced by type II alveolar epithelial cells
- phospholipid rich fluid
- forms a monomolecular film over internal walls of the terminal sacs and mature alveoli
- lowers surface tension at the air-alveolar interface
- produced from end of 6th month
What is the alveolar period (8 months - childhood)
- increased production of surfactant
- only about 5% of mature alveoli form before birth
- primordial alveoli increase in size, type I epithelial cells become thinner and capillaries form an even closer association as they mature
- most postnatal increase in lungs size is due to increased divisions to form respiratory bronchioles and continued primordial alveoli production
Changes in lungs before birth
Amount of surfactant produced increases before birth , mostly in last 2 weeks
- breathing movements occur before birth to stimulat lung development and respiratory muscles
- amniotic fluid is aspirated
Changes in lungs at birth
At birth lungs are half filled with fluid. This is removed by:
1) pressure on thorax during delivery Expelling fluid through mouth and nose
2) absorbed into circulation via pulmonary circulation.
3) absorbed into lymphatics
Thin coating of surfactant is left lining alveolar cell membrane
What occurs in the lungs of a stillborn
1st breath is not taken so no air in lungs. Lungs are full of fluid and will sink if placed in eater at autopsy
4 embryonic components of the diaphragm
Transverse septum
Pleuroperitoneal membranes
Dorsal messengers of oesophagus
Muscular in growth from lateral body walls
Describe the transverse septum (diaphragm)
Mesodermal in origin
- grows dorsal from ventrolateral Body wall
- forms early in development.
- forming liver embedded in tissue
- caudal to pericardial cavity- partially separating it from peritoneal cavity
- primordium of central tendon of diaphragm
How does the pleuroperitoneal membranes form (diaphragm)
Form from the lateral wall of the pleural and peritoneal cavities
- first appear at start of 5th week
- forms posterior and lateral parts of the diaphragm, by fusing with the transverse septum and dorsal mesentery in 7th week
Formation of dorsal mesentery of oesophagus (diaphragm)
Will form the median region of the diaphragm
- forms muscle bundles anterior to the aorta, the ‘crura of the diaphragm’
- derived from myoblasts that had previously migrated into the dorsal mesentery of oesophagus
Formation of the primordial diaphragm
Occurs by fusion of the pleuroperitoneal membranes, dorsal mesentery of oesophagus and septum transversum. This partitions the thoracic and abdominal cavities
What is respiratory distress syndrome
Premature baby may not have enough surfactant in lungs so surface tension will be high at air-blood interface
- risk of alveoli collapsing during expiration
Treated by artificial surfactant treatment with glucocorticoids
What is oesophageal atresia and tracheooesophagus fistulas
Abnormal separation of the oesophagus and trachea by oesophagotracheal septum
- most common defect of lower resp tract
Atresia- narrowing or withering away
Fistula- abnormal opening or passage
What are congenital cysts of the lungs
- terminal bronchi abnormally dilated
- usually at lung periphery
- may be small and numerous or few and large
- causes poor draining and can cause chronic lung infections
What is a congenital diaphragmatic hernia
Failure of fusion of pleuroperitoneal membrane with 3 other components
- usually a posterolateral defect
- 90% of cases are on the left side
What is erythropoiesis
Essential to maintain RBC level
Controlled by erythropoietin (polypeptide hormone)
Released by peritubular cells in the kidney in response to hypoxia (low oxygen) eg anaemia, at altitude, chronic lung disease
Increases the number of stem cells committed to erythropoiesis
- recombinant erythropoietin used clinically
Describe the structure of haemoglobin
RBC- 640 million molecules of Hb
- tetrameric: 4 glob in chains, each made of a polypeptide with haem prosthetic group
Haem: ferrous iron, Fe2+ at the centre of a protoporphyrin complex
Globin chains are linked by non-covalent bonds
How are RBCs degraded
Occurs in reticuloendothelial system of spleen, liver and bone marrow
Proteins are degraded and recycled, iron retained in stores, porphyrin from haem converted to bilirubin in liver
What is the difference between adult and fetal Hb
Adult Hb contains a2Bs subunits
Fetal contains a2 gamma2 (rapidly destroyed at birth) - can lead to jaundice due to high levels of bilirubin
Described the significance oh haemoglobin
1 litre of plasma holds 3ml of O2
1 litre of blood holds 195ml of O2
This is because haemoglobin has such a high oxygen carrying capacity
What does haemoglobin being an allosteric molecule mean
Once 1 O2 is binded, the non covalent bonds undergo a conformational change which means that the second oxygen binds more avidly etc
How can Non-steroidal anti-inflammatory drugs (NSAIDS) eg aspirin, ibuprofen affect asthma
They increase leukotriene production
Why should beta blockers not be given to patients with asthma
They bind to beta 2 adrenoreceptors in the lungs and worsen asthma
What is the difference between infections of the upper and lower respiratory tract
Lower respiratory tract infections involve the airways below the larynx
Upper respiratory tract infections occur in structures in or above the larynx
What are the 4 different paranasal air sinuses
- frontal
- sphenoidal
- maxillary
- ethmoidal (air cells)
What are the 9 cartilages of the larynx
Unpaired: epiglottis, thyroid, cricoid
Paired: arytenoid, corniculate, cuneiform
What structures are found in each part of the mediastinum
Anterior: internal thoracic aa and vv (and anterior intercostal branches); thymus (possibly); sternopericardial ligaments
Middle: heart and pericardium (serous and fibrous); phrenic nn and pericardiophrenic aa and vv; IVC (diaphragm to RA)
Posterior: descending aorta (and branches); azygous vv (and tributaries); oesophagus; thoracic duct; sympathetic trunks (and branches)
What are the accessory muscles of respiration
Scalene muscles - prevent rib 1 and 2 from descending
Pecs and trapezius- ‘fix’ the pectoral girdle to raise rib cage
How do babies breathe
Babies only breathe via abdominal breathing
- newborn ribs are more horizontal so cant use pump / bucket handle movements (weak intercostals)
- abdominal breathing is done by contracting the diaphragm
- as the diaphragm is located horizontally between the thoracic and abdominal cavities, air enters the lungs and abdominal cavity expands
- reliance on the diaphragm for breathing means there is a high risk for respiratory failure if the diaphragm is not able to contract
How do children breathe
Nasal breathers until 4-6 weeks
- short neck and shorter, narrower airways- more susceptible to airway obstruction / respiratory distress
- tongue is larger in proportion to the mouth (more likely to obstruct airway if child is unconscious)
- smaller lung capacity and underdeveloped chest muscles
- have a higher respiratory rate
Why is the use of the accessory muscles while at rest a sign of respiratory distress
- lungs fail to provide enough oxygen to a persons body
2 main types: - neonatal respiratory distress syndrome which affects newborns
- acute respiratory distress syndrome (ARDS) which can affect people regardless of age
Describe neonatal respiratory distress syndrome
- affects prem babies, if they are born before their lungs are fully developed and capable of working properly
- the more prem the baby, the more likely it is that they will have respiratory distress syndrome
- approx half of all babies born before 28 weeks will develop NRDS
- leading cause of death in newborns (20%)
Describe acute respiratory distress syndrome (ARDS)
- fluid / proteins leak from the blood vessels into the alveoli
- lungs become stiff and so don’t work properly
- breathing becomes difficult
- mainly affects the over 75s
- approx 1/6000 people per year affected in England
- common causes are an infection in the lungs eg pneumonia
- lung clots or injury eg from a car crash could also trigger the condition
Define the different types of breathlessness
Dyspnoea - breathlessness
Orthopnea - breathlessness on lying down
Exertional dyspnoea - breathlessness on exercise
Paroxysmal nocturnal dyspnoea - episodic breathlessness at night
Describe the parasympathetic and sympathetic control of bronchial calibre
Parasympathetic : A.Ch. Acts on muscarinic M3 receptors which causes bronchoconstriction and increased mucus
Sympathetic:
Circulating adrenaline acting on beta 2 adrenoceptors on bronchial smooth muscle to cause relaxation
Plus sympathetic fibres releasing NA, acting at adrenoceptors on parasympathetic ganglia to inhibit transmission
Beta2-adrenoceptors also on mucus glands to inhibit secretion
What is an asthmatic attack
A genetic predisposition provoked by:
- allergens
- cold air
- viral infections
- smoking
- exercise
May be characterised by early (immediate) phase followed by late phase
Clinical features of an asthma attack
Wheezing Breathlessness Tight chest Cough Decreases in FEV1, reversed by a B2 agonist
How do bronchodilators treat asthma attacks
Reverse bronchospasm (early phase) Rapid relief (relievers)
Prevention:
May be used to prevent an attack
Can be anti-inflammatory
How do muscarinic receptor antagonists treat asthma
They block parasympathetic bronchocon-striction
Inhalation: prevents anti muscarinic side effects
- limited / little value in asthma, used in COPD
How do anti-inflammatory agents treat asthma
Preventative: do not reverse an attack
Corticosteroids:
Eg beclometasone
- anti-inflammatory by activation of intracellular receptors, leading to altered gene transcription (decrease cytokine production) and production of lipocortin
What are the 3 principle compartments of the respiratory system
Conduction zone: conditioning of inhaled air
Respiratory zone: site of gas exchange
Musculo-elastic ventilation apparatus: drives ventilation
What is a restrictive deficit
Lung expansion is compromised- alterations in lung parenchyma, disease of the pleura or chest wall
- lungs do not fill to capacity hence they are less full before expiration
Eg pulmonary fibrosis and scoliosis
FVC is reduced but the FEV1 is relatively normal
What is an obstructive deficit
Characterised by airway obstruction
If airways are narrowed, lungs can still fill to capacity
Resistance is however increased on expiration
Eg asthma, COPD
FEV1 will be reduced but FVC will be relatively normal
What is the diffusion conductance test
Measures how easily CO crosses from alveolar air to blood
The patient inhales a single breath of dilute CO followed by a breath hold of 10 seconds
The diffusion capacity is calculated from the lung volume and the percentage of CO in the alveoli at the beginning and the end of the 10s breath hold
This is relevant in fibrosis of the lungs where gas diffusion is compromised
Borders of the heart
Superior: from L costal cartilage 2 to R costal cartilage 3
Right: convex to R; from R cc3 to R cc6; mainly R atrium with SVC and IVC
Inferior: lies on diaphragm central tendon; from R cc6 to L intercostal space 5; mainly R ventricle and part of L ventricle
Left: convex to L; from L ics5 and back to L cc2; mainly L ventricle and maybe some L atrium
What are the positions for different valve sounds
For auscultation, sounds (lub-dup) are heard best downstream of valve positions
Pulmonary: L ics2 near sternal edge: ‘dup’ sound
Aortic: R ics2 near sternal edge; ‘dup’ sound
Bicuspid or mitral: L ics5 at midclavicular line; ‘lub’ sound
Tricuspid: L ics5/6 near lower sternal edge; ‘lub’ sound
Why are pleural reflections important to know
For correct interpretation of chest X-ray
To perform procedures such as thoracentesis correctly
Describe the right lung
Has 3 lobes (superior, middle and inferior) separated by the oblique and horizontal fissures;
Oblique fissure from T2 vertebra posteriorly to rib 6 anteriorly
Horizontal fissure from rib 4 to oblique fissure
Superior and middle lobes mainly anterior
Inferior lobe mainly posterior
Describe the left lung
Has 2 lobes (superior and inferior) separated by the oblique fissures;
Oblique fissure from T2 vertebra posteriorly to rib 6 anteriorly;
Superior lobe mainly anterior and has lingula
Inferior lobe mainly posterior
What is atresia and fistula
Atresia - narrowing or withering away
Fistula- abnormal opening or passage
