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Respi patho Flashcards

1
Q

What holds open the large airways?

A

Cartilage

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2
Q

What controls the calibre of the small airways?

A

Smooth muscles

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3
Q

What type of cells line the alveoli?

A

Type 1 pneumocytes

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4
Q

Fn of type 2 pneumocytes

A

Produce surfactant

Repair of alveolar damage

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5
Q

What perforates alveolar walls?

A

Pores of Khon

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6
Q

Fn of pores of Khon

A

Permit passage of exudate and bacteria btw adjacent alveoli -> enable infection to spread

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7
Q

Requirements for lung to freely exchange O2

A

Alveoli must be open
- surface tension kept low

Lungs must be compliant
- easy to stretch and expand

Air must move freely

Sufficient area for diffusion

Barrier to diffusion must be thin

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8
Q

What is rhinitis?

A

URTI

Inflammation of the nasal cavity

Usually viral in origin

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9
Q

Pathogenesis of rhinitis

A

Viral necrosis of surface epithelial cells -> exudation of fluid and mucus from the damaged surface

Submucosal oedema -> swelling and nasal obstruction

Infection can spread to lower tract -> predispose to bacterial infection

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10
Q

What is allergic rhinitis?

A

Hypersensitivity to environmental agents

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11
Q

Pathogenesis of allergic rhinitis

A

Antigenic stimulus persists -> mucosa becomes swollen and polypoid w/ formation of nasal polyps

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12
Q

What are nasal polyps?

A

Localised outgrowths of lamina propria due to accumulation of oedema fluid, inflammation and fibroblast proliferation

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13
Q

Features of nasal polyps

A

Multiple

Bilateral

Involve nasal cavity and paranasal sinuses

Amt and composition of inflammatory component highly variable

Take shape of nasal cavity

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14
Q

What is sinusitis?

A

URT

Inflammation of the paranasal sinus linings of the maxillary, ethmoid and frontal sinuses

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15
Q

Pathogenesis of sinusitis

A

Mucosal oedema -> impaired drainage of secretions -> predispose to sec bacterial infection

Severe -> spread to meninges

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16
Q

What is the nasopharynx?

A

Part of pharynx lying immediately behind nasal cavities
- inaccessible -> hard to detect tumor until it’s grown in size

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17
Q

What lines the nasopharynx?

A

Respiratory columnar epithelium
w/ associated mucosa-associated lymphoid tissue

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18
Q

Is nasopharyngeal carcinoma (NPC) common in SG?

A

Yes

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19
Q

3 histological classification of NPC

A

Non-keratinising carcinoma

Keratinising squamous cell carcinoma

Basaloid squamous cell carcinoma

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20
Q

Characteristics of non-keratinising NPC

A

Tumor is poorly differentiated

Intermingled lymphocytes amongst carcinoma cells

Diff appearance to other squamous cell carcinoma of the head and neck

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21
Q

Characteristics of keratinising NPC

A

Resembles squamous cell carcinoma of other sites in the head and neck region

Associated w/ smoking and alcohol consumption

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22
Q

Risk factors for NPC

A

Epstein Barr Virus (EBV) infection at young age

Salt-preserved food

Family history

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23
Q

Features of EBV infection

A

Subclinical in childhood

Virus associated w/ later development of several malignancies

Infection in adolescence more likely to be symptomatic

Infects and maintain latency in nasopharyngeal epithelium and tonsillar B lymphocytes

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24
Q

Link btw NPC and EBV

A

NPC pts have elevated Ab titres to EBV viral antigens
- Ab titres precede tumor development by several years, correlated w/ tumor burden, remission and recurrence
- further linked to development of NPC thru EBV DNA, RNA and/or gene pdts in tumor cells

EBV stimulates normal cell to divide -> cancer

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25
Q

Basis of screening test for NPC

A

Ab against viral capsid antigen

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26
Q

Why may NPC originate from a single progenitor cell infected w/ EBV b4 clonal expansion?

A

EBV episome is identical in every tumor cell

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27
Q

Symptoms of NPC

A

Increased diplopia due to invasion of VI cranial nerve

Increased nasal obstruction, epistaxis, serous nasal discharge

Increased metastases in cervical lymph nodes

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28
Q

Pathogenesis of C. diptheriae infection

A

Infect upper airway mucosa -> produce exotoxin -> necrosis of epithelium -> pseudomembrane -> airway obstruction

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29
Q

What does H. influenzae infection cause?

A

Acute epiglottitis -> airway obstruction (due to swelling of epiglottis)

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30
Q

Compulsory vaccinations in SG

A

Diphtheria and measles

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31
Q

Vaccination for C. diphtheriae and H. influenzae

A

DTaP-IPV + HIB

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32
Q

Most common pathogen for acute pharyngitis and laryngitis

A

Virus

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33
Q

Symptoms related to larynx

A

Sore throat

Hoarseness

Cough

Tracheal soreness

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34
Q

What is stridor?

A

Breathing sound due to large airway obstruction, usually worsen in inspiration

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35
Q

What is croup in children?

A

Cough + stridor due to infection

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36
Q

What are some complications of URTI

A

Indivs w/ poor cough reflex (i.e: elderly/debilitated/unconscious) -> infected material not coughed up -> pass into smaller airways and rest of lung -> bronchopneumonia

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37
Q

What is allergic pharyngolaryngeal oedema?

A

Life-threatening type 1 hypersensitivity rxn
- may be associated w/ facial oedema and bronchospasm

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38
Q

How is acute toxic laryngitis acquired?

A

Via inhalation of toxic gases

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39
Q

Impt cause of death in fires

A

Acute toxic laryngitis

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40
Q

Risk factor for chronic laryngitis

A

Heavy smoker

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41
Q

How does chronic laryngitis lead to cancer?

A

Chronic irritation of epithelium -> squamous metaplasia -> increased risk of dysplasia and squamous cell carcinoma

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42
Q

What are singer’s nodules?

A

Benign lesions of the larynx
- reactive nodular thickenings of vocal cords seen in singers and chronic smokers

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43
Q

Where does carcinoma of the larynx occur?

A

Occur at/above/below level of vocal cords

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44
Q

Presentation of glottic tumors

A

Early

Hoarseness (change of voice)

Lower stage at presentation compared to supraglottic and subglottic tumors

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45
Q

Why do glottic tumors tend to be lower stage at presentation compared to tumors at the supraglottic and subglottic tumors?

A

Poor lymphatic supple of glottic region -> less likely to spread

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46
Q

Growth patterns of carcinomas

A

Polypoid -> space occupying

Ulcerative

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47
Q

What is atelectasis?

A

Collapse of the lung

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48
Q

Complications of atelectasis

A

Inadequate expansion of lung -> loss of lung vol -> affect ventilation

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49
Q

Causes of atelectasis

A

Resorption atelectasis
- airway obstruction
- air will get absorbed from alveoli but no replenishing of fresh air -> alveoli collapse

Compression atelectasis
-air/fluid in pleural space w/ compression of lung
-post-operative poor lung expansion

Contraction atelectasis
- scarring of lung/pleura
- loss of normal surfactant

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50
Q

What are the normal defences of the lung?

A

Mucus -> trap large microbes in URT

Ciliary action -> transport trapped microbes to back of throat where swallowed

Cough reflex

Alveolar macrophage -> phagocytose smaller organisms

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51
Q

Features of URTI

A

Common

Usually self-limiting viral disease

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52
Q

Bacterial vs viral infection of URTI

A

Bacterial infection is more serious

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53
Q

What can damage hose defences?

A

Smoking

Intubation

Previous infection

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54
Q

Factors that increase chance of infection

A

Poor swallowing and reduced cough reflex

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55
Q

Common pathogen for bronchitis and bronchiolitis

A

Viruses
- same ones that cause URTI

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56
Q

What is pneumonia?

A

Infective inflammation and consolidation of lung
- filling of airspaces by inflammatory exudate -> renders affected area solid and airless

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57
Q

What is pneumonitis?

A

Inflammatory disease dominated by interstitial inflammation

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58
Q

Causes of pneumonitis

A

Infection

Inhaled toxins and allergens

Drug rxn

Irradiation

Connective tissue disease

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59
Q

What is bronchopneumonia?

A

Primary infection centered on the bronchi, spreads to involve adjacent alveoli

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60
Q

Features of bronchopneumonia

A

Initially patchy, may become confluent

Common in infancy and old age

Affects lower lobe more

Terminal in debilitated pts

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61
Q

Lobar vs bronchopneumonia

A

Lobar pneumonia has no bronchial-lobe centric appearance
- infection confined to alveolar spaces

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62
Q

Pathogenesis of lobar pneumonia

A

Organisms gain entry to distal airspaces rather than colonising bronchi -> spread rapidly thru alveolar spaces and bronchioles (more virulent) -> infect whole lobe
- NOTE: little tissue destruction

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63
Q

Common organisms causing lobar pneumonia

A

S. pneumoniae

Klebsiella

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64
Q

What is an air bronchogram?

A

Phenomenon of air-filled bronchi being made visible by opacification of surrounding alveoli

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65
Q

What kind of organisms cause community-acquired pneumonia (CAP)?

A

Gram pos
-eg
- S. pneumoniae
- H. influenzae
- Legionella
- Mycoplasma
- M. tuberculosis

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66
Q

What kind of organisms cause hospital-acquired pneumonia (HAP)?

A

Gram neg
- eg
- Klebsiella
- Pseudomonas
- E coli

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67
Q

Risk factors for HAP

A

Being on a ventilator

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68
Q

How do you directly sample a lung?

A

Bronchoalveolar lavage (BAL)

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69
Q

What is tuberculosis?

A

Chronic pneumonia that is communicable, granulomatous

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70
Q

What organism causes tuberculosis?

A

Mycobacterium tuberculosis

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71
Q

Diseases that increase risk of tuberculosis

A

Diabetes

Chronic lung disease

Alcoholism

HIV infection

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72
Q

Features of mycobacteria

A

Slender rod-shaped bacteria

Waxy cell wall -> resistant to destruction by neutrophils
- only macrophage can effectively phagocytose and contain mycobacteria

Can live intracellularly -> proliferate in macrophages

Readily bind Ziehl-Neelsen stain

Resist decolourisation (AFB)

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73
Q

Pri vs sec TB

A

Pri
- no prev exposure (unsensitised host), pattern of disease

Sec
- prev exposure and sensitised, pattern of disease

Main diff is where the immune rxn is predominant

Prev exposure but poor immune sys = pattern of pri TB

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74
Q

Outcomes of TB

A

Both pri and sec TB may heal/spread
- TB spread via bronchi, lymphatics/into pleural space

Miliary TB
- TB enters blood supply

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75
Q

Describe the cell-mediated immunity of TB

A

Host develops targeted cell-mediated immunity

Antigens presented to CD4+ T cells -> secrete cytokines and activate macrophages to kill bacteria

Immune response comes at cost of hypersensitivity and accompanying tissue destruction

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76
Q

Pathogenesis of pri TB

A

Infection and necrosis at periphery of the lung, often just beneath the pleura -> Ghon focus
- small focus of infection due to few immune recognition sites within lung

Bacteria conveyed to local lymph nodes at lung hilum -> immune recognition -> enlarge through granulomatous inflammation and caseation (necrosis)
- immune recognition ONLY at lymph nodes at hilum
- lesions are small

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77
Q

Control of infection for pri TB

A

Cell-mediated immunity controls infection

Area of caseation heals -> only leave small calcified nodule at site of infection

Viable organisms lie dormant in these foci -> latent TB
- can’t transmit organism to others

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78
Q

Progression of pri TB

A

Progress w/ severe pneumonia and dissemination (uncommon)

Continuing enlargement of caseating granulomas in lymph nodes

Spread occurs by enlarging nodes eroding either thru the wall of a bronchus/thin-walled blood vessel

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79
Q

Distinctive pattern of miliary TB on chest x-ray

A

Many tiny spots distributed throughout the lung fields
- doesn’t follow airway

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80
Q

Pathogenesis of sec TB

A

Common presentation in immunocompetent adults

New organism/re-activate pri complex years aft pri infection

Occurs in apex of lung but if other organs seeded during pri infection -> re-activate elsewhere

Reactivation -> rapid mobilisation of defence rxn at site of entry and increased tissue destruction -> cavitation

Immune sys recognises infection in lung and tries to contain it there -> little lymph node involvement

Apical lesions (Assmann focus) begins as central area of necrosis surrounded by granulomas

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81
Q

Histopathology of focus of TB infection

A

Granuloma

Laanghan’s giant cell

T lymphocytes

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82
Q

Outcomes of sec TB

A

Vigorous immune response -> healing of apical lesions -> central area of caseous necrotic material surrounded by thick, dense collagenous wall which often calcifies (fibrocaseous TB)

Weakened immune response and residual organisms present -> latent TB lead to spreading infection -> reactivated fibrocaseous TB

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83
Q

Progression of sec TB

A

Poor immune response -> progrossive enlargement of apical lesion w/ continued destruction of lung tissue -> risk of erosion into blood vessels/airways

Spread is similar to pri TB (bronchopneumonia, miliary TB)

84
Q

Risk factors for aspiration pneumonia

A

Unconsciousness

Impaired swallowing

85
Q

Pathogenesis of aspiration pneumonia

A

Mixed organisms (commonly anaerobes and oropharyngeal bacteria) +/- gastric acid +/- food -> infective pneumonia + chemical damage

Frequently leads to lung abscess

86
Q

Features of atypical pneumonia

A

Pt has symptoms of pneumonia but there is absence of consolidation on x-ray

Marked infiltration of alveolar septa/interstitium by chronic inflammatory cells

87
Q

What are some organisms that cause atypical pneumonia?

A

Mycoplasma

Chlamydia

Rickettsia

88
Q

Describe the immune rxn of viral pneumonia

A

Interstitial inflammatory response dominated by lymphoid cells

Severe -> cytokine storm -> acute respi distress syndrome

89
Q

Common pathogens for viral pneumonia

A

Influenza
- H5N1

Sars-CoV-1/2

90
Q

What are some traits of pneumonia caused in immunocompromised pt?

A

Caused by opportunistic pathogens
- pathogens that normally won’t cause infection in immunocompetent hosts

Common pathogens can cause more severe pneumonia

Disease disseminated early

91
Q

Situations where organisms of low pathogenicity can cause infection?

A

Immunocompromised pts

Pts w/ prev damage to lung resulting in stagnant secretions

92
Q

Presenting illness of HIV+ pts

A

Opportunistic infections
- Pneumocystis jirovecii
- Candida

93
Q

What is bronchiectasis?

A

Permanent abnormal dilatation of the main bronchi

94
Q

Complications caused by bronchiectasis

A

Airways dilated -> may contain purulent secretions, chronic inflammation of wall w/ loss of normal epithelium

Pts have recurrent infection

Haemoptysis (cough up blood)

Spread of infection from bronchi to surrounding lung

95
Q

2 main factors predisposing to bronchiectasis

A

Interference w/ drainage secretions

Recurrent and persistent infection

96
Q

Outcomes of bronchiectasis

A

Chronic suppuration w/ its sequelae

Spread of infection beyond lung

Massive haemoptysis

Loss of normal lung tissue w/it sequelae -> respi failure

97
Q

What is a lung abscess?

A

Localised area of suppurative necrosis, usually forming large cavities

98
Q

What are some infections predisposing pts to lung abscess?

A

Pulmonary infarction

Aspiration

Bronchial obstruction

Bronchiectasis

S. aureus

99
Q

What are the main complications of lung abscess?

A

Rupture into pleura -> empyema and pneumothorax

Haemorrhage from erosion into pulmonary vessel

Bacteraemia

100
Q

Obstructive vs restrictive lung disease

A

Obstructive
- limitation of airflow -> affect ventilation
- normal total lung capacity
- reduced expiratory flow rate

Restrictive
- total lung capacity reduced,
- normal expiratory flow rate

101
Q

What does spirometry measure?

A

Lung vol and flow rate of air
- distinguish btw obstructive and restrictive lung disease

102
Q

Features of obstructive lung disease

A

Problem w/ ventilation, usually at level of small branches of bronchial tree

Exhalation usually more affected and req more effort

Wheeze heard

103
Q

What is obstructive sleep apnoea (OSA)?

A

Ep of partial/complete closing of the upper airways during sleep
- pt wake up repeatedly to gasp for air
- jaw and tongue fall backward and obstruct airway

104
Q

What can OSA result in?

A

Hypoxaemia

Poor sleep

105
Q

What is asthma?

A

Chronic disease affecting bronchioles
- recurring ep of bronchospasm (reversible) and excessive production of mucus

106
Q

Precipitating factors for asthma attacks

A

Atopic -> allergens

Non-atopic -> hypersensitive airways and irritants trigger attack

107
Q

What can repeated ep of asthma cause?

A

Over-reactivity of airways

Remodelling of airways

108
Q

What is status asthmaticus?

A

Prolonged bronchospasm and mucus plugging -> respi failure
- no time for body to be oxygenated btw attacks

109
Q

What is ‘model’ asthma?

A

Complex inflammatory response in bronchial mucosa

110
Q

Pathogenesis of ‘model’ asthma

A

Prev sensitisation causes IgE mediated response -> activation of mast cells and direct stimulation of nerve receptors

Mast cells release chemical mediators -> recruitment of eosinophils, cause bronchoconstriction and increase in vascular permeability and mucus secretion

Recruited eosinophils and T helper cells release further mediators -> amplify and sustain inflammatory response

111
Q

Structural changes in asthma

A

Hyperactivity and hypertrophy of smooth muscle bronchus

Hypersecretion of mucus

Mucosal oedema

Infiltration of bronchial mucosa by eosinophils, mast cells, lymphoid cells and macrophages

Deposition of collagen beneath bronchial epithelium

112
Q

Which grp of people are predisposed to COPD?

A

Chronic smokers

113
Q

Diff btw asthma and COPD

A

In COPD, airflow limitation is not fully reversible and disease is usually progressive (slow reduction to respi capacity)

114
Q

Exacerbation of COPD

A

Relatively mild concomitant illness/poor air quality
- due to loss of normal lung fn

115
Q

3 main pathologies contributing to COPD

A

Emphysema (affect alveoli) -> destruction of airspaces and loss of elastic recoil -> reduction in gas exchange capacity

Chronic bronchitis -> mucus hypersecretion and luminal narrowing of airways

Bronchiolitis -> narrowing of small airways by inflammation and scarring

116
Q

What is emphysema?

A

Permanent dilatation of airspaces distal to the terminal bronchiole w/ destruction of tissue in absence of scarring

117
Q

Pathogenesis of emphysema

A

Parenchymal destruction by extracellular proteases/elastases

Normally proteases secreted by inflammatory cells are inactivated by extracellular protease inhibitors in the lung but cigarette smoke inhibits effect of protease inhibitors, alpha-1-antitrypsin -> tissue destruction

Free radicals from cigarette smoke cause tissue damage

Persistent irritation -> increased inflammatory cells in lungs -> increased release of mediators and enzymes

118
Q

Who is at risk of developing emphysema?

A

Pts w/ congenital alpha-1-antitrypsin deficiency

119
Q

Clinical definition of chronic bronchitis

A

Cough productive of sputum on most days for 3 months of year for at least 2 successive years

120
Q

What is chronic bronchitis?

A

Airway obstruction related to luminal narrowing and mucus plugging, resulting in alveolar hypoventilation

121
Q

What is bronchiolitis?

A

Inflammation of airways <2mm in diameter

122
Q

What happens in bronchiolitis?

A

Macrophages and lymphoid cells infiltrate airway wall

May progress and lead to scarring and narrowing of airways -> functional airways obstruction

123
Q

Risk factors for COPD

A

Lifetime smoking exposure

Less common:
- recurrent childhood infections
- occupational exposure to dust

124
Q

Common causes of death for pts w/ COPD

A

Respi failure

Sec right heart failure

125
Q

What are diffuse parenchymal lung diseases?

A

Grp of lung diseases characterised by widespread inflammatory pathology, predominantly in interstitium -> reduced compliance in lungs
- acute/chronic/progressive

126
Q

Main histological patterns of rxn in lung following damage

A

Haemorrhage and fibrin exudation into alveoli -> hyaline membranes (glassy, uniformly pink)

Oedema and inflammation of interstitium

Macrophage accumulation in alveolar spaces

Fibrosis in interstitium/alveolar spaces

127
Q

What is acute respi distress syndrome (ARDS)?

A

Severe form of acute lung injury
- acute form of diffuse parenchymal disease

Clinical syndromes caused by alveolar and capillary damage

128
Q

Most common cause of ARDS

A

Systemic sepsis

Severe trauma/burns

Inhalation of toxic fumes -> damage both endothelial and epithelial cells

129
Q

Pathophysiology of ARDS

A

Injury of penumocytes and pulmonary endothelium -> damage to alveolar lining cells/alveolar capillary endothelium -> interstitial edema and high protein exudation into alveoli (hyaline membrane) -> regeneration of type 2 alveolar lining cells and inflammation of interstitium -> interstital fibrosis

Death in acute phase occurs due to interstitial edema and high protein exudation into alveoli

Fibrosis
- mild -> recovery w/ minimal residual respi dysfunction
- severe -> marked interstitial fibrosis (honeycomb lung) -> death due to chronic severe respi impairment

130
Q

Phases of ARDS

A

Acute exudative phase
- interstitial oedema and high protein exudation into alveoli -> fibrin-rich fluid + necrotic epithelial cells -> hyaline membranes

Late organisation phase
- regeneration of type 2 alveolar lining cells, organisation of hyaline membranes w/ fibrosis

131
Q

Causes of diffuse parenchymal lung disease

A

ARDS

Atypical pneumonias

Sarcoidosis

Smoking-related

Idiopathic

NOTE: these are only some of the many

132
Q

What is honeycomb lung?

A

End stage chronic pulmonary fibrosis

133
Q

How does honeycomb lung lead to death?

A

Leads to chronic respi impairment and reduced diffusion capacity -> death due to combination of respi and cardiac failure

134
Q

Histopathological features of honeycomb lung

A

Holes are bigger and thicker (like honeycomb)

135
Q

What is idiopathic pulmonary fibrosis?

A

Commonest chronic diffuse parenchymal disease

Progressive restrictive lung disease

136
Q

What does lung biopsy show in idiopathic pulmonary fibrosis?

A

Usual interstitial pneumonia (UIP) pattern

137
Q

What is hypersensitivity pneumonitis/extrinsic allergic alveolitis?

A

Lung disease due to hypersensitivity to inhaled organic antigens

138
Q

What does hypersensitivity pneumonitis/extrinsic allergic alveolitis cause?

A

Chronic fibrosing lung disease

139
Q

Most common grp of allergens for hypersensitivity pneumonitis/extrinsic allergic alveolitis and the clinical problems caused

A

Animal proteins and microbial agents in veg matter

Acute (respi symptoms 4-8h aft exposure)/chronic (insidious development of pulmonary fibrosis in pt that has not exp acute symptoms)

140
Q

What is pneumoconiosis?

A

Disease of lungs caused by inhalation of dust
- interaction of dust w/ defence mechanism of lung -> inflammation -> release of cytokines -> stimulation of fibrosis
- worsened by smoking

141
Q

Common particles associated w/ pneumoconiosis

A

Silica

Coal dust

Asbestos

*all are occupational hazards and have characteristic radiological and histological features

142
Q

Features of asbestos

A

Fibrogenic

Oncogenic

Persist in lungs

143
Q

Lung diseases associated w/ asbestos

A

Pleural plaques

Pleural effusions and thickening

Asbestosis -> progressive chronic lung fibrosis
- increase chance of mesothelioma

144
Q

What are granulomas?

A

Histological manifestation of cell mediated immunity -> activated macrophages necessary to tackle intracellular bacteria, large organisms and foreign material

145
Q

Causes of granulomas in lung

A

Infection (eg: TB)

Foreign material/antigens

146
Q

Why are granulomas often seen in lymph nodes?

A

Immune recognition takes place in draining lymph nodes

147
Q

What is sarcoidosis?

A

Systemic disease of unknown cause characterised by non-necrotising granulomas in many tissues and organs (eg: spleen, liver, bone marrow, etc)

148
Q

Common site of metastasis from other cancers

A

Lung

149
Q

Correlation btw smoking and lung cancer

A

Risk of cancer increases w/ no. of cigarettes smoked and age at which smoking was started (pack years)

Passive smokers have double risk compared to those not exposed

Stopping smoking reduces risk but doesn’t return to normal

150
Q

Classification of lung cancer

A

Small cell carcinoma (SCLC)
- aggressive

Non small cell carcinoma (NSCLC)
- squamous cell carcinoma
- adenocarcinoma
- others

151
Q

Location of lung cancer

A

Central -> near airways

Peripheral -> far from airways

152
Q

Possible spread of lung cancer

A

Local

Lymphatic

Transcoelomic (pleural and pericardial effusions)

Hematogenous

153
Q

Histological features of squamous cell carcinoma

A

Central cavitation

Preceded by squamous metaplasia/dysplasia

154
Q

Features of squamous cell carcinoma

A

Commoner in males

High association w/ smoking

155
Q

Features of adenocarcinoma

A

Equal gender incidence

Not strongly linked w/ smoking
- most common lung cancer in non-smokers

Minimally invasive

Spreads along alveolar septa

Looks like consolidation rather than mass on x-ray

156
Q

Features of small cell carcinoma

A

Central

Rapid rate of growth

High association w/ smoking

Poor prognosis

Tumor cells show neuroendocrine differentiation

157
Q

Histological features in small cell carcinoma

A

Enlarged nuclei w/ little cytoplasm

158
Q

Why does lung cancer usually have poor prognosis?

A

No early symptoms

Many lesions found on chest x-ray screening have alr spread

Only way to pick up small lesions is by CT scan

Metastatic spread present in most pts at presentation

159
Q

Associated syndrome w/ lung cancer

A

Paraneoplastic syndrome -> immune rxn to cancerous tumor

160
Q

Outcome of NSCLC

A

Surgery is best hope of cure if cancer hasn’t spread out of lung

Most cases inoperable

161
Q

Outcome of SCLC

A

Sensitive to radiotherapy and chemotherapy

162
Q

What kind of cells line the pleura?

A

Mesothelial cells

163
Q

Describe fluid cycle in pleura (bad phrasing of qn)

A

Constant generation of fluid from parietal pleura and resorption by visceral pleura

164
Q

Transudate vs exudate

A

Transudate
- low protein fluid -> due to high hydrostatic pressure, low oncotic pressure
- little cells

Exudate
- high protein fluid -> due to damaged vessel walls/inflammatory rxn to tumor/infection
- lots of cells

165
Q

Common causes of pleural effusions

A

Cardiac failure

Infections

Neoplasm

166
Q

Diagnosis of pleural effusion on chest x-ray

A

Loss of air in costal phrenic angle

167
Q

What is pleurisy?

A

Acute inflammation of the pleura, usually due to infection

168
Q

Histopathological features of pleurisy

A

Fibrinous/purulent exudate seen on pleural surface

Neutrophils predominate in most bacterial infection (except: TB -> lymphocytes predominate)

Fibrinous exudate organised to form fibrous pleural adhesions

169
Q

Common causes of pneumothorax

A

Thin, young mem

Congenital subpleural apical bleb

Rupture of emphysematous bulla

Asthmatics

Trauma

Iatrogenic (illness caused by medical examination or treatment)

170
Q

Features of pneumothorax in chest x-ray

A

Lack of lung markings

171
Q

Most common tumor of the pleura

A

Metastatic carcinoma

172
Q

Pri neoplasm associated w/ asbestos exposure

A

Malignant mesothelioma

173
Q

Features of malignant mesothelioma

A

Tubular (epitheloid)/spindle cell (sarcomatoid) pattern

Spread ard lung and mediastinal structures

Poor prognosis

174
Q

Common mediastinal mass lesions adults

A

Metastases

Pri TB

Thymoma

Lymphoma
- specifically -> T cell lymphoblastic lymphoma, pri mediastinal large B cell lymphoma and Hodgkin lymphoma

Germ cell tumors

175
Q

Common mediastinal mass lesions adults

A

Lymphoma/leukaemia

Neuroblastoma/other neural tumors

176
Q

What kind of cells make up the thymus?

A

Lymphoid cells and specialised epithelial cells

177
Q

What happens to the thymus as one ages?

A

Regresses after puberty

178
Q

How does thymic tumors present and what are the main tumors of the thymus?

A

Anterior mediastinal masses

Main tumors
- thymoma
- lymphoma
- germ cell tumor

179
Q

What is thymoma?

A

Neoplasm derived from thymic epithelial cells
- lymphocytes preset but are non-neoplastic
- proportion of cases associated w/ myasthenia gravis

180
Q

Histological features of thymoma

A

Nest of epithelial cells

Lymphocytes

181
Q

What is atresia?

A

Condition in which an orifice/passage in the body is abnormally closed/absent

182
Q

Common developmental abnormalities causing lung disease in children

A

Bronchial atresia

Bronchogenic cysts -> accessory bronchial buds which become sealed off from the rest of airway

Bronchopulmonary sequestration -> area of lung tissue that develops abnormally (no connection w/ bronchial tree) -> no respi fn

183
Q

Alternative name for neonatal respi distress syndrome

A

Hyaline membrane disease

184
Q

Pathogenesis of neonatal respi distress syndrome

A

Deficiency of surfactant in lungs usually due to prematurity -> alveoli collapse -> hypoxia, damage to endothelial and alveolar lining cells and fibrin exudation

185
Q

Childhood diseases that affect fn of lungs

A

Immotile cilia fn -> cilia have abnormal structure/can’t beat in coordinated pattern

Cystic fibrosis -> production of abnormally viscous mucus that can’t be cleared -> repeated infections and bronchiectasis
- autosomal recessive

186
Q

Main cause of pulmonary oedema

A

Pulmonary capillary pressure due to left heart failure

187
Q

Common symptom of pulmonary oedema and pathophysio behind it

A

Capillary rupture -> leakage of RBC into interstitium -> RBC phagocytosed by alveolar macrophages (heart failure cells)

188
Q

Causes of pulmonary arterial hypertension

A

Sec to left heart disease where pressure is transmitted to entire pulmonary sys

Shunts from left to right heart

Chronic lung disease

Sequelae of pulmonary emboli

Unknown cause

189
Q

Consequences of pulmonary hypertension

A

Sustained increased pulmonary arterial pressure -> irreversible structural changes in pulmonary arteries -> medial hypertrophy in muscular arteries and intimal proliferation -> narrowing/occlusion -> further increased pressure

190
Q

What is cor pulmonale?

A

Heart failure sec to lung disease
- long term need to pump at higher pressures causes heart to fail

191
Q

Outcome of pulmonary emboli

A

Depends on size of thrombus and local haemodynamics
- large -> circulatory collapse
- infarction
- no infarction but ventilation-perfusion mismatch
- recurrent small thromboemboli -> organisation of thrombi in small arteries -> permanent occlusion -> progressive reduction in pulmonary vasculature -> pulmonary hypertension

192
Q

What is pulmonary vasculitis? What are some eg of diseases w/ prominent lung manifestations?

A

Inflammatory destruction of blood vessels ->bleeding into lungs
- repeated ep -> vessel damage -> pulmonary hypertension

Granulomatosis w/ polyangiitis (GPA) = Wegener granulomatosis

Eosinophilic granulomatosis w/ polyangiitis (EGPA) = Churg-Strauss syndrome

193
Q

What is respi failure?

A

Inadequate gas exchange due to dysfn of 1/more of essential components of respi sys

194
Q

Consequence of respi failure

A

Inability to maintain O2 and/or CO2 lvls at normal lvls -> hypoxia/hypercapnia

195
Q

Normal physio response to low pO2 lvls

A

Increased RR

196
Q

Measurement of oxygenation

A

Pulse oximeter

Arterial blood gas
- more accurate

197
Q

Components that may fail in respi failure

A

CNS and nerves

Chest wall/diaphragm

Airways

Alveolar-capillary units

Pulmonary circulation

198
Q

Main symptoms of respi failure

A

Breathlessness

Consequences of hypoxia

199
Q

Consequence of longstanding hypoxia

A

Pulmonary hypertension and sec right heart strain

Polycythaemia due to stimulation of erythropoietin release from kidney
- high lvl of RBC to compensate for hypoxia

200
Q

Clinical definition of type 1 respi failure

A

Hypoxaemia w/o hypercapnia
- main problem is failure of alveolar-capillary units -> gas exchange affected more than ventilation

201
Q

Clinical definition of type 2 respi failure

A

Hypoxaemia w/ hypercapnia
- have component of poor ventilation resulting in retention CO2

202
Q

Why does type 1 respi failure often lead to type 2 respi failure?

A

Progression of disease/exhaustion of pt reach a point where compensatory measures fail

Exhaustion and insufficient O2 to brain -> ventilation problems w/ hypercapnia

203
Q

What are the diff clinical phenotypes of respi failure in pts w/ advanced COPD

A

Pink puffers

Blue bloaters

204
Q

Describe pink puffers

A

Pink complexion

Obv breathing effort -> just enough alveoli to stay alive but breathe hard to make sure each one is always ventilated

Emphysema is pri underlying pathology

Pt compensates for less surface area for gas exchange by hyperventilating

Few unventilated areas of lung -> CO2 retention no an issue

205
Q

Describe blue bloaters

A

Chronic bronchitis is pri underlying pathology

Marked ventilation/perfusion mismatch -> unable to shift enough air -> blood leaving lungs not oxygenated

Poor ventilation -> hypoxaemia and hypercapnia

Heart works hard to perfuse lung more -> right heart failure

Slow process -> brainstem re-setting to tolerate levels of hypxaemia and hypercapnia

206
Q

Principles of therapy for pts w/ COPD

A

Treat cause

Give O2

Bronchodilators

Assist ventilation when necessary

207
Q

Principles of therapy for blue bloaters

A

Blue bloaters have dulling of CO2 reflex -> too much O2 reduce rate of ventilation and exacerbate problems -> need to control O2 delivery and monitor closely

Respi (16 decks)

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