Asthma Flashcards

1
Q

Outline the structure of the respiratory airway and describe how this relates to its function.

A

the respiratory system consists of the trachea, bronchi, alveoli and lungs. this helps us to draw air in and has a large surface area for gas exchange.

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2
Q

Describe the basic gas laws, calculate partial pressures, and convert kPa to mmHg.

A

dalton’s law of partial pressure: Pressure exerted by each gas in a mixture of gases is independent of the other gases present. The total pressure of a mixture of gases is equal to the sum of the individual gas pressures.

1kPa = 7.50mmHg

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3
Q

Calculate the pulmonary and alveolar ventilation rates, and define the different types of dead space, state their normal values, and explain how they are related.

A

The pulmonary ventilation rate is the frequency/respiration rate x tidal volume.

The dead space ventilation rate is the physiological dead space (typically 0.17L) x the respiration rate.

The alveolar ventilation rate is the pulmonary ventilation rate - the dead space ventilation rate.

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4
Q

Define airways resistance and describe its distribution in the respiratory tract.

A

Factors that influence airway resistance are airway smooth muscle tone, gravity and posture, lung compliance, age and disease.

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5
Q

Explain why the distribution of inspired gas differs across the lung.

A

At the base of the lungs, there are more alveoli present than at the apex of the lungs. When a person is upright, the blood volume is increased at the base of the lungs due to gravity. When a person is lying down, the blood flow is distributed evenly throughout the lung. Airways resistance is then increased when lying down (supine) compared to the upright position. Compression when lying down can also narrow the airways.

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6
Q

Describe how the processes of gas diffusion apply in the lungs.

A

Inhalation - 21% oxygen and 0.03% to 0.04% carbon dioxide.

Exhalation - 14% oxygen and 5% carbon dioxide.

Oxygen kPa - 13.3kPa in arterial blood and alveoli, 5.3kPa in venoud blood.

Carbon Dioxide kPa - arterial blood and alveoli is 5.3kPa, 6.0kPa in venous blood.

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7
Q

Define ventilation/perfusion ratio, give a normal value for the lung as a whole, and explain how and why it varies within the lung.

A

VA - pulmonary ventilation rate and the alveolar ventilation rate

Perfusion (Q) - the process by which deoxygenated blood passes through the longs and becomes reoxygenated.

The ventilation-perfusion ratio (VA/Q ratio) is defined as a ratio of alveolar ventilation to blood flow. A normal value is 1.

Dead space - normal ventilation, but there is no perfusion. No gas exchange occurs between the alveoli and the blood. The alveoli equilibrates with the atmosphere.

Shunt - no ventilation, but normal perfusion. No new oxygen enters the system, and the alveoli equilibrates with venous blood.

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8
Q

Outline the functional and clinical anatomy of the chest wall.

A

there are 3 layers of intercostal muscles: external, internal, and innermost. the neurovascular bundle lies between the internal and innermost muscles.

superior thoracic aperture - opening for structures to enter and leave the neck and thorax, thoracic outlet syndrome can occur.

inferior thoracic aperture - opening at the lower part of thoracic cavity and is closed by the diaphragm.

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9
Q

Outline the functional and clinical anatomy of the ribs and thoracic vertebrae

A

1st rib - atypical, scalene muscle attaches to subclavian tubercle, has subclavian vein and artery groove

facet on the vertebrae attaches to the tubercle of the rib - costotransverse joint

head of the rib articulates with 2 vertebrae and their intervertebral disc - costovertebral joint

there are 12 thoracic vertebrae

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10
Q

Outline the functional and clinical anatomy of the breast and pectoral muscles.

A

breast - known as mammary gland, 15-20 lobes, breast is separated from the pectoralis major muscle by a retromammary space

pectoralis major - attached to clavicle and sternum, joins to bicipital groove of humerus, accessory of respiration when pectoral girdle is flexed, innervated by medial and lateral pectoral nerves

pectoralis minor - attached to coracoid process of scapular and near to costal cartilage, innervated by medial pectoral nerve

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11
Q

Outline the functional and clinical anatomy of the mediastinum and its contents.

A

central part of thoracic cavity that lies between pleural cavities.

boundaries are sternum, thoracic inlet, thoracic vertebral column, diaphragm

superior mediastinum - behind manubrium

inferior mediastinum:

anterior - Internal thoracic aa and vv, thymus, sternopericardial ligaments

middle - Heart and pericardium, phrenic nn and pericardiophrenic aa and vv, inferior vena cava

posterior - Descending aorta, azygos vv, oesophagus, thoracic duct, sympathetic trunks

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12
Q

Describe the layout of the respiratory system.

A

the nasal cavity, larynx, trachea, bronchi, lungs, alveoli, pleural cavity

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13
Q

Describe the structure of the walls of the thorax and to indicate the normal and accessory muscles of respiration function.

A

the diaphragm is the main muscle of respiration, intercostal muscles, pectoral muscles, sternocleidomastoid, scalene muscles and trapezius are accessory muscles of respiration.

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14
Q

Explain the differences between respiratory movements in adults and children.

A

babies - horizontal ribs, abdominal breathing by contacting diaphragm, shorter airways, larger tongue in proportion, smaller lung capacity and undeveloped chest muscles

adults - muscles of respiration contract to expand the thoracic cavity, increases thoracic volume and decreases intrathoracic pressure. Air is drawn into the lungs from the outside and passes into the terminal bronchioles and alveoli to oxygenate the blood. The diaphragm relaxes, the lungs recoil, thoracic volume decreases, intrathoracic pressure increases and air is expelled.

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15
Q

Give examples of respiratory distress and appreciate some clinical problems associated with the respiratory system.

A

There are two main types of respiratory distress: neonatal respiratory distress syndrome, which affects newborn babies, and acute respiratory distress syndrome (ARDS), which can affect people regardless of age. The symptoms of respiratory distress are blue coloured extremities, rapid and shallow breathing, and a rapid heart rate.

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16
Q

Demonstrate the main anatomical features and surface landmarks of the thoracic vertebrae, ribs and sternum

A

thoracic vertebrae - lamina, facet for tubercle of rib, body, hole for spinal cord

ribs - tubercule, head, body, angle (1st rib - subclavian artery and vein groove, scalene tubercle)

sternum - jugular notch, manubrium, sternal angle, body, xiphoid process.

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17
Q

Describe the anatomy of the joints between the ribs, vertebrae, costal cartilages and sternum.

A

Costovertebral Joint – the joint of the head of the rib, in which the head articulates with two adjacent vertebral bodies and the intervertebral disc between them.

Costotransverse Joint - the tubercle of the rib articulates with the transverse process of a vertebra (facet).

The ribs join to the sternum via the sternal notches. Ribs 7,8 and 9 fuses to connect to the 7th sternal notch. The clavicle joins at the sternoclavicular joint.

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18
Q

Describe the anatomy of the intercostal muscles. Describe a neurovascular bundle in a typical intercostal space and outline the structures its components supply

A

intercostal muscle - external, internal, innermost

neurovascular bundle - intercostal vein, intercostal artery, intercostal nerve, present between interal and innermost intercostal muscles.

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19
Q

Appreciate the thoracic contents in situ

Appreciate the muscles of the anterior thoracic wall

A

thoracic contents - lungs, heart, bronchi, trachea, pleural cavity

muscles of anterior thoracic wall - pectoral muscles, serous anterior

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20
Q

Describe the pathophysiology of asthma.

A

asthma is a reversible increase in airway resistance, involving bronchoconstriction and inflammation

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21
Q

List the clinical features of asthma.

A

wheezing, breathlessness, tight chest, cough, decrease in FEV1

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22
Q

Describe how asthma may be diagnosed and managed.

A

taking PEF measurements, to see if a beta-2 agonist reduces symptoms, rule of cardiovascular conditions or COPD, auscultate

managed by inhaling a steroid as a preventative measure, use a beta-2 agonist, xanthines in an emergency, omalizumab in servere cases

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23
Q

Describe the pharmacological actions of a short-acting betaadrenoceptor agonist such as salbutamol.

A

Salbutamol is a beta2-adrenoceptor agonist and acts on beta2-adrenoceptors in the smooth muscle to increase cAMP levels. This dilates the airways.

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24
Q

Describe the pharmacological actions of a long-acting betaadrenoceptor agonist such as salmeterol.

A

stimulates beta 2 adrengenic receptors and causes bronchodilation

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25
Q

Describe the pharmacological actions of an inhaled corticosteroid such as beclometasone.

A
  • prevents inflammation by the activation of intracellular receptors, leading to altered gene transcription and production of lipocortin.
  • corticosteroids penetrate the cell and bind to an intracellular receptor. This complex then goes to the nucleus and controls DNA transcription. mRNA and proteins are produced, such as lipocortin, which stops the production of phospholipase 2, which causes inflammation through the arachidonic acid pathway.
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26
Q

Describe the pharmacological actions of a leukotriene receptor antagonist such as montelukast.

A

They are preventative and bronchodilators. They antagonise the actions of leukotrienes, which are constrictors and inflammatory.

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27
Q

Describe the pharmacological actions of a muscarinic receptor antagonist such as ipratropium.

A

Ipratropium is a muscarinic antagonist, a type of anticholinergic, which works by causing smooth muscles to relax.

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28
Q

Describe the pharmacological actions of a xanthine such as theophylline.

A
  • bronchodilators, but they are not as good as beta-adrenoceptor agonists.
  • taken orally, or can be administered intravenously in an emergency.
  • adenosine receptor antagonists and phosphodiesterase inhibitors.
  • narrow therapeutic window.
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29
Q

Describe the pharmacological actions of a cromone such as sodium cromoglicate.

A

stabilisation of mast cell membranes, thereby inhibiting the release of pharmacological mediators of anaphylaxis when the cells are triggered in a selective manner

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30
Q

Describe the clinical features of chronic obstructive pulmonary disease and state how it may be managed by drugs.

A
  • chronic bronchitis, which causes increased mucus, airway obstruction, and intercurrent infections
  • emphysema, which is the destruction of alveoli.
  • More than 90 percent of cases are smoking related. FEV1 is reduced and there is little variation in PEF (peak expiratory flow).
  • roflumilast is a selective PDE IV inhibitor licensed for COPD.
31
Q

Describe how betaadrenoceptor antagonists and nonsteroidal anti-inflammatory drugs (NSAIDs) may both cause bronchospasm.

A

Bronchoconstriction occurs because sympathetic nerves innervating the bronchioles normally activate β2-adrenoceptors that promote bronchodilation.

32
Q

Outline the histological structure of the upper respiratory system

A
  • The epithelium in the upper respiratory system is the same as in the lower respiratory system. The upper respiratory system is the nasal cavity, the nasopharynx and the esophagus.
  • airways are kept open by either bony or cartilaginous scaffolds. Turbinate bones in the nasal cavity create turbulence, increasing surface to air volume ratio.
  • large particles are prevented from entry by vibrissae
  • smaller particles are trapped by mucus which covers the lining all the way to the terminal bronchioles.
33
Q

Describe the detailed histological structure of the airways and outline the differences between the different parts of the airway

A

The trachea splits into two main bronchi, which split into two left lobar bronchi and the right lobar bronchi. This splits into segmental bronchi and then the bronchioles, and finally the terminal and respiratory bronchioles.

The respiratory epithelium is formed of:

  • pseudostratified columnar ciliated epithelium and basement membrane.
  • mucosa.
  • lamina propria contains connective tissue, blood and lymph.
  • submucosa is formed of seromucous glands, smooth muscle and elastin fibres.
  • cartilage present is hyaline cartilage, which is c-shaped in the trachea and less prominent as the tubes get smaller.
34
Q

Describe the structure of the alveoli and the air-blood interface

A

The alveoli are blind ended sacs with thin walls for gaseous exchange, lined by two types of epithelium. These are type I and type II pneumocytes.

Type I pneumocytes are flattened squamous epithelial cells with very thin cytoplasm to allow gaseous diffusion. The basement membrane is fused with capillary basement membrane.

Type II pneumocytes are rounded cells with prominent secretory granules for production and secretion of surfactant.

35
Q

Describe the structure and function of the lung interstitium

A

This is a connective tissue with blood vessels, macrophages and fibroblasts. There is no collagen. Instead there is elastin. it is a scaffolding for the lung and reservoir for vital structures and homeostatic cellular processes.

36
Q

Describe the defence mechanisms employed by the respiratory system to protect the lungs from infection

A

nasal hair, immunoglobulin secretion, saliva, cough, epiglottic reflexes, macrophages, neutrophils, mucus, phagocytes

37
Q

Give a basic account of obstructive and restrictive lung disease in the context of lung histology and function

A

An obstructive disease is where there is limitation of airflow due to obstruction, which causes increased airway resistance. Airway narrowing (asthma), loss of elasticity (emphysema) or increased secretions (bronchitis/asthma) can occur.

Restrictive diseases district normal lung movement during respiration, reduced expansion of lung tissue and decreased total lung capacity.

38
Q

Explain simple flow volume curves and the use of peak expiratory flow rate.

A

PEF - Total lung capacity to peak expiratory flow is effort dependent. Peak expiratory flow to residual volume is not.

39
Q

Define the various respiratory volumes which can be measured (VC, RV, FRC, IRV, ERV, TV and TLC).

A

spirometry:
VC - vital capacity, is the maximum amount of air expelled from the lungs after first filling the lungs to a maximum then expiring to a maximum

TV - tidal volume, the volume of air entering and leaving the lung with each normal breath

IRV - inspiratory reserve volume, the extra volume of air inspired above the normal tidal volume with full force

ERV - expiratory reserve volume, the extra volume of air expired by forceful expiration at the end of normal tidal expiration

helium dilution/nitrogen washout
FRC - the total volume exhaled

RV - the volume of air remaining in the lungs after the most forceful expiration

TLC - the maximum volume of air that the lungs can hold

40
Q

Outline the functional and clinical anatomy of the mediastinum and its contents.

A

The mediastinum contains the heart and its vessels, the esophagus, the trachea, the phrenic and cardiac nerves, the thoracic duct, the thymus and the lymph nodes of the central chest.

41
Q

Outline the functional and clinical anatomy of the heart and great vessels.

A

heart:

  • sternocostal surface - the right (with bit of left) ventricle.
  • diaphragmatic side - left (with a bit of right) ventricle.
  • posterior - left (and a bit of right) atrium and pulmonary veins.
  • pulmonary surface - left ventricle, in the cardiac notch of the left lung.
  • superior border - left costal cartilage 2 to right costal cartilage 3.
  • inferior border - diaphragm central tendon from right costal cartilage 6 to left intercostal space 5, right ventricle and part of the left ventricle.

great vessels:

  • superior vena cava - deoxygenated blood from the head region and upper limbs.
  • inferior vena cava - deoxygenated blood from the abdominal regions and the lower limbs.
  • pulmonary trunk goes into the pulmonary arteries, which carry deoxygenated blood to the lungs. The pulmonary veins carry oxygenated blood from the lungs.
  • proximal aorta goes - arch of the aorta, which splits into the right subclavian, right common carotid arteries and the left common carotid and the left subclavian artery.
  • thoracic aorta - posterior intercostal arteries coming off of it.
  • superior vena cava has the azygos vein attached to it. - posterior intercostal veins drain the posterior thoracic wall. The accessory hemiazygos vein and the hemiazygous veins drain into the azygos vein.
42
Q

Outline the functional and clinical anatomy of the lungs and pleura.

A

The right lung has 3 lobes, superior, middle and inferior, separated by the oblique and horizontal fissures. The oblique fissure is from T2 to rib 6. The horizontal fissure from rib 4 to the oblique fissure. The superior and middle lobes are mainly anterior and the inferior lobe is mainly posterior.

The left lung has 2 lobes, the superior and inferior, separated by the oblique fissures. The oblique fissure is from T2 to rib 6. The superior lobe is mainly anterior and has a lingula, and the inferior lobe mainly is posterior.

43
Q

Distinguish the sources of the antigens recognised, and the materials damaged by, the adaptive response in antimicrobial immunity, allergy and autoimmunity.

A

There are four main types of hypersensitivity: type I, II, III an IV.

Type I is antibody mediated activity by IgE antibodies as well as allergen and mast cells. It is also known as atopic allergy.

Type II is mediated by IgG antibodies that bind to cytokines.

Type III is known as immune complex hypersensitivity and is antibody mediated by IgG, IgA and IgM.

Type IV is a cell mediated response, and can be known as delayed type hypersensitivity. T cells activate macrophages that can lead to tissue damage.

44
Q

Describe the role of IgE and mast cells in type I hypers

Explain the role of Th2 cells in promoting IgE production and eosinophil development.ensitivity.

A

The first exposure to an allergen is sensitization. T helper 2 cells produce cytokines that aid a B cell to class switch to produce IgE antibodies.

second exposure to the same allergen is elicitation. IgE antibodies are on the surface of the mast cell. These are cross linked by the allergen and cause the mast cell to degranulate and release its preformed and newly formed mediators.

45
Q

Explain how the route of exposure to allergens may influence the type of atopic disorder(s) that result.

Describe atopic disorders that affect different tissues, including allergic rhinitis, asthma, urticaria, eczema, food allergies, anaphylaxis.

A

Systemic anaphylaxis can be caused by drugs, serum, venom and peanuts. The route of entry is intravenous. The response is edema, increased vascular permeability, tracheal occlusion, circulatory collapse and death.

Allergic rhinitis and asthma can be caused by inhalation of pollens and dust-mite feces. This can lead to bronchoconstriction, increased mucus production and airway inflammation.

Food allergies are caused by oral entry. This can lead to vomiting, diarrhea, itching, hives and anaphylaxis.

46
Q

Outline the skin prick test.

A

an allergen is introduced to the skin and an allergic reaction will be produced.

47
Q

Describe the acute and chronic phases of atopic reactions.

A

In the acute response, inflammatory mediators cause increased mucus secretion and smooth muscle contraction, leading to airway obstruction. There is then a recruitment of cells from the circulation. The chronic response is caused by cytokines and eosinophil products.

48
Q

Outline the mechanism of type II hypersensitivity and how it is exemplified by haemolytic anaemia associated with certain drug allergies.

A

In type II hypersensitivity these escaped self-reactive B cells become activated and produce IgM or, with the help of CD4 positive T helper cells, IgG antibodies that attach to antigens on host cells.

49
Q

Outline the mechanism of type III hypersensitivity and how it is exemplified by allergic alveolitis.

A

In type III hypersensitivity reaction, an abnormal immune response is mediated by the formation of antigen-antibody aggregates called “immune complexes.”

50
Q

Outline the mechanism of type IV hypersensitivity and how it is exemplified by contact dermatitis, with the underlying Th1driven mechanisms being similar to those seen in tuberculosis and leprosy.

A

type IV HS results primarily from the actions of effector T cells and macrophages.

51
Q

Explain the immunological basis of tissue transplant rejection.

A

the immune system does not recognise the surface antigens and so attacks the organ.

52
Q

Explain how the respiratory system develops.

A

lung formation:

  1. pseudoglandular stage - weeks 5 to 16, terminal bronchioles form, all the major components of the lung are formed, pericardioperitoneal canals become separated from the pericardial cavity by the pleuropericardial folds.
  2. canalicular period - week 16 to 26, lumens of the bronchi and terminal bronchioles enlarge, tissue becomes vascularised, terminal sacs form at the end of the respiratory bronchioles.
  3. terminal sac period - week 26 to birth, primordial alveoli form, type I alveolar epithelial cells, type II alveolar cells which form in-between the flat type I alveolar cells.
  4. alveolar period - 8 months old into childhood, increased production of surfactant, primordial alveoli increase in size, type I epithelial cells become thinner and capillaries mature.

diaphragm:

  • transverse septum is mesodermal in origin and grows dorsally from the ventrolateral body wall, forming liver is embedded in the tissue, from the caudal to pericardial cavity, which partially separates it from the peritoneal cavity. Primordium of central tendon of diaphragm.
  • Pleuroperitoneal membranes form from the lateral wall of pleural and peritoneal cavities and first appear at the start of the 5th week. This forms the posterior and lateral parts of diaphragm, by fusing with the transverse septum and dorsal mesentery in the 7th week.
  • dorsal mesentery of oesophagus will form the median region of the diaphragm. It forms muscle bundles anterior to the aorta, the crura of the diaphragm. This is 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.
  • muscular ingrowth from lateral body walls contributes muscle to the peripheral region of diaphragm external to the region that is derived from the pleuroperitoneal membranes. This has occurred by the twelfth week.
53
Q

Explain the changes that occur before and at birth.

A

before birth:
The amount of surfactant produced increases before birth, mostly in the last 2 weeks of gestation. Breathing movements occur before birth to stimulate lung development and respiratory muscles. Amniotic fluid is aspirated.

at birth:
the lungs are half filled with fluid. This fluid is removed from the lungs by pressure on the thorax during delivery, expelling fluid through mouth and nose, absorbed into circulation via the pulmonary circulation, and absorbed into the lymphatics. A thin coating of surfactant is left lining the alveolar cell membranes.

54
Q

Explain how some important defects form.

A

Respiratory Distress Syndrome:
- not enough surfactant and surface tension will be high at the air-blood interface. There is a risk of alveoli collapsing during expiration, leading to RDS.

Oesophageal Atresia and Tracheoesophageal Fistulas: - abnormal separation of the oesophagus and trachea by the oesophagotracheal septum.

  • Atresia is the narrowing or withering away and fistula is an abnormal opening or passage.
  • Excessive amounts of fluid in the mouth and upper respiratory tract means that gastric contents may reflux into the trachea and lungs. Coughing, choking and pneumonia can occur.

Congenital Cysts of the Lungs:

  • terminal bronchi are abnormally dilated, usually at the lung periphery.
  • The cysts may be small and numerous or few and large. Problems associated can be poor drainage which leads to chronic lung infections.

Congenital Diaphragmatic Hernia:

  • failure of fusion of pleuroperitoneal membrane with other 3 components.
  • usually a posterolateral defect, and 90% of cases are on the left side. It can cause abdominal viscera to be present in the thoracic cavity. It is associated with hypoplastic lung and the mediastinum may be pushed to the right.
55
Q

Describe the layout in the adult

A

Development explains many features of the respiratory system. Three lobes of the lungs on right and two on left originates from the first division of the lung buds. Separation of thoracic, abdominal and pleural cavities occur when cavities become completely separate units in development. The formation of the diaphragm is derived from 4 embryological components.

56
Q

Describe the regulation of erythropoiesis. Define the term reticulocyte.

A

Control of erythropoiesis is essential to maintain the red blood cell level. It is controlled by erythropoietin, which is a polypeptide hormone.

a reticulocyte is an immature red blood cell

57
Q

List the different major components of haemoglobin.

A

haem is made from ferrous iron, Fe2+, at the centre of a protoporphyrin complex. Blobin chains are linked by non-covalent bonds.

58
Q

State the differences in chemical composition between foetal and adult haemoglobin.

A

adult haemoglobin is tetrameric, and is formed of four polypeptide chains with alpha2 and beta 2 subunits. Fetal hemoglobin is formed of alpha 2 and gamma 2 subunits

59
Q

List the stages in iron metabolism and state the roles of ferritin and transferrin.

A
  • Fe3+ from the diet is reduced to Fe2+ by the stomach acid.
  • Fe3+ is produced by the mucosal cells of duodenum. It binds to apoferritin to produce ferritin (which is an iron store).
  • Iron is released into the blood to bind with transferrin for transport and delivers iron to the bone marrow (which are ferritin stores). Iron is then haemoglobin.
60
Q

State how oxygen is carried in the blood.

A

Ferrous (Fe2+) iron in haem binds O2. Four oxygen molecules bind per haemoglobin.

61
Q

Draw and label haemoglobins oxygen dissociation curve. Compare the curve with that for foetal haemoglobin.

A

Hemoglobin is an allosteric protein. The binding of one oxygen molecule enhances (by a conformational change) the binding of another oxygen molecule to another haem in the same molecule. This leads to an sigmoidal-shaped curve.

Fetal haemoglobin has a much higher affinity for oxygen, so its curve is further left than hat of adult haemoglobin.

62
Q

Describe the Bohr effect.

A

Acidity enhances the release of oxygen from haemoglobin. Increasing carbon dioxide at constant a pH also lowers haemoglobin’s affinity for oxygen. Therefore, oxygen is more readily given up to metabolically active tissues (which produce hydrogen and carbon dioxide).

63
Q

Describe the effects of diphosphoglycerate on the carriage of oxygen.

A

2,3-DPG reduces the oxygen affinity of haemoglobin. DPG binds to deoxyhaemoglobin to shift equilibrium, which reduces oxygen binding. this liberates oxygen to the tissues.

Fetal haemoglobin is unable to bind DPG and has a higher affinity for oxygen because of this. DPG levels are increased when arterial oxygen is reduced chronically, so that oxygen is more readily liberated to tissues.

64
Q

Describe the binding of carbon monoxide to haemoglobin and the pathological consequences.

A

Haemoglobin has a much greater affinity for carbon monoxide than oxygen and will form carboxyhaemoglobin. This compound does not readily dissociate and the tissues will become starved of oxygen.

65
Q

Define the term methaemoglobinaemia and list its possible causes.

A

Iron is in the ferric (Fe3+) state, not the ferrous state. Therefore, the patient cannot carry O2. The patient may have symptoms of anoxia, can be due to a hereditary lack of glucose-6-phosphate dehydrogenase, which keeps Hb in reduced state, and may be caused by drugs such as antimalarial drugs.

66
Q

Describe how carbon dioxide is carried in the blood.

A
  • 30 percent of carbon dioxide forms carbaminohaemoglobin.
  • 60 percent of the carbon dioxide is present as HCO3-, its formation catalysed by carbonic anhydrase the red blood cells.
  • 10% of carbon dioxide is dissolved in the body.
67
Q

Understand why shortness of breath (SOB) can be a presenting symptom for both Respiratory and Cardiovascular disease.

A
  • respiratory disease can cause someone to not be able to take in enough oxygen due to problems with the airways
  • cardiovascular disease can cause breathlessness as the heart may not be pumping enough blood around the body.
68
Q

Understand how V/Q mis-match causes SOB, and why physiological compensation is limited.

A

low perfusion means that the blood is not being oxygenated properly and will therefore cause shortness of breath

69
Q

Be able to distinguish respiratory and cardiovascular causes of SOB from the patient history and examination.

A

ask the patient questions about their lifestyle, about the type of shortness of breath they are experiencing, what is causing it

70
Q

Name the routine investigations for someone with SOB and understand their strengths and weaknesses.

A

auscultation, take PEF measurements, pulse oximeter

71
Q

Know what confirmation bias is.

A

Confirmation bias is the tendency to search for, interpret, favor, and recall information in a way that confirms or supports one’s prior beliefs or values.

72
Q

Consider the surface anatomy of the nose and neck (larynx)

A

The nasal cavity is divided by the septum, made of the vomer, ethmoid and cartilage.

superior boundary - frontal bone, sphenoid bone and the ethmoid bone.
floor - hard palate.
lateral wall - superior, middle and inferior concha. superior, middle and inferior meatus underlie the concha.

73
Q

Identify on X-rays, CT scans and sections of the head: the nasal septum, conchae, meati, and paranasal air sinuses.

A

The sinuses are named the frontal, sphenoidal, maxillary and ethmoidal sinuses.

frontal sinus - drains through the frontonasal duct into the middle meatus.
sphenoid sinus - drains into the sphenoethmoidal recess.
maxillary sinus - drains into the middle meatus. The posterior ethmoidal cells drain into the superior meatus.
anterior and middle ethmoidal cells - drain into the middle meatus.
nasolacrimal duct - drains into the inferior meatus.