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Resp Flashcards

1
Q

What is partial pressure and how is it calculated?

A
  • The pressure which a gas exerts within a mixture

- Proportional the the volume of gas in the mixture ie air is 21% oxygen so will generate a partial pressure of 21kPa

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2
Q

Describe the intrathorasic pressure changes during inspiration and expiration

A
  • Inspiration = lungs expand and volume increases whilst pressure falls below atmomspheric pressure allowing air to flow into lungs
  • Expiration = lungs deflate and volume decreases whilst pressure rises forcing air out
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3
Q

What is saturated vapour pressure?

A

-The amount of pressure exerted by liquid molecules as they evaporate at a liquid-gas interface after equilibrium is reached

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4
Q

What is the effect of saturated water vapour on nitrogen and oxygen as it is breathed in?

A

-Lowers the partial pressure as it contributes to the total pressure in the airways

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5
Q

What is gas tension? What dertermines gas tension

A
  • The amount of pressure exerted in a liquid by gas condensing into it
  • Same as partial pressure in the air as it will reach equilibrium
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6
Q

What epithelium lines the upper respiratory tract?

A

-Pseudostratified columnar ciliated epithelium with goblet cells

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7
Q

What are the function of the conchae/turbinates?

A

-To increase the surface area in order to warm and humidify air, to mix air

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8
Q

What are the functions of the nose?

A
  • Organ of smell
  • Filter (hairs and mucus) and humidify air
  • Receive local secretions form sinuses and nasolacrimal duct
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9
Q

Which sinuses correspond to which meatus in the nose?

A
  • Frontal, anterior ethmoid and maxillary into middle
  • Sphenoid and posterior ethmoid into superior
  • Nasolacrimal to inferior
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10
Q

Why can upper resp tract infections cause middle ear infections?

A

-Track up eustachian tube

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11
Q

Describe the positioning of the vocal cords during respiration, swallowing, speech and coughing

A
  • Respiration -> open
  • Swallowing -> closed
  • Speech -> partially closed
  • Coughing -> initially closed then open
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12
Q

What is the glottis?

A

-Two vocal cords and opening between them

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13
Q

What moves the vocal cords and what nerve supplies these muscles? How can this relate to a horse voice?

A
  • Intrinsic muscles of larynx
  • Recurrent laryngeal nerve (branch of vagus)
  • Any damage to the RLN eg thyroid goitre, apical lung tumour, stroke, can lead to hoarse voice
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14
Q

Which bronchi is most likely to aspirate a foreign body and why?

A

-Right as the path is more vertical

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15
Q

Describe the defect in CF and how this causes symptoms

A
  • Defective ion channel named cystic fibrosis transmembrane regulator causing comprimised cl transport across the membrane
  • Water does not leave epithelium producing thick, viscous and sticky mucus which is hard to clear. this produces severe pulmonary infections, pancreatitis and gi disturbances
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16
Q

How do the bronchioles remain open during inspiration if they have no supporting cartilage? What happens during expiration? In which pathology can this be problematic and why?

A
  • The tension from the surrounding alveoli keep them open. during expiration they willl collapse as the alveoli are not filled with air
  • COPD/emphysema- Increased airway resistance due to destruction of supporting alveolus tissue causing early closure of the bronchioles during expiration
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17
Q

What cells secrete surfactant and why is it so crucial to lung function?

A
  • Clara cells/type II pneumocytes
  • Surfactant decreases the surface tension in alveoli in order to keep the pressures in each alveolus similar and prevent bullae formation. This is because smaller alveolus will have a larger surface tensio.Surfactant has a greater effect in smaller alveoli as there is less surface area for it to cover therefore the pressure in each alveolus becomes equal
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18
Q

What is emphysema?

A
  • Desctruction of the alveolar walls as a result of a1-antitrypsin deficiency or smoking
  • results in difficulty breathing due to early closure of bronchioles
  • Air become trapped within the alveoli
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19
Q

In which direction do the upper and lower ribs move?

A
  • Upper increase AP diameter

- Lower increase transverse diameter

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20
Q

Describe the intercostal muscles and their function

A
  • External -> end close to costal cartilage and elevate the ribs during quiet inspiration
  • Internal -> end close to vertebral column and depress the ribs during forced expiration
  • Innermost -> only lie laterally and depres the ribs in forced expiration
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21
Q

Where would you place a chest drain and why?

A
  • 5th intercostal space mid axillary line at the superior border of 6th rib
  • Avoid any thick musculature and avoid neurovascular bundle which runs along each inferior rib
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22
Q

From where do the intercostal arteries arise?

A
  • Posterior from thoracic aorta

- Anterior from internal thoracic (from subclavian)

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23
Q

What is the main source of venous drainage of the thoracic wall?

A

-Azygous system

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24
Q

What is the function of the diaphragm? Where/why are the openings in the diaphragm

A
  • Main muscle of inspiration
  • T8 -> IVC aperture
  • T10 -> oesophageal aperture
  • T12-> Aortic aperture
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25
Q

Where is the upper border of the liver during expiration?

A

-5th rib

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26
Q

Describe the nerve supply of the diaphragm and why this can cause shoulder tip pain?

A
  • C3,4,5 (phrenic)

- Referred pain upon diaphragmatic irritation to dermatomes C3,4,5

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27
Q

State the muscles used in normal inspiration. What are the accessory muscles of inspiration?

A
  • Diaphragm and external intercostals
  • Scalene
  • Sternocleidomastoid
  • Pec major
  • Serratus anterior
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28
Q

What are the muscles of quiet and forced expiration?

A
  • Quiet expiration is by elastic recoil of lungs and chest wall -> passive, no muscles involved
  • Forced -> abdominal muscles and internal/innermost intercoastals
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29
Q

What are the four parts of the pleura?

A

-Cervical, mediastinal, costal and diaphragmatic

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30
Q

What is the pleural seal? What happens when it is broken?

A
  • Formed by the surface tension of the pleural fluid, prevents the parietal and visceral pleura from being pulled apart coupling movements on the thoracic wall with movement of the lungs
  • Break in the seal causes air to rush inside the pleural cavity due to negative pressure -> pneumothorax
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31
Q

What is the costophrenic recess? Why is it clinically significant?

A
  • The pleural lined gutter which covers the upward convexity of the diaphragm
  • Loss of this recess on an xray indicates pathology
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32
Q

What are the possible extrapulmonary presentations of an apical lung tumour?

A
  • Horners (ptosis, myosis and anhydrosis)
  • Lower brachial plexus injury
  • Hoarse voice
  • Cushings syndrome
  • SIADH
  • Hyperparathyroidism
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33
Q

Describe the surface markings of the lungs and pleura

A
  • Lungs -> begin at clavicle and descend beside sternum to 4th rib, then move laterally to be at 6th rib mid clavicular line, then 8th rib anterior axillary line then 10th rib posteriorly
  • Pleura -> begins at clavicle an descends beside sternum until 6th rib, then moves laterally to mid clavicular line at 8th rib, anterior axillary line at 10th rib and 12th rib posteriorly
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34
Q

What is lung compliance? Name a disease in which over compliance is an issue. Name a disease in which low compliance is an issue

A
  • How stretchy the lungs are -> higher compliance = easier stretch
  • Emphysema -> loss of elastic recoil causes barrel shaped chest as lung expands more easily
  • Fibrosis
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35
Q

What is Respiratory distress syndrome?

A
  • Occurs in neonates which are born prematurely. Lungs are not well enough developed to produce surfactant meaning the surface tension in alveoli is too great to keep alveoli open and bullae are formed and the lungs are very stiff causing compromised gas exchange
  • Occurs in adults after major trauma
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36
Q

Why do obstructive airway diseases affect expiration and not inspiration

A
  • During inspiration there is a lower intrathoracic pressure as the airways are expanding meaning the bronchioles are open so inspiration is fine
  • During expiration the intrathoracic pressure rises and the smaller airways which have no cartilage collapse earlier than they would without disease due to an increase in resistance to airflow causing air to become trapped
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37
Q

Why is O2 affected more than CO2 in a diseased lung? how can the pressure gradient of CO2 be so small?

A
  • O2 is less soluble than CO2

- CO2 is so soluble that a very small pressure gradient can be present and diffusion will still occur

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38
Q

What is the partial pressure of O2 and CO2 in the alveoli and blood in a normal lung?

A
  • 13.3% O2

- 5.3% CO2

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39
Q

By what 3 mechanisms is CO2 carried around the body

A
  • Dissolved in plasma
  • Bound to haemoglobin
  • As bicarb in the plasma
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40
Q

Why is it important that deoxygenated blood is saturated with O2 by 1/3 of its distance across the alveolus?

A

-When HR increased the transit time of blood spent in contact with the alveolus is halved -> allows full saturation still

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41
Q

Why is it significant that it takes multiple new breaths to replace all the alveolar air?

A

-Guards against sudden changes in blood gas levels on interruption of respiration -> allows more respiratory stability

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42
Q

What determines the partial pressure in the alveolus?

A
  • Rate of air entry into alveolus

- Rate os absorption into RBC

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43
Q

What is the alveolar ventilation rate?

A
  • The amount of air which actually reaches the alveolus per minute
  • Pulmonary ventilation rate - dead space ventilation rate
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44
Q

What is alveolar ventilation mismatching?

A

-When the ventilation and perfusion of the lungs is not equal
Normally:
-Alveolar ventilation rate is approx 5L/min
-Lung perfusion is approx 5L/min
-So ventilation matches perfusion producing a V/Q ratio of 1

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45
Q

What is dead space?

A
  • Air which is exchanged in each breath which doesnt take part in respiration ie the air in the trachea and conducting bronchioles or damaged airways
  • Serial/anatomical = conducting airways (0.15L)
  • Distributive = dead/damaged alveoli/ poorly perfused alveoli
  • Serial+dstributive =physiological
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46
Q

How do you calculate dead space ventilation rate?

A

-Physiologocal dead space x RR

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47
Q

Define tidal volume, inspiratory reserve volume and expiratory reserve volume, residual volume

A
  • The amount of air breathed in and out during quiet respiration
  • The amount of air which can be breathed in above quiet respiration
  • The amount of air which can be breathed out above quiet respiration
  • The amount of air remaining in the lung after maximal expiration
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48
Q

Define inspiratory capacity, vital capacity, functional residual capacity and total lung capacity

A
  • inspiratory reserve volume plus tidal volume
  • max inspiration to max expiration -> IRV +TV + ERV
  • volume of air in lungs at resting expiratory level -> ERV + RV
  • VC + RV
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49
Q

What does a vitalograph show? What will an obstructive pattern look like? What will a restrictive pattern look like?

A
  • Volume expired over time ie forced vital capacity (FVC -> maximum volume which can be expired from full lungs)
  • Volume which is expired in first second (FEV1)
  • Air expired more slowly so FEV1 reduced and FVC relatively normal
  • FEV1 the same as no obstruction but total FVC reduced -> lungs unabe to fill
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50
Q

Give some causes of obstructive/restrictive airway disease

A
  • Obstructive -> Asthma, COPD

- Restictive -> Interstitial lung disease, pneumothorax, neuromuscular disorder, chest wall deformity

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51
Q

What does a flow volume curve show? Describe obstructive and restrictive patterns

A
  • Measures flow against volume
  • Obstructive will be same but then scooped in as volume progresses as airways narrow early decreasing flow and expiration
  • Restrictive will be same pattern but narrower due to less total volume being expired
52
Q

How do you measure residual volume, serial dead space and diffusion conductance?

A
  • RV -> Helium dilution
  • Serial dead space -> nitrogen washout
  • Diffusion -> CO transfer
53
Q

Describe and explain the oxygen dissociation curve. Whatt is meant by cooperativity?

A
  • Hb saturation % on Y axis
  • pO2 on x axis
  • Sigmoidal shape -> Low saturation at low pO2 due to promotion of the T state and high saturation at high pO2 due to promotion of the R state
  • Once one O2 molecule bound it is easier to bind the next
54
Q

What is the pO2 at the lungs and tissues? At what pO2 is Hb normally fully saturated? Is all the O2 dissociated at the tissues? How do the oxygenation saturation properties of Hb make it ideal for its function?

A
  • Alveoli = 13.3 kPa, Tissue pO2 = 5kPa
  • Above 9kPa
  • No, only about half is dissociated
  • Tightly binds O2 in the lungs due to high pO2 and then dissociates at the tissues where there is low pO2 thus delivers o2 to tissues
55
Q

What is 2,3-BPG? When are there higher levels of 2,3-BPG and why is this beneficial?

A
  • 2,3-biphosphoglycerate
  • biproduct of glycolysis which decreases Hb affinity for oxygen by promoting the T state
  • Anaemia or altitude -> More oxygen dissociation increases delivery to tissues
56
Q

Describe the requirements of the capillary pO2 at tissues. Which tissues have a lower pO2?

A
  • Must remain high enough to drive diffusion into cells but low enough to ensure enough O2 dissociates from Hb
  • Those with a higher capillary density as distance to drive diffusion is shorter eg heart
57
Q

Describe the bohr shift and how this contributes to normal O2 delivery
How does temperature effect oxygen dissociation?

A
  • The bohr shift refers to the principle that with a lower pH, The T state of Hb is promoted and the oxygen dissociation curve shifts to the right and gives up more oxygen at higher pO2s
  • In tissues there is a local lower pH due to metabolising tissues producing CO2 which reacts with water to produce H2CO3 and dissocates into H+ and HCO3-.
  • Higher temp curve shifts right -> more o2 given up
58
Q

What is cyanosis? What is the cause of peripheral and central cyanosis? Do you have to have both at same time?

A
  • Blue discolouration of the skin due to decreased presence of saturated Hb
  • Peripheral is due to poor circulation
  • Central is due to poor Hb saturation
  • Can have peripheral without central but cannot have central without peripheral
59
Q

How does CO2 help maintain arterial pH?

A

-Dissolved CO2 in the blood reacts with H2O in plasma and RBCs forming the reversible reaction:
CO2 + H2O <> H2CO3 <> H+ + HCO3-
-The rate and direction of this reaction depends on the amounts of reactant/products thus high pCO2 in blood drives the forward reaction and more H+ produced

60
Q

Ultimately what does the pH of blood depend on? What are their normal concentrations in plasma?

A
  • The ratio between CO2 and HCO3-

- CO2= 1.2mmol/L and HCO3 =25mmol/L

61
Q

Where/how is HCO3 produced? How is HCO3 controlled?

A
  • Red blood cells
  • CO2 + H2O <> H2CO3 <> H+ + HCO3-
  • In the RBC H+ is scavenged by Hb and the HCO3- is pumped out into plasma by AE
  • Can also be produced by the kidney
  • Controlled by excretion/resorption in the kidney
62
Q

What is the henderson-hesselbach equation?

A
  • Used to calculate pH

- pH=pK (6.1@37 degrees) +log(HCO3/[pCO2 x 0.23])

63
Q

What controls the PCO2 in arterial blood?

Describe how CO2 is transported from the tissues to the lungs to be breathed out

A
  • Alveolar ventilation rate
  • Lower pH at tissues promotes T state Hb -> binds more H+ -> allows more HCO3- to be produced and pumped into plasma so no pH change
  • At lungs -> R state promoted -> H+ unbinds -> Reacts with HCO3- in RBC -> CO2 produced and diffuses into alveoli
64
Q

How does the body respond to persisting hypoxia? Eg COPD

A
  • Hypoxia detected by peripheral chemoreceptors in carotid and aortic bodies which causes an increase in ventilation
  • This causes a decrease in pCO2 so ventilation decreases again
  • Hypoxia still present so increases ventilation and the low pCO2 is accepted as normal -> choroid plexus adds H+ into CSF to compensate
  • Increased EPO production by kidneys to raise Hb levels
65
Q

What is respiratory acidosis/alkalosis?

A
  • Acidosis = A decrease in blood pH caused by an increased level of pCO2 due to a respiratory change
  • Alkalosis = An increase in blood pH caused by a decrease in PCO2 due to hyperventilation meaning more CO2 is blown off
66
Q

What is metabolic acidosis/alkalosis?

A
  • Acidosis = A decrease in blood pH due to increased H+ caused by a metabolic disturbance eg anaerobic respiration
  • Alkalosis = An increased in blood pH most commonly caused by a loss of H+ ions through vomiting meaning a relative increase in HCO3
67
Q

What is the bodies response to a large decrease in pO2? What detects large decreases in pO2? What detects small changes in pCO2 and how?

A
  • Hyperventilation, increase HR and Prioritise organs ie divert blood flow from gut
  • Peripheral chemoreceptors
  • Central chemoreceptors -> small increase in H+ in csf detected as the csf has no HCO3 buffering capacity only a fixed amount
68
Q

What % saturations is considered hypoxia? When does tossue damage occur?

A
  • <94%

- <90%

69
Q

What are the defining features of T1 resp failure? Give some causes

A
  • Low pO2 normal pCO2 as pCO2 more soluble
  • Diffusion defects eg fibrosis, emphysema, pulmonary oedema
  • Ventilation-perfusion mismatch eg pneumonia, PE
70
Q

What are the defining features of T2 resp failure? Give some causes

A
  • Decreased pO2 and increased pCO2
  • Ventilatory pump failure eg resp depression in opioid overdose, MND, pneumothorax
  • Hard to ventilate lungs eg COPD, severe asthma
71
Q

What is hypoxic pulmonary vasoconstriction? When can it become problematic?

A
  • Physiological response to ensure ventilation perfusion matching. Vessels to alveoli which are not well ventilated undergo vasoconstriction to divert blood to over well ventilated areas
  • Chronic hypoxia causes prolonged hypoxic pulmonary vasoconstriction and can lead to pulmonary hypertension or cor pulmonale
72
Q

Describe the pathophysiology of asthma

A

-Bronchial hypersensitivity causing an exaggerated response to normally non-allergenic non-noxious stimuli resulting in mucosal oedema, mucus hypersecretion and bronchoconstriction which leads to reversible airway narrowing. Over time this lead to goblet cell hyperplasia, smooth muscle hypertrophy and airway remodelling .

73
Q

What cellular/immune components are involved in asthma

A
  • Histamine release from mast cells
  • IgE and eosinophils
  • TH2 Lymphocytes
74
Q

Name some precipitants of asthma

A
  • Atopy -> t1 hypersensitivity to dust, pollen, animals
  • Stress -> cold air, viral urti, exercise, emotion
  • Toxins -> smoking, hairspray
75
Q

What are the signs and symptoms of asthma

A
  • Cough +/- sputum
  • Wheeze
  • Dysponea
  • Diurnal variation
76
Q

What things would you want to illicit in a history to point towards asthma?

A
  • Precipitants
  • diurnal variation
  • Exercise tolerance
  • Life Effects
  • Other Atopy
  • Home/job environment
77
Q

Give 2 differentials for asthma

A
  • COPD
  • Pulmonary oedema
  • Bronchiectasis
78
Q

Differentials of acute severe asthma

A
  • Pneumothorax
  • Pulmonary embolism
  • Pulmonary oedema
  • Acute exacerbation of COPD
79
Q

Describe the immediate and latephase response to stimuli in asthma

A
  • Immediate = interaction of allergen with IgE, mast cell degranulation which releases chemical mediators initiating an immune response
  • Late phase = all inflammatory cells which have been recruited secrete mediators and cytokines wich worsen the inflammation
80
Q

How do you diagnose asthma?

A

-History + Decreased peak flow and spirometry for reversible FEV1:FVC ratio

81
Q

Why is an asthmatic cough worse at night?

A
  • Increases parasympathetic drive at night causes bronchoconstriction
  • Diurnal variation of cortisol means anti-inflammatory is lowest at night
82
Q

What 2 conditions does COPD generally encompass? Briefly describe each

A
  • Emyphysema -> destruction of the elastin in teriminal brochioles and alveolar walls producing enlarged air spaces known as bullae. Small airways close earlier on expiration due to the increasing intrathoracic pressure not being withstood -> airflow obstruction
  • Chronic bronchitis -> smooth muscle hypertrophy and mucus hypersecretion causing airway narrowing and a productive cough
83
Q

What are the major causes of COPD?

A
  • Smoking

- A1-antitrypsin deficiency

84
Q

Describe the signs and symptoms of COPD. What are pink puffers and blue bloaters

A
  • Symptoms = cough, sputum, wheeze, progressive dysponea,
  • Signs = tachyponea, hyperinflation, cyanosis, cor pulmonale, purselip breathing, accessory muscle use, oedema
  • Pink puffer -> emphysema causing breathlessness but not cyanosis -> progressing to T1 respiratory failure
  • Blue bloater -> chronic bronchitis -> Cyanosed but not breathless, rely on hypoxic drive -> type 2 resp failure
85
Q

What is the MRC Dysponea score? describe its classification

A
  • A systematic approach to grading breathlessness
    1) only on vigorous exercise
    2) On hurrying/walking up stairs
    3) Walking slowly/has to stop
    4) stops after a few mminutes
    5) In normal ADLs/struggles to leave the house
86
Q

Name some complications associated with COPD

A
  • Acute exacerbations +/- infection
  • Pneumothorax
  • Cor Pulmonale
  • Lung Carcinoma
87
Q

What investigations would you perform if you suspected COPD?

A
  • Bloods (FBCs, A1-antitrypsin, ABG)
  • CXR
  • ECG
  • Spirometry
88
Q

What signs may you see on a CXR of someone with COPD

A
  • Hyperinflation -> >6 ribs anteriorly
  • Flattened diaphragm
  • Cardiomegaly
  • Prominent pulmonary arteries
89
Q

State the main differences between COPD and asthma

A
  • COPD nearly always smoker
  • COPD commonly presents over 35 asthma is under
  • COPD common to have chronic productive cough
  • COPD persistent and progressive breathlessness, asthma is variable
  • Asthma wakes from nightime cough and wheeze
  • Asthma has diurnal symptom pattern or day-day variability
90
Q

How is an acute COPD exacerbation treated?

A
  • O2 (titrated be careful of hypoxic drive)
  • Salbutamol
  • Hydrocortisone or prednisolone
  • Ipratropium
  • Thephylline
  • Abx
  • Physiotherapy
91
Q

What bacterium is associated with pneumonia in a COPD patient?`

A

-Haemophilus influenzae

92
Q

Describe the spirometry results in a patient with COPD. How is it scored?

A
  • Decreased FEV1/FVC ratio
  • 80% or above but with symptoms = mild
  • 50-79% Predicted FEV1 = moderate
  • 30-49% predicted = severe
  • > 30% = very severe
93
Q

What is the most common URTI?

A

-Rhinovirus

94
Q

What are the most common organisms in community acquired pneumonia?

A
  • Strep. pneumoniae
  • Haemophilus
  • Morexella Catterhalis
  • Staph aureus
95
Q

How does pneumonia present?

A
  • Non-productive cough
  • SOB
  • Pleuritic chest pain
  • Fever, rigors, N+V, tachycardia
  • Cyanosis
  • Stony dull percusion
  • Bibasal crackles
  • Tactile fremitus
96
Q

Describe the defences of the resp tract

A
  • Mucociliary esculator
  • Cough reflex
  • Macrophages
  • Nasal hairs
  • Mucosal associated lymphatic tissue
97
Q

What is acute bronchitis? What symptoms and signs does it produce? How do you differentiate from pneumonia? Give some causative organisms

A
  • Inflammation of the medium airways with increased mucus secretion
  • Productive cough, SOB, fever,
  • No xray changes in acute bronchitis
  • Viruses, H.influenzae, S.pnemoniae
98
Q

Give 3 atypical causes of pneumonia. Is it more or less serious than typical pnemonia?

A
  • Leigionella Pneumophilia
  • Mycoplasma pneumoniae
  • Chlamydophilia pneumoniae
  • Less
99
Q

What is CURB65?

A 
-A tool to measure severity of pneumonia
Confusion?
Urea>7mmol/L
Resp rate >30
BP<90/60
Over 65?
100
Q

What investigations may you do for pneumonia?

A

-FBC, U+E, CRP, CXR, blood culture if fever present, sputum culture, urine dip

101
Q

What organisms commonly cause hospital acquired pneumonia? Does it tend to be more or less serious than CAP?

A
  • Straph aureus (MRSA)
  • Psuedomonas Aeruginosa
  • Enterobacteriaciae
  • More serious as the organisms are likely to be drug resistant and the patient is already ill as in hospital
102
Q

What is lobar pneumonia? What is most common organism? How does it characteristically look? What is bronchopneumonia?

A
  • Pneumonia which is confined to one lobe, usually unilateral
  • Step pneumoniae
  • Goes through hepatisation
  • Pneumonia which has patchy areas of consolidation scattered throughout the lung. Often bilateral and effects the base of the lungs
103
Q

What is interstitial pneumonia? Aspirational pneumina?

A
  • Pneumonia which is confined to the interstitium of the lung rather than the actual parenchyma
  • Pneumonia which is caused by aspiration of a substance/object
104
Q

What Pneumonia is associated with HIV?

A

-Pneumocystis Jiroveci

105
Q

Describe the organism Mycoplasma tuberculosis

A
  • Bacilli
  • Acid fast due to waxy cell wall and allows evasion of immune system
  • Obligate aerobe
106
Q

Describe the pathogenesis of TB and latent TB

A
  • TB organism inhaled to lower respiratory tract
  • Engulfed by alveolar macrophages -> cannot destroy as organism secretes protein to prevent fusion with lysosome
  • Multiplication producing a localised infection with flu-like symptoms -> Primary TB
  • About 3 weeks after infection cell-mediated immunity kicks in ->Granuloma formation around infection in attempt to wall off infection -> Central caseating necrosis = Ghons focus. TB infects nearby lymph nodes by immune cells or direct spread = Ghons complex
  • After this either the immune system prevails and there is resolution or TB remains viable but become dormant. When the immune system becomes comprimised again, The ghons focus becomes reactivated and the infection begins to spread throughout the lungs again (to upper lobes as aerobes)
107
Q

What can you see on an Xray of TB

A
  • Fibrosed and calcified Ghons complex

- Cavitation

108
Q

Why is reactivated TB worse than the primary TB?

A

-Memory T cells become activated producing a rapid inflammatory response to the new outbreak -> multiple areas of caseous necrosis which cavitates and allows dissemination of the bacteria to lymphatics and other parts of the lung. Can also access vascular system and cause systemic miliary TB

109
Q

What symptoms can occur in systemic miliary TB

A
  • Renal TB -> Sterile pyuria
  • Meningitis
  • Pott disease
  • Addisons disease
  • Hepatitis
  • Cervical lymphadenitis (scrofula)
110
Q

Give some symptoms of TB

A
  • Night sweats
  • Cough/haemoptysis
  • SOB
  • Fever
  • Malaise/myalgia
111
Q

What invstigations are undertaken in suspected tb?

A
  • 3 Early morning sputum samples
  • CXR
  • FBCs, U+E CRP
  • Sputum culture/NAAT
112
Q

Describe the tuberculin skin test

A
  • Tuberculin a protein produced by TB is injected in between the layers of the dermis
  • Inspected 48-72 hours later for an adequate induration
  • If positive suggests exposure to TB but cannot now if active or latent so sent for CXR
113
Q

State some risk factors for lung cancer

A
  • Smoking
  • Increasing Age
  • Radon
  • Occupational carcinogens
  • Genetics
114
Q

Where do lung cancers commonly metastasise?

A
  • Brain
  • Breast
  • Bone
  • Draining lymph nodes
  • Adrenals
115
Q

What is TNM staging?

A

-Staging system based on size of tumour, number of lymph nodes involved and metastases

116
Q

What are symptoms of lung cancer?

A
  • Weight loss
  • Haemoptysis
  • Prolonged cough (non-productive)
  • Asymptomatic
  • SOB
  • Malaise
  • Paraneoplastic syndromes
117
Q

State some paraneoplastic syndromes of lung cancer

A
  • Cushings from ectopic ACTH production -> Small cell
  • SIADH -> small cell
  • Hyperparathyroid -> PTHrp from squamous
  • Anaemia
118
Q

Give 3 signs which may be present on examination of a person with lung cancer

A
  • Pale conjunctiva
  • Clubbing
  • Cachexia
  • Cervical lymphadenopathy
119
Q

ILD, restrictive or obstructive?

A

-Restrivtive

120
Q

Give some causes of ILD

A
  • Idiopathic
  • Occupational -> Asbestosis, pneumoconiosis
  • Tx related -> Methotrexate, amiodarone, bleomycin, nitrofurantoin
  • CT disease -> RA, SLE
  • Immunological -> Sarcoidosis
  • Smoking
121
Q

How does ILD affect ventilation and perfusion?

A
  • Thickening of interstitium increases diffusion distance
  • Inflammatory exudate may infiltrate alveoli
  • Fibrosis makes it harder to expand lungs
  • Destruction of capillaries
122
Q

Give some signs and symptoms of ILD

A
  • Non productive cough
  • Progressing dyspnoea
  • Diffuse bilateral crackles
  • Tachypnoea
  • clubbing
  • Cor Pulmonale
123
Q

What is a primary malignancy of the pleura? With what is it associated?

A
  • Mesothelioma

- Asbestosis

124
Q

What is a primary pneumothorax? Secondary pneumothorax?

A
  • Spontaneous filling of the pleural space with air compressing the lung in otherwise healthy people
  • Pneumothorax which occurs secondary to underlying disease eg COPD, cancer
125
Q

What are the signs of a tension pneumothorax?

A
  • Hyperresonance
  • Deviated trachea
  • Low BP
  • Tachycardia
  • Dyspnoea
  • Cyanosis
  • Absent breath sounds
  • Decreased chest expansion
126
Q

Give some causes of pleural effusion

A
  • Kidney failure
  • Cardiac failure
  • Liver failure
  • Infection
  • Maligancy
127
Q

What 2 signs on CXR suggest pleural effusion?

A
  • Meniscus

- Loss of costophrenic angle

PPE (15 decks)

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