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LSS 1 - Thorax anatomy, Respiratory and Circulatory system > RS Lecture 7 and 8 - Respiratory Pathology and Breathlessness and Control of Breathing > Flashcards

RS Lecture 7 and 8 - Respiratory Pathology and Breathlessness and Control of Breathing Flashcards

1
Q

What is the epidemiology of lung cancer?

A

3rd most common cause of death in the UK

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2
Q

What are some risk factors for lung cancer?

A

Tobacco, radon, asbestos

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3
Q

What are the clinical features of lung cancer?

A

Haemoptysis, unexplained or persistent: cough, shoulder/chest pain, chest signs, dyspnoea, hoarseness, finger clubbing

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4
Q

What are the 2 lung cancer types?

A

Small cell and non-small cell carcinoma

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5
Q

How do we classify lung cancers?

A

TNM -> Tumour location, Lymph nodes affected, metastasis

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6
Q

What is the pathway of treatment for Small cell carcinoma?

A

If fit and early detected, then chemo and radiotherapy; if unhealthy and detected, then palliative

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7
Q

What is the pathway of treatment for non-small cell carcinoma?

A

Surgery if diagnosed early

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8
Q

Which cell type divides the quickest and the slowest in cancers?

A

Small cells (fastest) and adenocarcinomas (slowest)

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9
Q

How long does it take to ID a lung cancer?

A

Around 10-15yrs when the cancer has probably already metastasised and before symptoms present

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10
Q

What is the treatment of lung cancer based on?

A

Cell types, staging, performance status of patient

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11
Q

What is the prognosis for lung cancer?

A

80% die within a year -> 5yr survival/cure rate less than 6%

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12
Q

What is the clinical presentation of lung cancer?

A

Most asymptomatic (when tumour close to middle of the lungs and not irritating the airways) with incidental finding of mass on chest X-ray BUT symptomatic with cough, haemoptysis, recurrent infections

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13
Q

How is the diagnosis of lung cancer made?

A

Cytology (sputum, bronchial washings/brushings, pleural fluid, endoscopic fine needle aspiration) and histology (biopsy at bronchoscopy)

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14
Q

What are the main types of lung cancer?

A

Tumours arise from epithelial, mesenchymal and lymphoid cell types -> forming benign or malignant lung tumours

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15
Q

What are benign lung tumours?

A

Do not metastasise, can cause local complications (airway obstruction) -> eg: chondroma

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16
Q

What are malignant lung tumours?

A

Potential to metastasise, but variable clinical behaviour from relatively indolent to aggressive (small cell carcinoma) -> commonest are epithelial tumours

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17
Q

What are some examples of non-small cell carcinoma?

A

Squamous cell carcinoma (20-40%), adenocarcinoma (20-40%), large cell carcinoma (uncommon)

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18
Q

Why has the incidence of adenocarcinoma increased and small cell carcinoma decreased?

A

Smoking -> decline in smoking (which has small cell carcinoma as most common type, so it declined too) Adenocarcinoma is more common in non-smokers and in periphery of lungs Asbestos -> has a latent period of growth

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19
Q

Is there genetic predisposition to lung cancer?

A

Increased risk for first degree relatives of young age -> susceptibility genes also exist: nicotine addiction, chemical modification of carcinogens, susceptibility to chromosome breaks and DNA damage

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20
Q

How is carcinoma developed?

A

Multistep pathway of morphological changes associated with accumulation of mutation which result in disordered growth, loss of cell adhesion, invasion of tissue by tumour and stimulation of angiogenesis around tumour

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21
Q

How is squamous cell carcinoma developed?

A

Ciliated epithelium, become hyperplasic then undergoes metaplasia to squamous epithelium, then dysplasia, then carcinoma in situ and then invasive carcinoma -> acquire more and more mutations

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22
Q

What is squamous cell carcinoma?

A

25-40% pulmonary carcinoma -> closely associated with smoking

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23
Q

Where are squamous cell carcinomas located?

A

Central arising from bronchial epithelium but recent increase in peripheral cases

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24
Q

How do squamous cell carcinomas spread?

A

Local spread and metastasise late

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25
Q

How is adenocarcinoma developed?

A

Atypical adenomatous hyperplasia -> proliferation of atypical cells lining the alveolar walls -> increases in size and can become invasive

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26
Q

What is the incidence of adenocarcinoma?

A

25-40% of carcinomas -> common in far east, females and non-smokers

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27
Q

Where are adenocarcinomas located?

A

Peripheral and more often multicentric

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28
Q

How do adenocarcinomas spread?

A

Extrathoracic metastases common and early

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29
Q

What is large cell carcinoma?

A

Poorly differentiated tumours composed of large cells with no histological evidence of glandular/squamous differentiation (unless on electron microscope) -> poorer prognosis

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30
Q

What is small cell carcinoma and where is it located?

A

20-25% tumours -> often centred near bronchi with VERY CLOSE association with smoking

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31
Q

How do patients present with small cell carcinoma and what is the prognosis?

A

80% present with advanced disease -> very chemosensitive but very bad prognosis

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32
Q

What is the difference between small cell and non-small cell carcinoma?

A

SCC -> survival 2-4months untreated, 10-20 months with current therapy using chemoradiotherapy. NSCC -> Early stage=60% 5yr survival; late stage=5% 5yr survival; 20-30% have early stage tumours suitable for resection - less chemosensitive

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33
Q

Why do you need to distinguish between NSCC (adeno/squamous cell carcinoma)?

A

Some adenocarcinomas respond well to anti-EGFR drugs -> some SqCC develop fatal haemorrhage with Bevacizumab

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34
Q

What is the TNM staging system?

A

T(1-4) -> size of tumour, invasion of pleura/other structures. N(0-3) -> lymph node metastasis M(0-1) -> distant metastasis. Measure of how advanced tumour is -> giving info on prognosis and operability

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35
Q

What are the effects of bronchogenic carcinomas?

A

Bronchial obstruction, invasion of local structures, extension through pleura/pericardium, diffuse lymphatic spread within lung

36
Q

What does bronchial obstruction from bronchogenic carcinomas cause in the patient?

A

Collapse of distal lung: shortness of breath. Impaired drainage of bronchus: chest infection (pneumonia/abscess)

37
Q

Which local structures are invaded by bronchogenic carcinomas and what do they cause in the patient?

A

Local airways/vessels: haemoptysis, cough. Around large vessels: SVC syndrome (venous congestion of head and arm oedema and ultimately circulatory collapse. Oesophagus: dysphagia. Chest wall: pain. Nerves: Horners syndrome

38
Q

What does the extension of cancer through pleura/pericardium from bronchogenic carcinomas cause in the patient?

A

Pleuritis or pericarditis with effusions -> breathlessness, cardiac compromise

39
Q

What does the diffuse lymphatic spread within the lung from bronchogenic carcinomas cause in the patient?

A

Shortness of breath, very poor prognostic features (lymphangitis carcinoma)

40
Q

What are the systemic effects of bronchogenic carcinoma?

A

Physical effect of metastatic spread -> brain (fits), skin (lumps), liver (liver pain, deranged LFTs), bones (bone pain/fractures). Paraneoplastic syndromes

41
Q

What are paraneoplastic syndromes?

A

Systemic effect of tumour due to an abnormal expression by tumour cells of factors not normally expressed by the tissue from which the tumour arose

42
Q

What are the 2 types of paraneoplastic syndromes?

A

Endocrine and NON-endocrine

43
Q

What substances do endocrine paraneoplastic syndromes release?

A

ADH (SCC mainly) -> Syndrome of innapropriate ADH causes hyponatraemia. ACTH (SCC mainly) -> Cushing’s syndrome. PTH-related peptides (SqCC) -> hypercalcaemia. Others -> calcitonin (hypocalcaemia), Gonadotrophin (gynecomastia), serotonin (carcinoid syndrome -> carcinoid tumours mainly, rarely SCC)

44
Q

What is caused by non-endocrine paraneoplastic syndromes?

A

Haematologic/coagulation defects, skin, muscular, miscellaneous disorders

45
Q

What is mesothelioma?

A

Malignant tumour of pleura -> usually from asbestos exposure, long lag time, with tumour developing decades after exposure -> fatal disease

46
Q

What symptoms do patients with mesothelioma present with and what is the prognosis?

A

Shortness of breath, chest pain -> very bad prognosis

47
Q

What are the functions of respiratory muscles?

A

Maintenance of arterial PO2, PCO2 and pH(most important); defense of airways/lungs), exercise, speech, control of intrathoracic and intra-abdominal pressures

48
Q

How is respiratory minute volume determined?

A

V.E=VT*f (tidal volume*frequency) OR V.E= VT* 60/TTOT (per min)

49
Q

What is TTOT?

A

Total time of respiratory cycle: frequency= 1/TTOT

50
Q

How can we determine the tidal breath from VE?

A

V.E= VT/TI (mean inspiratory flow or neural drive) * TI/TTOT (timing)

51
Q

How does the CNS control breathing?

A

Involuntary/metabolic centre in the medulla; Voluntary/behavioural centre in motor area of central cortex -> metabolic will always override behavioural; other cortex parts under involuntary control influence the metabolic centre (emotional); sleep via reticular formation also influences metabolic centre

52
Q

What is the action of the metabolic centre?

A

Responds to metabolic demands for and production of CO2 and determines in part the set point for CO2 (monitored as PaCO2)

53
Q

What is the action of the behavioural centre?

A

Controls acts such as breath holding, singing

54
Q

What other systems may influence the metabolic centre?

A

Limbic system [Survival responses (suffocation, hunger, thirst)], frontal cortex [emotions] and sensory inputs [pain, startle]

55
Q

Where are the centres for respiratory control located?

A

Automatic bulbopontine controller (brainstem), behavioural suprapontine control (widely distributed)

56
Q

What is the source of volitional drive?

A

Diaphragm centre in motor homonculus in cortex

57
Q

How is breathing control organised?

A

Metabolic controller has a H+ receptor which controls the TI/E via the phrenic nerve, and operates the respiratory muscles via the respiratory spinal motorneurones thatchange the V.E -> feedback from respiratory muscles (muscle spindles and tendon organs) and lungs (stretch and irritant receptors) returns to the metabolic controller. Other feedback from carotid bodies which detect changes in pH content in arterioles -> also ECF is sampled for pH by the metabolic controller. Metabolic controller causes upper airway muscles to open and close when inspiring/expiring

58
Q

How does the behavioural controller affect breathing control?

A
59
Q

What is the carotid body?

A

Well perfused chemoreceptor

60
Q

Where does the carotid body lie?

A

At the junction of the internal and external carotid arteries in the neck

61
Q

What is the function of the carotid body?

A

Rapid response system for detecting changes in arterial PCO2 and PO2

62
Q

How is respiratory rhythm coordinated?

A

Group pacemaker activity coming from about 10 groups of neurons in the medulla near nuclei of CNIX/X -> Pre-Botzinger complex in ventro-cranial medulla near 4th ventricle seems essential for resp rhythm generation (gasping centre) w/coordination between it and other centres to change gasping to orderly resp rhythm

63
Q

How is the respiratory cycle coordinated?

A

Discrete groups of neurons in medulla discharge at different points of resp cycle, w/different functions -> early inspiratory (initiates insp. flow via resp muscles), inspiratory augmenting (may dilate pharynx, larynx and airways), late inspiration (signal end of insp and brake start of expiration). Expiratory decrementing (brake passive expiration by adducting larynx/pharynx), expiratory augmenting (activate exp muscles when ventilatiion increases on exercise), Late expiratory (signal end of exp and onset of inspiration, dilate pharynx in prep for insp.)

64
Q

What reflex controls occur and which nerves do they stimulate to cause it?

A

CNV -> afferents from face/nose (irritant). CNIX -> from pharynx and larynx (irritant). CNX -> Bronchi/bronchioles (irritant and stretch). Irritant receptors lead to cough/sneezing - are defensive. Thoracic spinal cord -> from chest wall and resp muscles (spindles stretch)

65
Q

What are the Hering-Breuer reflexes?

A

Reflex from pulm. stretch receptors which sense lengthening/shortening and terminates insp/exp. -> weak in humans (CNX)

66
Q

Where does the metabolic controller get the sensory information from?

A

Central part in medulla responding to H+ in ECF; peripheral part at carotid bifurcation, H+ receptors of carotid body -> pH changes mirror PCO2 changes rapidly in carotid bodies, slowly in ECF bathing the medulla

67
Q

How does hypoxic breathing change the sensititvity of the acute CO2 response?

A

Increases the sensitivity -> effect mediated through carotid body

68
Q

What does chronic metabolic acidosis cause?

A

Increases the apneic threshold but not the sensitivity

69
Q

What does chronic metabolic alkalosis cause?

A

Decreases the apneic threshold but doesn’t alter the sensitivity

70
Q

What substances are being controlled by the medulla?

A

PaO2 not as tightly controlled as PaCO2 and H+ -> with SaO2 rather than PaO2 being maintained -> fall in ventilation=fall in PaO2, rise in PaCO2 and fall in PaO2 increases sensitivity of carotid body to PaCO2 and H+, so ventilation and PaO2 increases and PaCO2 decreases by negative feedback

71
Q

How is the diaphragm working in patients with chronic bronchitis and emphysema?

A

It is working much harder, even though the end VE is the same as normal people; so Diaphragm moves much faster, to make up for the lack of lung function, so TTOT is shorter

72
Q

What occurs in respiratory acidosis and what are the compensatory mechanisms?

A

Acute: hypoventilation causes PaO2 to fall, PaCO2/H+ to increase, stimulating the metabolic centre and carotid body to increase minute ventilation and restore blood gas/H+ levels. Chronic: ventilatory compensation may be inadequate for PaCO2 homeostasis but renal excretion of weak acids returns H+ to normal even though PaCO2 remains high

73
Q

What determines [H+]?

A

[H+] = constant* PaCO2/HCO3-. Strong ion difference: [Na+ plus H+] - Cl-

74
Q

What occurs in metabolic acidosis and what are the compensatory mechanisms?

A

Excess production of H+ -> compensatory mechanisms: ventilatory stimulation lowers PaCO2 and H+, renal excretion of weak (lactate and keto) acids, renal retention of chloride to reduce strong ion difference

75
Q

What occurs in metabolic alkalosis and what are the compensatory mechanisms?

A

Excess HCO3-, lowers H+ -> compensatory mechanisms: Hypoventilation raises PaCO2 and H+, renal retention of weak acids, renal excretion of Cl- to increase strong ion difference

76
Q

What are the central controller causes of hypoventilation?

A

Acute: metabolic centre poisoning. Chronic: vascular/neoplastic disease of metabolic centre, congenital central hypoventilation syndrome (decreased sensitivity PaCO2), obesity hypoventilation syndrome, chronic mountain sickness.

77
Q

What are the peripheral causes of hypoventilation?

A

Acute: muscle relaxant drugs, myasthenia gravis. Chronic: neuromuscular with respiratory muscle weakness

78
Q

How does COPD cause hypoventilation?

A

Mixture of central (won’t breathe, CO2 insensitvity) and peripheral (can’t breathe, hyperinflation/obstruction)

79
Q

How is hyperventilation caused?

A

Chronic hypoxaemia, excess H+ (metabolic cause), pulmonary vascular disease, chronic anxiety (psychogenic)

80
Q

What is breathlessness?

A

Suspended breathing with an emotional cause OR normal experience when exercise exceeds a threshold of comfort

81
Q

What is dyspnea?

A

Breathlessness with connotation of discomfort or difficulty -> at rest = difficulty with inspiration/expiration

82
Q

What are then 3 types of breathlessness?

A

Tightness: difficulty inspiring due to airway narrowing. Increased work and effort: breathing at high minute ventilation/at normal minute ventilation but high lung volume/against insp or exp resistance. Air hunger: sensation of powerful urge to breathe

83
Q

What is air hunger?

A

Mismatch between VE demanded and VE achieved -> cerebral cortex compares 2 afferent inputs: demand (copy of signal sent by metabolic controller to spinal motorneurones) and output (afferents from lung, chest wall and chemoreceptors)

84
Q

What scale measures breathlessness?

A

Borg scale or visual analogue scale

85
Q

What is the breath holding time?

A

Tests strength of behavioural vs metabolic controller -> break point prolonged by increasing lung volume, lowering PaCO2 or by taking an isoxic/isocapnic breath near break point -> expression of air hunger, product of stretch receptor drive * metabolic drive

LSS 1 - Thorax anatomy, Respiratory and Circulatory system (27 decks)

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