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Anatomy - Thorax / Asthma Flashcards

1
Q

What is the purpose of costal cartilage?

A

Provides resilience and stability

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2
Q

What are these parts called?

A
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3
Q

What are these lines called?

A
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4
Q

What are the properties of intercostal muscles?

A

In intercostal space

3 layers - external, internal, innermost

Respiration importance

Help keep intercostal space rigid

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5
Q

Where is pleura found and what are the 2 types?

A

Each lung is enclosed in serous pleural sac

2 continuous membranes - visceral (surface) and parietal (inner surface – lines pulmonary cavities)

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6
Q

What are these parts called?

A
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7
Q

What is a health problem related to the thorax?

A

Thoracic outlet syndrome - where important arteries and nerves are compressed

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8
Q

What are the 2 thoracic apertures and their function?

A
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9
Q

What number are these atypical ribs?

A
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10
Q

What are these parts called?

A
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11
Q

What is the purpose of the scalene tubercule on rib 1?

A

Where scalene anterior muscle attaches

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12
Q

Where does the pectoralis major attach to?

A

Clavicular head which attaches to clavicle

Sternocostal head which attaches to sternum + upper 6 costal cartilages

Fibres which converge on intertubercular groove or humerus

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13
Q

What is the function of the pectoralis major?

A
  • Adductor and medial rotator of arm at shoulder joint
  • Can act also as flexor (when arm extended) and as extensor (when arm flexed)
  • If pectoral girdle is ‘fixed’, it can act also as an accessory muscle of respiration
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14
Q

Which nerves innervate the pectoralis major?

A

Medial and lateral pectoral nerves (C5-8 and T1)

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15
Q

Where does the pectoralis minor attach to?

A

Coracoid process of scapula, ribs 3-5 near cartilage

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16
Q

What is the function of the pectoralis minor?

A

Depressor of scapula (and, hence, shoulder) and protractor of scapula

If pectoral girdle is ‘fixed’, it can act also as an accessory muscle of respiration

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17
Q

Which nerve innervates the pectoralis minor?

A

Medial pectoral nerve (C8 and T1)

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18
Q

What are these parts called?

A
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19
Q

What is the mediastinum?

A

Central part of thoracic cavity, between pleural cavities

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20
Q

What are the boundaries of th mediastinum?

A

Sternum (anterior)

Thoracic vertebral column (posteriorly)

Thoracic inlet and root of the neck (superiorly)

Diaphragm (inferiorly)

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21
Q

What are these parts called?

A
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22
Q

What are the contents superior mediastinum?

A
  • Thymus (lymphoid organ; large between birth and puberty but involutes in adult, especially after disease);
  • 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 (T4/5 in expiration); Oesophagus;
  • Thoracic duct
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23
Q

What are the divisions are the mediastinum?

A

Superior and inferior –> behind manubrium sterni and behind body and xiphoid process of sternum

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24
Q

What are these parts called?

A
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25
Q

What are the contents of the inferior mediastinum?

A
  • Divided into anterior, middle and posterior regions:
  • 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 right atrium)
  • Posterior: Descending aorta (and branches); azygos vv (and tributaries); oesophagus; thoracic duct; sympathetic trunks (and branches)
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26
Q

What are these parts called?

A
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27
Q

What are these parts called?

A
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28
Q

What is the purpose of trachea cartilage?

A

Keeps airways open

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29
Q

What are these parts called?

A
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30
Q

What are these parts called?

A
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31
Q

What happens during breathing?

A
  • At rest, diaphragm relaxed
  • Muscles of respiration contract to expand thoracic cavity - mainly diaphragm
  • This increases thoracic volume / decreases intra-thoracic pressure
  • Air drawn into lungs from outside (where pressure greater)
  • Air passes into terminal bronchioles / alveoli to oxygenate blood
  • Diaphragm relaxes, lungs recoil, thoracic volume decreases, intrathoracic pressure increases and air expelled
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32
Q

What are the properties of the diaphragm?

A

The 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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33
Q

What does a superior view of diaphragm look like?

A
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34
Q

What are the properties of 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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35
Q

What are A, B and C?

A

A = external intercostal muscle

B = internal intercostal muscle (interosseus part)

C = internal intercostal muscle (interchondral part)

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36
Q

What are these parts called?

A
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37
Q

What are the directions of movement of the sternum and ribs?

A

Sternum = pump handle movement

Ribs = bucket handle movement

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38
Q

What are the properties of the different types of pleura and lungs?

A

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

Parietal pleura = Outer; lines thoracic cavity

Visceral pleura = Inner; covers lung following lung fissures

Lungs = Go above 1st rib; covered by suprapleural membrane.

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39
Q

What causes thoracic cavity and lungs to expand?

A

Surface tension between 2 pleura layers

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40
Q

What are the properties of babies breathing?

A
  • Babies can only breathe via abdominal breathing
  • Newborn ribs more horizontal so cant use pump/bucket handle movements
  • Intercostals weak
  • 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 the thoracic 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
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41
Q

What are the properties of children’s breathing?

A
  • Nasal breathers until 4 – 6 wks
  • Short neck & shorter, narrow airways – more susceptible to airway obstruction / respiratory distress
  • Tongue is larger in proportion to the mouth - more likely to obstruct airway if child unconscious
  • Smaller lung capacity and underdeveloped chest muscles
  • Have a higher respiratory rate – newborns ~60 breaths/min, early teens ~20-30 breaths/min
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42
Q

What is a health problem related to breathing?

A

Harrison’s suculus - defect from rapid breathing causing rib deformation in children

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43
Q

What is the costodiaphragmatic recess?

A

Where fluid will accumulate in the lungs (look for this abnormality in X-rays)

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44
Q

What does the use of accessory muscles during rest indicate?

A

Respiratory distress as lungs cannot provide enough oxygen to the body

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45
Q

What is neonatal respiratory distress syndrome?

A
  • Affects premature babies, if they are born before their lungs are fully developed and capable of working properly
  • The more premature the baby, the more likely it is that s/he will have respiratory distress syndrome
  • Approx. half of all babies born before 28 weeks of pregnancy will develop NRDS
  • Leading cause of death in newborns (accounts for 20% of deaths)
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46
Q

What is acute respiratory distress syndrome (ARDS)?

A
  • Fluid / proteins leak from the blood vessels into the alveoli (air sacs)
  • Lungs become stiff and so don’t work normally
  • Breathing becomes difficult
  • Mainly affects people over 75
  • Approx 1 in 6,000 people per year affected in England
  • Common causes are an infection in the lungs e.g pneumonia
  • Lung clots or injury (e.g from a car crash), could also trigger the condition
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47
Q

What are the symptoms of respiratory distress?

A

Blue extremities

Rapid and shallow breathing

Rapid heart rate

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48
Q

What are the properties of asthma?

A

Common - ~ 5.4million people in UK receive treatment

An inflammatory disease of the airways of the lungs; persists long-term

  • Muscles around the walls of

the airways tighten - so airways

become narrower

  • The lining of the airways

becomes inflamed

Variable symptoms - shortness of breath, wheezing, tightness of chest, coughing

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49
Q

What are these parts called?

A
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50
Q

What is pneumothorax and the 2 types?

A
  • Perforation of parietal pleura = air in pleural cavity
  • Tension and non-tension pneumothorax
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51
Q

What is non-tension pneumothorax?

A

Hole so air in and out, no build-up

Less severe

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52
Q

What is tension pneumothorax?

A

Air breathed in cannot escape, so remains and builds with each breath

Flap of tissue covers opening

Heart is pushed over - leads to arrythmia

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53
Q

What happens during emphysema?

A
  • COPD
  • Over-inflated alveoli so ineffective gas exchange
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54
Q

How is asthma characterised?

A

Reversible decreases in FEV1:FVC (first expiratory volume in first second and total amount of air expelled)

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55
Q

How is asthma diagnosed?

A

Variations in PEF which improve with B2 agonist use

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56
Q

What are the properties of COPD?

A
  • Chronic bronchitis and emphysema
  • Chronic bronchitis = + airway mucus, airway obstruction and intercurrent infections
  • Emphysema = alveoli destruction
  • +90% related to smoking
  • FEV1 reduced
  • Little PEF (peak expiratory flow) variation
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57
Q

What is bronchial calibre control?

A

Parasympathetic + sympathetic

Sympathetic = circulating adrenaline acting on B2 adrenoceptors on bronchial smooth muscle, causing relaxation

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58
Q

What effect does parasympathetic system have on airways?

A
  • A.Ch. acts on muscarinic M3–receptors:
  • Bronchoconstriction
  • Increase mucus
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59
Q

What effect does sympathetic system have on airways?

A
  • Circulating adrenaline acting on beta2-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.
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60
Q

What activates sympathetic nerve?

A

Irritants, such as dust

Leads to bronchoconstriction

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61
Q

What are the properties of asthma attacks?

A

Genetic predisposition, provoked by:

Allergens

Cold air

Viral infections

Smoking

Exercise

May be characterised by Early (Immediate) phase followed by Late phase

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62
Q

What do lung function test graphs look like before and after b2 agonist use for someone with asthma?

A

Decrease in FEV1, reversed by B2 agonist

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63
Q

What are the 3 spasmogens?

A
  • Histamine
  • Prostaglandin D2
  • Leukotrienes (C4 and D4)
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64
Q

What are 2 chemotaxins and what do they do?

A

Leukotriene B4, PAF (platelet activating factor)

Lead to late phase

Attract leukocytes (+ eosinophils and mononuclear cells)

Leads to inflammation and airway hyperactivity

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65
Q

What are the 2 pharmacological therapy basis for asthma?

A

Bronchodilators - reverse bronchospasm in early phase and offer rapid relief

Prevention - prevent attacks, are anti-inflammatory

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66
Q

What are the properties of B2 adrenoceptor agonists?

A
  • Increase FEV1
  • Salbutamol
  • Increase cAMP on smooth muscle B2-adrenoceptors
  • Reduce parasympathetic activity
  • By inhalation
  • Prolonged use can lead to receptor down-regulation
  • Long acting beta agonists (LABA) given for long-term control (i.e. salmeterol)
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67
Q

What is an example of a xathine and its properties?

A

i.e. theophylline

Bronchodilators, not as good as beta adrenoceptor agonists

Oral or IV in emergency (aminophylline)

Adenosine receptor antagonist

Phosphodiesterase inhibitors

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68
Q

What are examples of muscarinic m-receptor antagonists and their properties?

A

i.e. ipratropium / tiotropium

Block parasympathetic bronchoconstriction

Inhalation = prevents antimuscarinic side effects

Little value in asthma, used for COPD

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69
Q

What are examples and properties of anti-inflammatory agents?

A

Preventative

Corticosteroids - i.e. beclomethasone (inhalation) or prednisolone (oral)

Anti-inflammatory = by activation of intracellular receptors, leading to altered gene transcription, less cytokine production, and production of lipocortin/ Annexin A1 (a protein)

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70
Q

What is the function of lipocortin (annexin A1)?

A

Inhibits prostaglandin and leukotriene synthesis

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71
Q

What are the properties of steroid treatment in asthma?

A
  • Given with B2-agonists
  • Reduce receptor down-regulation
  • Side effects - throat infections, hoarseness (inhalation) and adrenal suppression (oral)
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72
Q

What is an example and the function of leukotriene receptor antagonists?

A

i.e. montelukast

+ role as add on therapy

Preventative and bronchodilator

Antagonise actions of leukotrienes

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73
Q

What are the properties of omalizumab?

A

Role in difficult to treat asthma

Directed against free IgE but not bound IgE

Prevents IgE from binding to immune cells which lead to allergen-induced mediator release in allergenic asthma

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74
Q

What is stepped care and the clinical pharmacology?

A

Follow guidelines - if salbutamol is used +2 times per week, step up

Spacer devices (patients with – technique and reduce steroid impaction)

Bronchodilator before steroid

Rinse mouth after steroid

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75
Q

What is lung compliance and the properties it in regards to the lungs?

A

Lung compliance = stretchiness

High pressure = stiffer lung = low compliance

Base of lung = + compliant than apex for better ventilation

Compliance = ensued by elastic recoil

Decreased lung compliance = pulmonary fibrosis, alveolar oedema e.g.

Increased lung compliance = normal ageing lung

Healthy lung = + lung compliance, - alveolar surface tension due to surfactant

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76
Q

What are the 3 lung function tests?

A

Test mechanical condition of lungs (pulmonary fibrosis)

Test airway resistance (asthma)

Test diffusion across alveolar membrane (pulmonary fibrosis)

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77
Q

What does a spirometer graph tell us?

A

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

VC = vital capacity - maximum amount of air expelled from the lungs after first filling the lungs to a maximum then expiring to a maximum (TV+IRV+ERV)

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

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

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78
Q

What forced vital capacity (FVC), FEV1.0 and their ratio?

A

Total volume exhaled

Volume expired in the first second, usually >80% of FVC

FEV1.0 / FVC

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79
Q

What does the helium dilution test test and what are the equations?

A

Functional residual capacity tests

V1 = known initial volume of helium

C1 = known initial concentration of helium

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80
Q

What does the nitrogen washout test test and how does it work?

A
  • Functional residual capacity
  • 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
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81
Q

What is restrictive deficit and what diseases does it occur in?

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
  • E.g. pulmonary fibrosis and scoliosis
  • FVC is reduced, but the FEV1.0. is relatively normal
  • The FEV1/FVC also remains relatively normal/increased
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82
Q

What is obstructive deficit and when does it occur?

A
  • Characterised by airway obstruction
  • If airways are narrowed, lungs can still fill to capacity
  • Resistance is however increased on expiration
  • E.g. asthma, chronic obstructive pulmonary disease (COPD)
  • FEV1.0 will be reduced, but FVC will be relatively normal.
  • A low FEV1.0/FVC will be recorded
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83
Q

What is the function of a vitalograph?

A

Measures ability to move air out of the lungs FVC and FEV1.0

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84
Q

What is the Miller’s prediction quadrant?

A
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85
Q

What is peak expiratory flow (PEF) recorded as and how does it work?

A
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86
Q

What do flow-volume loops look like and what type of defecit is the red and orange ones?

A

Red = restrictive deficit

Orange = obstructive deficit

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87
Q

How do measure PEF and what is gas transfer-diffusion conductance?

A

Peak flow meter

  • Measures how easily CO crosses from alveolar air to blood
  • The patient inhales a single breath of dilute carbon monoxide 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
  • Clinical relevance - e.g. in fibrosis of the lungs where gas diffusion is compromised
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88
Q

What is the pericardium divided into and what is its function?

A

Fibrous (outer)

Serous (inner)

Surround the heart

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89
Q

What are the properties of the fibrous pericardium?

A
  • Tough and not distensible
  • Attached to diaphragm by pericardiophrenic ligaments
  • Blends into adventitia of great vessels
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90
Q

What are the properties of the serous pericardium?

A
  • Comprises visceral layer (epicardium) and parietal layer (lining fibrous pericardium)
  • Potential space between them (pericardial cavity)
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91
Q

What do the parietal and visceral pericardial layers line?

A

Parietal = lines inner surface of fibrous pericardium

Visceral = lines surface of the heart

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92
Q

What are the 4 surfaces of the heart?

A

Anterior or sternocostal: formed mostly of right (with bit of left) ventricle

Inferior or diaphragmatic: mostly L (with bit of R) ventricle

Posterior or base: mostly L (and bit of R) atrium and pulmonary vv

Pulmonary: mostly L ventricle, in cardiac notch of L lung

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93
Q

What are the 4 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

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94
Q

What are the 4 valve positions and what are all valves?

A

All valves = retrosternal in position and close to the midline

Pulmonary = medial to L cc3

Aortic = medial to L ics3

Bicuspid or mitral = medial to L cc4

Tricuspid = medial to R ics4

95
Q

What are the 4 valve sounds and their locations?

A

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

96
Q

What are the properties of the parietal pleura?

A
  • Lines thoracic cavity lateral to mediastinum
  • Supplied by intercostal and phrenic nerve
  • Is sensitive to pain
97
Q

What are the properties of the visceral pleura?

A
  • Covers lungs and follows lung fissures
  • Supplied by autonomic nerve
98
Q

What is a condition related to the pleura?

A

Inflammation of the pleura. The lung surfaces end up rough so the ‘pleural rub’ can be heard with a stethoscope. Leads to chest pain (usually sharp) when you take a breath or cough.

99
Q

What are the 4 types of pleura and their properties?

A

Dark green = Mediastinal: flat, faces mediastinum and has impressions of mediastinal structures; contains the hilum and pulmonary ligament

Light green = Diaphragmatic: concave and faces domes of diaphragm

Red = Costal: convex and faces ribs

Blue = Cervical: extends into neck, 2-3 cm above medial third of clavicle, as apex, dome or cupola

100
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

101
Q

What are the properties of the visceral pleural reflections?

A

Reflections closest at plane of sternal angle (rib 2);

Parallel down to rib 4; L indented (cardiac notch) butR continues to cc 6;

Cross rib 8 at midaxillary line;

Cross rib 10 at lateral borderof erector spinae m

102
Q

What are the properties of the parietal pleural reflections?

A

Again, asymmetry and close behind sternal angle (rib 2);

Parallel down to rib 4;

L indented (cardiac notch) but R continues to cc 6;

Rib 8 at midclavicular line;

Rib 10 at midaxillary line;

Rib 12 at lateral border of erector spinae m

103
Q

What are the properties of 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
104
Q

What are the properties of 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
105
Q

What is the main property of each bronchopulmonary segment?

A

Have own nerve, vein and artery supply

106
Q

What are the properties of the bronchi divisions?

A
  • Trachea divides into right and left
  • Right is wider and more vertical than left
  • Each bronchus divides into secondary bronchi (supplying lobes)
  • Secondary divide into tertiary bronchi (supplying segments)
  • Right lung has 3 lobes and 10 segments
  • Left lung has 2 lobes and 9/10 segments
107
Q

Why are the anatomical, functional and surgical units of the lungs required to be known?

A
  • X-ray interpretation
  • Surgical resection in disease (segment resection is preferred to lobe resection)
  • Draining fluids (fluids tend to accumulate in apical and posterior segments of inferior lobe)
108
Q

What are the great vessels of the heart?

109
Q

What are thedifferent parts of the aorta?

A

Descending aorta = divided into thoracic and abdominal aorta

110
Q

What is the function of the azygous vein?

A

Drainage of posterior thoracic wall

111
Q

What are these CT scans showing?

A

1 = left is right and right is left side of heart

2 = arch of the aorta

3 = ascending aorta and descending aorta

112
Q

What are the 3 respiratory system compartments?

A

Conduction zone - conditioning of inhaled air

Respiratory zone - site of gas exchange

Musculo-elastic ventilation apparatus - drives ventilation

113
Q

What is the main property of airway division?

A

Divides in successions of bifurcations

114
Q

How is turbulence created in the nasal cavity?

A

Created by turbinate bones in nasal cavity which form narrow passageways

115
Q

What is the function of the large venous plexus in submucosa?

A

Enhance temperature adjustment and moisturising

116
Q

What is the function of vibrissae?

A

Prevent large particles entering nose as large hairs at nasal cavity entry

117
Q

What is the function of mucus?

A

Traps small particles and covers lining all the way to terminal bronchioles

118
Q

What are these parts called?

119
Q

What are these parts called?

120
Q

What are these parts called?

What happens during infection?

A

Venous plexus swell during infeciton, blocking airway

121
Q

What are these parts called?

122
Q

What are the properties of the trachea?

A
  • Kept open by horse-shoe shaped cartilage
  • Has seromucous glands in submucosa
  • Smooth muscle completes rings, formed partially of cartilage
123
Q

What are the properties of the respiratory epithelium?

A
  • Pseudostratified, ciliated and varying in thickness
  • Has mucus producing goblet cells
  • Mucus is transported towards pharynx by cilia (mucociliary clearance)
124
Q

What are the properties of a bronchus?

A
  • Has cartilage in its wall of varying size
  • Lumen bordered by respiratory epithelium
  • Ring of smooth muscle located between epithelium and cartilage
  • May have submucosal glands
125
Q

What are the properties of a bronchioli?

A
  • Derived from bifurcations downstream of bronchi
  • No cartilage in wall
  • Fewer goblet cells in epithelium
  • Incomplete smooth muscle ring surrounds
  • No submucosal glands
126
Q

What are the properties of the smaller bronchiole?

A
  • Epithelium becomes cuboidal
  • Ciliated and non-ciliated club cells
  • Club cells have protective role
  • Club cells generate serous secretions
  • Incomplete smooth muscle ring surrounds epithelium
  • Higher ratio of muscle ring thickness to luminal diameter than bronchi
127
Q

What is the function of terminal bronchioles?

A

Give rise to respiratory bronchioles that have cuboidal epithelial and alveoli built in walls

128
Q

What do connective tissue of alveoli contain?

A

Numerous elastin fibres

129
Q

What is the blood air barrier formed of?

A

Thin capillary endothelium and type 1 cell wall

130
Q

Where do alveolar capillary networks get their blood supply from?

A

Pulmonary circulation

131
Q

What are the properties of pulmonary arteries?

A
  • Elastic arteries
  • Comparatively thin walls
  • Larger ones accompany bronchi and bronchioles
132
Q

Where do bronchi get their blood circulation from?

A

From the aorta

133
Q

What is the function of surfactant?

A

Reduces surface tension in alveoli

134
Q

What are these parts?

135
Q

Where are lymph vessels found and what is their function?

A

In septa next to vessels of pulmonary circulation

  • Drain into series of major lymph nodes along trachea
  • Network found in interstitial layer adjacent to pleura
136
Q

What is Waldeyer’s ring?

What does airway mucus contain?

A

Tonsils - aggregates of lymph follicles

Immunoglobulins mainly IgA

137
Q

What is the purpose of regulated immunological response?

What does exaggerated immunological response result in?

A

Protection

Tissue damage (hypersensitivity)

138
Q

What are the different types of hypersensitivity?

139
Q

What are the properties of mast cells?

A
  • Generate inflammatory response
  • Activated by 2+ type 1 allergens binding to receptors
  • Mediators released
  • Tissue damage
140
Q

What are the steps of an allergic reaction?

What is the purpose of IL-4 and IL-13?

When does allergic sensitisation occur?

A

IL-4 and IL-13 = cause B cell to switch and produce IgE antibodies instead

At first exposure

141
Q

What can Th2 cells promote?

A

Type 1 hypersensitivity

142
Q

What happens during skin test with IgE and IgE + T cells?

143
Q

What happens during actue and chronic repsonse to allergens?

144
Q

What happens during the triggering mechanism?

145
Q

What are examples of type 2 allergies and autoimmunities?

A

Allergies:

  • Allergeric haemolytic anaemia
  • Blood transfusion reactions
  • Haemolytic disease of newborn

Autoimmunities:

  • Autoimmune haemolytic anaemia
  • Myasthenia gravis
  • Grave’s disease
146
Q

How does haemolytic disease of newborn arise?

147
Q

What are exampkles of type 3 allergies and autoimmunities?

A

Allergies:

  • Dermatitis herpetiformis
  • Allergic alveolitis

Autoimmunities:

  • Systemic lupus erythmatosus
  • Rheumatoid arthritis
148
Q

What are examples of type 4 allergies and autoimmunities?

A

Allergies:

  • Contact dermatitis
  • Acute graph rejection

Autoimmunities:

  • Thyroiditis
  • Addison’s disease
  • Gastritis
  • Type 1 diabetes mellitus
149
Q

What is the process of immune complex transport and removal?

150
Q

How does the respiratory diverticulum form?

A

Forms as a blind-ending outgrowth from ventral wall of foregut

151
Q

What happens during trachea development?

A
  • In 4th week
  • Oesophagotracheal ridges fuse to form oesophagotracheal septum
152
Q

What are the 2 layers of the laryngotracheal tube and their funciton?

153
Q

What are the 4 stages of lung development?

A
  • Pseudoglandular stage
  • Canalicular period
  • Terminal sac period
  • Alveolar period
154
Q

What happens during the first stage of lung development (pseudoglandular stage)?

A

Terminal bronchioles form

All major lung components formed at end of period, expect those for gas exchange (5-16 weeks)

155
Q

What happens during the second stage of lung development (canalicular period)?

A
  • Enlargement of lumens of bronchi and terminal bronchioles
  • Tissues = vascularised
  • 24 weeks = each terminal bronchiole has formed 2+ respiratory bronchioles
  • First terminal sacs form at end of period at end of respiratory bronchioles
156
Q

What happens during the third stage of lung development (terminal sac period)?

A
    • terminal sacs form
  • Flat and thin epithelial cells of terminal sacs (type 1 alveolar cells/ pneumocytes)
  • Capillaries close to flat cells and bulge into primordial alveoli allowing gas exchange
  • Secretory round e cells form (type 2 alveolar cells) between flat cells
157
Q

What happens during the fourth stage of lung development (alveolar period)?

A
    • surfactant production
  • 5% of mature alveoli before birth
    • size of primordial alveoli
  • Thinner type 1 cells
  • Capillaries = closer as they mature
  • Postnatal + lung size due to + divisions to form respiratory bronchioles and continues primordial alveoli production
158
Q

What happens during pleural cavity development?

A

Pericardioperitoneal canals are separated from pericardial cavity by pleuropericardial folds (5th week)

Cavities narrow and are 2 separate cavities surrounding the heart but are separate from the heart

The pericardioperitoneal canals (which form the pleural cavities) remain connected to the peritoneal (abdominal) cavity until closed by fusion of the pleuroperitoneal folds during formation of the diaphragm

159
Q

What are the propertieds of type 1 and 2 alveolar epithelial cells?

A

Type 1 = thin, allowing efficient gas exchange

Type 2 = round, secretory formed from end of 6th month, produce surfactant

160
Q

What are the properties of 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 the end of 6th month, though at low levels
161
Q

What lung changes occur before birth?

A
  • 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
162
Q

What lung changes occur at birth?

A

This fluid is removed from the lungs by:

1) Pressure on the thorax during delivery expelling fluid through mouth and nose
2) Absorbed into circulation via the pulmonary circulation
3) Absorbed into lymphatics

A thin coating of surfactant is left lining the alveolar cell membranes

Lungs = half filled with fluid

Still born lungs = full of fluid if firth breath not taken or full of air if first breath taken

163
Q

What are the 4 embryonic components of the diaphragm?

A
  • Transverse septum
  • Pleuroperitoneal membranes
  • Dorsal mesentery of oesophagus
  • Muscular ingrowth from lateral body walls
164
Q

What are the properties of the transverse septum?

A
  • Mesodermal in origin
  • Grows dorsally 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
165
Q

What are the properties of the pleuroperitoneal membranes?

A
  • Form from the lateral wall of pleural and peritoneal cavities
  • First appear at the start of the 5th week
  • Forms posterior and lateral parts of diaphragm, by fusing with the transverse septum and dorsal mesentery in the 7th week
166
Q

What are the properties of the dorsal mesentery of the oesophagus?

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
167
Q

What 3 things fuse to form the full diaphragm and complete abdominal - thorax separation?

A

Pleuroperitoneal membranes

Dorsal mesentery

Transverse septum

168
Q

What is the purpose of muscle ingrowth during the 12th week?

A

Contributes muscle to peripheral region of diaphragm external to the region that is derived from the pleuroperitoneal membranes

169
Q

What are defects and problems associated with lung development?

A
  • Premature baby and respiratory distress syndrome
  • Oesophageal artesia and tracheoesophageal fistula
  • Congenital cysts of lungs
  • Congenital diaphragmatic hernia
170
Q

What happens during premature baby RDS?

A
  • Insufficient surfactant in lungs
  • High surface tension at air-blood interface
  • Risk of alveoli collapsing during expiration
  • RDS = 2% newborns
  • Rapid labored breathing
171
Q

What happens during oesophageal atresia and tracheoesophogeal fistula?

A
  • Abnormal separation of oesophagus and trachea by oesophageal septum
  • 1/3000 births
    • in males
  • Associated with CHD (fistula = abnormal opening / passage) (atresia = narrowing or withering away)
172
Q

What happens during congenital cysts of the lungs?

A
  • Abnormal terminal bronchi dilation
  • At lung periphery usually
  • Poor drainage
  • Chronic lung infections
173
Q

What happens during congenital diaphragmatic hernia?

A
  • Hole in diaphragm, usually posterior lateral
  • Abdominal contents become herniated and enter thorax
  • Lung = hypoplastic
  • Heart = under pressure
  • Mediastinum pushed to right
174
Q

What are the 5 main red cell physiologies?

A
  • Erythropoiesis
  • Haemoglobin structure
  • Haemoglobin biochemistry
  • O2 transport
  • CO2 transport
175
Q

How is erythropoiesis controlled and what is its funciton?

A
  • Essential to maintain RBC level
  • Controlled by ERYTHROPOIETIN - polypeptide hormone
  • Released by peritubular cells in kidney - in response to hypoxia (low oxygen) e.g.
    • Anaemia
    • At altitude
    • Chronic lung disease (e.g. COPD)
  • Increases number of stem cells committed to erythropoiesis
  • Recombinant erythropoietin (EPO) used clinically
  • Treat anaemias associated with renal failure.
  • Open to abuse by athletes?
176
Q

What is a reticulocyte?

What happens during red cell maturation?

A

An immature RBC

  • Immature RBC - nucleus extruded and taken up by bone marrow macrophages
  • mRNA in RETICULOCYTE allows haemoglobin to still be synthesised
  • The reticulocyte may enter blood stream - (0.5-2% of circulating RBCs)
  • Retic count elevated when erythropoiesis is increased:
    • bleeding
    • haemolysis
177
Q

What is the lifespan of RBCs and its properties?

A
  • 120 days
  • Measurement: incubate a sample of blood with 51Cr, which binds to Hb.
  • Measure disappearance from blood + sites of RBC destruction detected by surface counting.
  • Useful for haemolytic anaemias - increased disappearance + increased radioactivity at sites of destruction:
  • Spleen in spherocytosis
  • Liver in sickle cell anaemia
  • Degradation of RBCs: Occurs in reticuloendothelial system (mononuclear-phagocyte system) of spleen, liver + bone marrow.
  • Proteins degraded and recycled, iron retained in stores, porphyrin from haem converted to bilirubin in liver (+ bilirubin = jaundice).
178
Q

What is the structure of haemoglobin?

A
  • 2 components HAEM & GLOBIN
  • Tetrameric: 4 globin chains, each made of polypeptide with a haem prosthetic group
  • Haem: Ferrous iron, Fe2+ at the centre of a protoporphyrin complex
  • The Globin chains linked by non-covalent bonds
179
Q

What’s the difference between adult and fetal Hb?

A

Adult haemoglobin (Hb A) contains a2b2 subunits

Fetal Hb contains a2y2

180
Q

What are the properties of iron?

A
  • Iron - from diet:
  • Ferrous iron (Fe2+)
  • (Fe3+ reduced to Fe2+ by stomach acid) –ve effects of antacids, chelation by tetracycline
  • Fe3+ produced by mucosal cells of duodenum. Binds to apoferritin to produce ferritin (stores)
  • Release iron into blood to bind with transferrin (transport)
  • Delivers iron to bone marrow (ferritin stores)
  • Iron in Hb
  • Iron recycled - very efficient (90%) from breakdown of RBCs in liver and spleen
  • Iron uptake in guts increased when iron deficient: erythroid regulator from bone marrow & an iron stores regulator
181
Q

How is oxygen transported?

A
  • RBCs carry O2 from lungs to tissues and return CO2
  • Ferrous (Fe2+) iron in haem binds O2
  • 4 O2s per Hb
  • Hb is an ALLOSTERIC PROTEIN: the binding of 1O2 enhances (by a conformational change) the binding of another O2 to another haem in same molecule etc.
    • The 4th O2 binds some 300 x more readily than the 1st.
182
Q

What does an oxygen dissociation curve look like and what is the comparison between maternal and fetal curve?

A

First O2 binding = + affinity for 2nd to bind = enhances 3rd binding = enhances 4th binding

183
Q

What is the Bohr effect?

A
  • Acidity enhances the release of O2 from Hb
  • Increasing CO2 at constant pH also lowers Hb’s O2 affinity
  • Therefore, O2 is more readily given up to metabolically active tissues (which produce H+ and CO2).
184
Q

What is 2,3-diphosphoglycerate (DPG)?

A
  • Present in RBCs at same molar conc as Hb
  • Reduces O2 affinity of Hb - in its absence Hb would yield little O2 to tissues
  • DPG binds to deoxyhaemoglobin to shift equilibrium. Reduces O2 binding
  • Fetal Hb unable to bind DPG - hence higher O2 affinity
  • DPG increased when arterial O2 reduced chronically (e.g. at altitude, severe COPD) so O2 more readily liberated to tissues
185
Q

What is carboxyhaemoglobin?

A
  • Is CO + haemoglobin
  • Hb has a much greater affinity for carbon monoxide than oxygen - carboxyhaemoglobin
  • CO-Hb does not readily dissociate
  • Tissue becomes starved of O2
  • CO - cigarette smoke so smokers have higher levels of CO-Hb - contributes towards vascular diseases due to smoking
186
Q

What is methaemoglobinaemia?

A
  • Iron in Ferric (Fe3+) not ferrous state
  • Cannot carry O2
  • Patient may be
    • Cyanosed
    • Symptoms of anoxia (dizziness, respiratory distress, tachycardia)
  • Hereditary lack of glucose-6-phosphate dehydrogenase, which keeps Hb in reduced state
  • May be caused by drugs - e.g. antimalarials, sulphonamides through oxidant stress
187
Q

How is carbon dioxide transported?

A
  • 10% dissolved
  • 30% bound to Hb - combines to form carbaminohaemoglobin
  • 60% as HCO3-
  • CO2 + H2O –> HCO3- + H+
  • catalysed by carbonic anhydrase in RBC
  • Hb buffers H+
  • HCO3- may leave cell, Cl- enters (Chloride shift) to maintain charge
188
Q

What are the problems with NSAIDS?

A

Can provoke asthma by increasing leukotriene production

i.e. aspirin, ibuprofen

189
Q

What are the properties of beta blocker use in asthma and COPD?

A

Asthma = contraindicated

COPD = used with caution

190
Q

What are some causes of breathlessness?

A
  • Respiratory –> asthma, COPD, pneumonia, lung cancer
  • Cardiovascular –> heart failure, pulmonary oedema (accumulation of fluid on lungs), pulmonary embolism (blood clot on lungs), atrial fibrillation
  • Other –> functional breathlessness (i.e. obesity), anaemia (full blood count required)
  • Pneumothorax
  • Iatrogenic (caused by medicines)
  • Foreign bodies
  • Panic attacks
191
Q

What are the 3 steps of differential diagnosis?

A
  • What is likely to be wrong
  • What is unlikely to be wrong
  • ‘Conformation bias’ (closed minded so only focus on a certain condition/s)
192
Q

What history do you need to take when someone reports with breathlessness?

A
  • Age
  • Onset of symptoms
  • Variability
  • Smoking history
  • Drug history
  • Occupation
  • Pets
  • Associated symptoms
  • Orthopnoea (breathlessness from changing posture – related to heart failure)
193
Q

What are the 2 signs of respiratory disease and potential diagnoses?

A
  • Digital clubbing
    • Lung cancer
    • Bronchiectasis
    • Pulmonary fibrosis
    • Cardiac eg Fallot’s tetralogy
  • Cyanosis (bluish colour)
    • Central:
      • Reduced O2 saturation, tongue and lips
      • Cardiac/resp with shunting of blood
    • Peripheral:
      • Hand and feet due to poor blood flow
194
Q

What do you look for during physical examination for breathlessness?

A
  • Palpation and percussion
  • Auscultation
    • Wheeze: expiration, limitations of flow in asthma and COPD
    • Crackles: opening of closed bronchiole
      • Early Inspiratory associated with diffuse airflow limitation
      • Late inspiratory associated with pulmonary oedema, fibrosis and bronchiectasis
    • Pleural rub
      • Inflammation of pleural surfaces
195
Q

What are the 2 methods for measuring blood gases?

A

Arterial blood gas monitoring

Pulse oximetry (<92% = hypoxia symptom)

196
Q

What do lung function graphs tell us and how do normal, asthma and COPD compare on the graph?

A

FEV1 = volume of air expelled in the first second

FVC = total volume of air expelled after 6 seconds

197
Q

What diseases can chest X-rays show us?

A

Fluid

Tumours

TB

198
Q

What is V/Q scanning and how does it work?

A

Ventilation / perfusion (bloodflow)

  • Pulmonary 99mTc scintigraphy: under-perfused areas
    • Technetium (99mTc) albumin macroaggregated
  • Inhalation of Xenon-133 gas to detect under-ventilated areas
  • Pulmonary embolism: striking perfusion/ventilation mismatch
199
Q

What are the symptoms of chronic heart failure?

A
  • Left ventricular failure
  • Pulmonary oedema
  • Dyspnoea [Breathlessness] – sensation of drowning. ‘Cardiac asthma’
  • Cough
  • Orthopnoea – breathless on lying which is relieved by sitting up. Nocturnal problem? (paroxysmal nocturnal dyspnoea)
  • Inspiratory crepitations
200
Q

What are the properties of pneumonia?

A
  • An inflammation of the alveoli in the airways - usually due to infection
  • Infection: bacterial or viral
  • Aspiration e.g. vomit
  • Fluid accumulates in the alveoli and impairs gaseous exchange
201
Q

Which nerves are shown here?

202
Q

Which nerves are shown here?

203
Q

Which nerves are shown here?

204
Q

What are each of these in the hilum of the right lung?

205
Q

What are each of these in the hilum of the left lung?

206
Q

What are each of these impressions from?

207
Q

Where are the vomer, hyoid bone, palatine bone, conchae and turbinate bones located in the skull?

208
Q

Where is the thyroid cartilage, circoid cartilage, tracheal cartilage and arytenoid cartilage?

209
Q

What are the nasal branches of the maxillary artery?

210
Q

What are these nerves?

211
Q

What muscle is this?

212
Q

What are each of these sinuses?

213
Q

What is shown by this radiograph?

A

Hyoid bone

Air in pharynx and larynx

Soft palate

Nasopharynx

Oropharynx

214
Q

What are the key features of this radiograph?

A

Maxillary sinus

Nasal septum

Frontal air sinus

Entrance to nasopharynx

215
Q

What are hilar shadows on X-ray mainly made up of?

A

Pulmonary vessels

216
Q

What are numbers 6, 7, 17, 20, 21, 22, 23?

A

6 = Oesophagus

7 = Trachea

17 = T5 vertebral body

20 = Arch of aorta

21 = Anterior mediastinum

22 = superior vena cava

23 = Arch of azygous vein

217
Q

What are numbers 18, 22, 23, 24, 25, 27, 28, 29?

A

18 = T6 vertebral body

22 = Superior vena cava

23 = Arch of azygous vein

24 = Ascending aorta

25 = Descending aorta

27 = Pulmonary trunk

28 = Right pulmonary artery

29 = Left pulmonary artery

218
Q

What does the upper respiratory tract consist of vaguely?

What is the function of the pharynx and the larynx?

A

Nose

Nasal cavity

Pharynx

Larynx

Pharynx = respiration and digestive passageway

Larynx = voice, maintains open airway and directs food and drink appropriately

219
Q

What is the order of the respiratory tract bifurcations?

A

Trachea

Bronchi

Conductive bronchiole

Terminal bronchiole

Respiratory bronchiole

Alveoli

220
Q

What are the 3 steps of respiration?

A

Pulmonary ventilation - Air into lungs

Pulmonary respiration - Air from gas exchange at alveoli

Tissue respiration - Air from capillary to tissue cell

221
Q

What does Boyle’s law state?

A

Pressure = inversely proportionate to volume at a constant temperature

P ≈ 1 / V

222
Q

What is the role of water vapour in respiration?

A
  • Inspired air = saturated with water vapour
  • Dilutes gases
  • At 37 degrees, partial pressure = 6.3 KPa
  • Moist air enables efficient gas exchange
223
Q

How do you convert KPa into mmHg?

A

1 KPa = 7.50 mmHg

224
Q

What does Dalton’s law of partial pressure state?

A

Pressure exerted by each gas = independent of other gases present

Total pressure = sum of all individual pressures

225
Q

How do you work out pulmonary ventilation rate (PVR) and what are its units?

A

Respiration rate X Tidal volume

Units = L/min

During exercise can reach 120 L/min

226
Q

What is dead space in the lungs?

How do you work out dead space ventilation rate?

What is alveolar ventilation rate (AVR) and how do you work it out?

A

Serial dead space = volume of conducting airways (0.15L typically)

Distributive dead space = part of lungs that aren’t airways and dont’ support gas exchange (i.e. dead alveoli) (0.02L typically)

Physiological dead space = serial + distributive dead space (0.17L typically)

Physiological dead space X respiration rate

Actual amount of air that reaches alveoli

AVR = PVR - dead space VR

227
Q

When does dead space ventilation occur?

A

With rapid shallow breathing, reducing alveolar ventilation

228
Q

What factors affect airway resistance?

A
  • Airway smooth muscle tone —> During asthma attack, airways reduced in size causing obstructed airflow
  • Gravity and posture —> + airway resistance when in supine (led down) position than upright position as even blood flow distribution
  • Lung compliance —> increases with age due to loss in elastic recoil (emphysema = + lung compliance, pulmonary fibrosis = - lung compliance)
  • Age
  • Disease
229
Q

How do you detect airway resistance?

A

Auscultation:

  • High and turbulent airflow in bronchi produces breath sounds
  • Laminar flow in small bronchioles produces no breath sounds
  • Small airways = silent zones = hard to detect disease of small airways
230
Q

What does low diffusion resistance depend on?

A

Respiratory membrane

Gas permeability

231
Q

What are 2 respiratory membrane disorders?

A

Oedema fluid on interstitial space

Lung fibrosis

  • Increased diffusion resistance
  • Interferes with normal gas exchange
232
Q

What are the 2 ways gas transfer is controlled and where are they found?

A

Neural regulation —> cerebral cortex (voluntary breathing), pons and medulla (involuntary breathing)

Chemical regulation —> central chemoreceptors (on medulla), peripheral chemoreceptors (in aortic arch and carotid arteries), ventilation-perfusion matching

233
Q

What is perfusion?

When is ventilation-perfusion matching used?

A

Process where deoxygenated blood passes through lungs and becomes re-oxygenated

Detection of pulmonary embolism

Medicine 1 (28 decks)

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