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Medicine 2 > RCM Week 1 (asthma) > Flashcards

RCM Week 1 (asthma) Flashcards

1
Q

What are intercostal muscles

A

Located in intercostal spaces between ribs

3 layers of muscles: external, internal and innermost. Important in respiration and keeping ICS rigid

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2
Q

What is the pleura of the lungs

A
  • 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
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3
Q

Why may you have to insert a needle into an intercostal space

A

To drain or sample fluid (pleural fluid, blood or pus) from the pleural cavity or to anaesthetise an intercostal nerve

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4
Q

How do you avoid damaging neurovascular bundles when inserting a needle into an intercostal space

A

Insert the needle close to the upper border of the lower rib

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5
Q

What is the difference between the superior thoracic aperture and the inferior thoracic aperture

A

Superior : opening for structures to enter / leave the neck / thorax

Inferior: opening at lower part of thoracic cavity (closed by diaphragm)

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6
Q

What is thoracic outlet syndrome

A

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

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7
Q

Attachments, actions and nerve supply of the pectoralis major

A

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

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8
Q

Attachments, actions and nerve supply of the pectoralis minor

A

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)

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9
Q

Describe the location of the breast

A

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

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10
Q

Describe the structure of the breast

A

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

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11
Q

Why is lymphatic drainage of considerable clinical importance

A

Because of the frequency of breast cancer and its spread to other parts of the body by lymph and blood vessels

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12
Q

What is the mediastinum

A

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

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13
Q

What are the boundaries of the mediastinum

A

Anteriorly: sternum

Posteriorly: thoracic vertebral column

Superiorly: thoracic inlet and root of the neck

Inferiorly: diaphragm

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14
Q

Describe the divisions of the mediastinum

A

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)
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15
Q

What are the contents of the superior mediastinum

A

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

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16
Q

Describe the structure of the inferior mediastinum

A
  • 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)

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17
Q

Explain the process of breathing

A

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

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18
Q

Describe the diaphragm

A 
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
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19
Q

Describe the role of the intercostal muscles

A
  • 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
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20
Q

What is pleura

A

Serous membrane divided into parietal and visceral layers; surround the lungs; contain the pleural cavities; separated by serous fluid

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21
Q

What is the difference between parietal and visceral pleura

A

Parietal: outer; lines thoracic cavity

Visceral: inner; covers lung following lung fissures

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22
Q

Define asthma

A

Reversible increases in airway resistance, involving bronchoconstriction and inflammation

Reversible decreases in the FEV1 : FVC

Variations in PEF which improve with a B2 agonist

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23
Q

What is asthma provoked by

A

Genetic predisposition

  • allergens
  • cold air
  • viral infections
  • smoking
  • exercise
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24
Q

Clinical features of asthma

A 
Wheezing 
Breathlessness 
Tight chest 
Cough (worse at night / exercise) 
(Nocturnal in children)

Decreases in FEV1, reversed by a B2 agonist

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25
Q

How do B2 agonists help treat asthma

A
  • 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
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26
Q

How do xanthines treat asthma

A
  • bronchodilators, not as good as beta-adrenoceptor agonists (2nd line use)
  • oral or iv aminophylline in emergency
  • adenosine receptor antagonist
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27
Q

How can steroids be used to treat asthma

A

Given with B2 agonists - reduce receptor down-regulation

Side effects:

  • throat infections, hoarseness (inhalation)
  • adrenal suppression (oral)
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28
Q

How do leukotriene receptor antagonists treat asthma

A

Eg montelukast

  • increased role as add on therapy
  • preventative and bronchodilators
  • antagonise actions of LTs
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29
Q

How does omalizumab treat asthma

A

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

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30
Q

How do airways cope with changing pressure

A

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

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31
Q

How is temperature adjustment and moisturising enhanced in nasal cavity

A

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

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32
Q

What are the 3 components of the lower respiratory system

A

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)

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33
Q

Components of the airway system

A
  • trachea
  • 2 main bronchi
  • 2 left lobar bronchi and 3 right lobar bronchi
  • segmental bronchi
  • bronchioles (terminal and respiratory)
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34
Q

5 layers of the airway

A
  • 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
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35
Q

Describe the components of respiratory epithelium

A
  • 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

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36
Q

What is metaplasia

A

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
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37
Q

Describe structure of trachea

A

Anterior C shaped plates of cartilage with posterior smooth muscle. Mucous glands. Trachealis muscle (fibroelastic tissue) controls diameter

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38
Q

Describe structure of the bronchi

A

Discontinuous foci of cartilage ie cartilage plates, more prominent smooth muscle layer. Mucous glands

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39
Q

Describe the structure of the bronchioles

A

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

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40
Q

Describe the structure of the alveolar duct

A

Flat epithelium, no glands, no cilia

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41
Q

Describe the structure of the alveoli

A

Type I and II pneumocytes

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42
Q

What are the 2 types of alveoli epithelium

A

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

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43
Q

What is surfactant

A

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

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44
Q

Why are lungs vulnerable to infection

A

Due to constant exposure to the external environment
- constant inhalation of nasopharyngeal flora

Lung parenchyma remains sterile by coughing, sneezing and lung defence mechanisms

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45
Q

What are the host defence mechanisms of the upper airways (nasopharynx and oropharynx)

A 
Nasal hair 
Turbinates 
Mucociliary apparatus 
Immunoglobulin A (IgA) secretion 
Saliva 
Sloughing of epithelial cells 
Local complement production 
Interference from resident flora
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46
Q

What are the host defence mechanisms of the conducting airways (trachea and bronchi)

A

Cough, epiglottis reflexes, sharp-angled branching of airways, mucocilary apparatus, immunoglobulin production (IgG, IgM, IgA)

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47
Q

What are the host defence mechanisms of the lower respiratory tract (terminal airways, alveoli)

A

Alveolar lining fluid (surfactant, Ig, complement, fibronectin)

  • cytokines (interleukin 1, tumour necrosis factor)
  • alveolar macrophages
  • neutrophils
  • cell mediated immunity
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48
Q

Lung defence mechanisms

A

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

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49
Q

Further defence mechanisms that operate after development of adaptive immunity

A

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

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50
Q

Examples of obstructive diseases of the lungs

A 
COPD 
Bronchitis 
Emphysema 
Asthma 
Bronchiectasis 
Cystic fibrosis
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51
Q

Examples of restrictive diseases of the lungs

A

Fibrosis

Pneumoconiosis (asbestosis, silicosis, coal workers disease)

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52
Q

What does the ratio of FEV1 / FVC as % show

A

The proportion of total volume of air that can be expired in the first second of expiration

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53
Q

How is FEV1 and FVC affected in obstructive disease and restrictive disease

A

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

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54
Q

What is interstitial fibrosis

A

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

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55
Q

What is pulmonary fibrosis

A

Scarring of the lung tissue - stretchiness of lung is compromised which has an effect on lung capacity

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56
Q

What is tidal volume

A

Volume of air entering and leaving the lung with each normal breath

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57
Q

What is inspiratory reserve volume (IRV)

A

Extra volume of air inspired above the normal tidal volume with full force

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58
Q

What is expiratory reserve volume (ERV)

A

Extra volume of air expired by forceful expiration at the end of normal tidal expiration

59
Q

What is vital capacity (VC)

A

Maximum amount of air expelled from the lungs after first filling the lungs to a maximum then expiring to a maximum (TV + IRV + ERV)

60
Q

What is residual volume (RV)

A

Volume of air remaining in the lungs after the most forceful expiration

61
Q

What is functional residual capacity (FRC)

A

Amount of air that remains in the lungs at the end of normal expiration (ERV + RV)

62
Q

What is total lung capacity (TLC)

A

The maximum volume of air the lungs can hold (VC + RV)

63
Q

What is nitrogen washout in a lung function test

A

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

64
Q

Effects of obstructive deficits

A

Eg asthma, COPD

  • FEV1 will be reduced but FVC will be relatively normal
  • a low FEV1/FVC will be recorded
65
Q

What is the fibrous pericardium and the serous pericardium

A

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

66
Q

4 surfaces of the heart and pericardium

A

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

67
Q

What is the apex of the heart

A

L ventricle usually posterior to L ics5 in adults

Location of ‘apex beat’

68
Q

4 borders of the heart and pericardium

A

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

69
Q

What are the valve positions

A

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
70
Q

What are the valve auscultation sites (sites where you hear the lub-dup sound through the stethoscope)

A

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

71
Q

What is the pleura

A

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

72
Q

What is the difference between parietal pleura and visceral pleura

A

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

73
Q

Describe the different surfaces of the lungs

A

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

74
Q

What are pleural reflections

A

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

75
Q

Summary of the surface anatomy of the visceral pleura

A

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

76
Q

Summary of the surface anatomy of the parietal pleura

A

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

77
Q

Describe the right lung

A

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

78
Q

Describe the left lung

A

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

79
Q

What are the 4 types of hypersensitivity reactions

A

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

80
Q

What are mast cells

A

Found in all tissues - generate rapid inflammatory response

Activated by complement when pathogen comes into body causes cell to release inflammatory mediators

81
Q

What is the role of IgE antibodies in type I hypersensitivity (atopic allergy)

A

Recognise other allergens

82
Q

What is the first stage of type I hypersensitivity

A

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

83
Q

What is stage 2 of type I hypersensitivity

A

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

84
Q

What is systemic anaphylaxis (IgE mediated allergic reaction)

A

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

85
Q

What is acute urticaria (IgE mediated allergic reaction)

A

Allergens: insect bites or allergy testing

Route: subcutaenous

Response: local increase in blood flow and vascular permeability

86
Q

What is allergic rhinitis ‘ hay fever (IgE mediated allergic reaction)

A

Allergens: pollens, dust mites

Route: inhalation

Response: edema of nasal mucosa, imitation of nasal mucosa

87
Q

What is asthma (IgE mediated allergic reaction)

A

Allergens: danders, pollens, dust mite

Route: inhalation

Response: bronchial constriction, increased mucus production , airway inflammation

88
Q

What is food allergy (IgE mediated allergic reactions)

A

Allergens: tree nuts, peanuts, shellfish, milk, eggs, fish

Route: oral

Response: vomiting, diarrhoea, pruritis (itching), hives, anaphylaxis (rare)

89
Q

In development of the trachea what does the endoderm and splanchnic mesoderm give rise to

A

Splanchnic mesoderm- gives rise to cartilage, connective tissue and muscles

Endoderm- gives rise to epithelium and glands of trachea and pulmonary epithelium

90
Q

4 stages of lung maturation

A

Pseudoglandular stage

Canalicular period

Terminal sac period

Alveolar period

91
Q

What is the pseudogladnular stage of lung maturation

A

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
92
Q

What is the canalicular period of lung maturation

A

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
93
Q

What is the terminal sac period of lung maturation

A

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
94
Q

What are type II alveolar epithelial cells

A

Rounded secretory epithelial cells lining alveolar sacs

  • formed from the end of the 6th month
  • produce surfactant
95
Q

What is surfactant

A

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
96
Q

What is the alveolar period (8 months - childhood)

A
  • 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
97
Q

Changes in lungs before birth

A

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
98
Q

Changes in lungs at birth

A

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

99
Q

What occurs in the lungs of a stillborn

A

1st breath is not taken so no air in lungs. Lungs are full of fluid and will sink if placed in eater at autopsy

100
Q

4 embryonic components of the diaphragm

A

Transverse septum
Pleuroperitoneal membranes
Dorsal messengers of oesophagus
Muscular in growth from lateral body walls

101
Q

Describe the transverse septum (diaphragm)

A

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
102
Q

How does the pleuroperitoneal membranes form (diaphragm)

A

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
103
Q

Formation of dorsal mesentery of oesophagus (diaphragm)

A

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
104
Q

Formation of the primordial diaphragm

A

Occurs by fusion of the pleuroperitoneal membranes, dorsal mesentery of oesophagus and septum transversum. This partitions the thoracic and abdominal cavities

105
Q

What is respiratory distress syndrome

A

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
106
Q

What is oesophageal atresia and tracheooesophagus fistulas

A

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

107
Q

What are congenital cysts of the lungs

A
  • 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
108
Q

What is a congenital diaphragmatic hernia

A

Failure of fusion of pleuroperitoneal membrane with 3 other components

  • usually a posterolateral defect
  • 90% of cases are on the left side
109
Q

What is erythropoiesis

A

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

110
Q

Describe the structure of haemoglobin

A

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

111
Q

How are RBCs degraded

A

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

112
Q

What is the difference between adult and fetal Hb

A

Adult Hb contains a2Bs subunits

Fetal contains a2 gamma2 (rapidly destroyed at birth) - can lead to jaundice due to high levels of bilirubin

113
Q

Described the significance oh haemoglobin

A

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

114
Q

What does haemoglobin being an allosteric molecule mean

A

Once 1 O2 is binded, the non covalent bonds undergo a conformational change which means that the second oxygen binds more avidly etc

115
Q

How can Non-steroidal anti-inflammatory drugs (NSAIDS) eg aspirin, ibuprofen affect asthma

A

They increase leukotriene production

116
Q

Why should beta blockers not be given to patients with asthma

A

They bind to beta 2 adrenoreceptors in the lungs and worsen asthma

117
Q

What is the difference between infections of the upper and lower respiratory tract

A

Lower respiratory tract infections involve the airways below the larynx

Upper respiratory tract infections occur in structures in or above the larynx

118
Q

What are the 4 different paranasal air sinuses

A
  • frontal
  • sphenoidal
  • maxillary
  • ethmoidal (air cells)
119
Q

What are the 9 cartilages of the larynx

A

Unpaired: epiglottis, thyroid, cricoid

Paired: arytenoid, corniculate, cuneiform

120
Q

What structures are found in each part of the mediastinum

A

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)

121
Q

What are the accessory muscles of respiration

A

Scalene muscles - prevent rib 1 and 2 from descending

Pecs and trapezius- ‘fix’ the pectoral girdle to raise rib cage

122
Q

How do babies breathe

A

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
123
Q

How do children breathe

A

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
124
Q

Why is the use of the accessory muscles while at rest a sign of respiratory distress

A
  • 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
125
Q

Describe neonatal respiratory distress syndrome

A
  • 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%)
126
Q

Describe acute respiratory distress syndrome (ARDS)

A
  • 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
127
Q

Define the different types of breathlessness

A

Dyspnoea - breathlessness
Orthopnea - breathlessness on lying down
Exertional dyspnoea - breathlessness on exercise
Paroxysmal nocturnal dyspnoea - episodic breathlessness at night

128
Q

Describe the parasympathetic and sympathetic control of bronchial calibre

A

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

129
Q

What is an asthmatic attack

A

A genetic predisposition provoked by:

  • allergens
  • cold air
  • viral infections
  • smoking
  • exercise

May be characterised by early (immediate) phase followed by late phase

130
Q

Clinical features of an asthma attack

A 
Wheezing 
Breathlessness
Tight chest 
Cough 
Decreases in FEV1, reversed by a B2 agonist
131
Q

How do bronchodilators treat asthma attacks

A 
Reverse bronchospasm (early phase) 
Rapid relief (relievers)

Prevention:
May be used to prevent an attack
Can be anti-inflammatory

132
Q

How do muscarinic receptor antagonists treat asthma

A

They block parasympathetic bronchocon-striction

Inhalation: prevents anti muscarinic side effects
- limited / little value in asthma, used in COPD

133
Q

How do anti-inflammatory agents treat asthma

A

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

134
Q

What are the 3 principle compartments of the respiratory system

A

Conduction zone: conditioning of inhaled air
Respiratory zone: site of gas exchange
Musculo-elastic ventilation apparatus: drives ventilation

135
Q

What is a restrictive deficit

A

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

136
Q

What is an obstructive deficit

A

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

137
Q

What is the diffusion conductance test

A

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

138
Q

Borders of the heart

A

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

139
Q

What are the positions for different valve sounds

A

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

140
Q

Why are pleural reflections important to know

A

For correct interpretation of chest X-ray

To perform procedures such as thoracentesis correctly

141
Q

Describe the right lung

A

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

142
Q

Describe the left lung

A

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

143
Q

What is atresia and fistula

A

Atresia - narrowing or withering away

Fistula- abnormal opening or passage

Medicine 2 (16 decks)

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