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Respiratory System > Patho > Flashcards

Patho Flashcards

1
Q

What are 2 etiologies of rhinitis?

A

1) Allergic (type 1 to allergens in atopic individual)

2) Infective (usually viral)

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2
Q

What is the pathogenesis of viral rhinitis?

A

Viral necrosis of surface epithelial cells
→ exudation of fluid and mucus
→ submucosal edema → swelling and nasal obstruction

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3
Q

Viral infection of the upper respiratory tract may spread to ___________ and predisposes the px to ______________.

A

Spread to lower tract and predisposes px to secondary bacterial infection

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4
Q

What is the pathogenesis of allergic rhinitis?

A

Prior exposure to allergen → activate Th2 and Tfh → B cells IgE switching → bind to FcεRI on mast cell

1) Repeat exposure to allergen → bind to IgE on Mast cell FcεRI

2) FcεRI crosslink → activte mast cells →

i) histamines
- ↑vascular permeability → exudate + mucosal edema
ii) Chymase
- stimulate mucus secretion

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5
Q

In allergic rhinitis, if the antigenic stimulus persists, the mucosa may become swollen and polyploid, leading to the formation of ______________.

A

Nasal polyps

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6
Q

What is a nasal polyp

A

Localised outgrowths of lamina propria due to accumulation of oedema fluid, inflammation and fibroblast proliferation
- Often multiple and bilateral and involve nasal cavity and paranasal sinuses
- usually 2­° to prolonged allergic rhinitis

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7
Q

What is sinusitis?

A

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

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8
Q

Sinusitis is often a/w ______, predisposes a px to __________ and in severe cases may spread to _______.

A

a/w rhinitis

predispose to 2° bacterial infection (↓drainage of secretions)

spread to meninges

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9
Q

True or false:
Nasopharyngeal carcinomas are often detected early.

A

False.
Nasopharynx is an inaccessible site, tumours often undetected until they are sizeable or have spread

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10
Q

True or false.
Nasopharyngeal carcinoma is rare throughout most of the world but is endemic/common in SG.

A

True

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11
Q

What are 2 types of nasopharyngeal carcinoma?

A

1) Non-keratinizing carcinoma (95%)
2) Keratinizing squamous cell carcinoma
3) Basaloid squamous cell carcinoma

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12
Q

How is non-keratinising NPC differentiated from keratinising NPC?

A

Non-keratinising
- poorly differentiated
- intermingled lymphocytes amongst carcinoma cells

Keratinising
- resembles SCC
- a/w smoking and alcohol consumption
- keratin pearls

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13
Q

What are 3 main risk factors for NPC?

A

1) EBV infection @ young age
2) Salt-preserved food
3) FHx

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14
Q

True or false:
EBV infection alone is sufficient to incite the pathogenesis of NPC.

A

False.
Other factors must contribute to NPC development

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15
Q

Primary EBV infection is typically (severe/subclinical) in childhood, and is associated with later development of several malignancies, including __________ as EBV infects the nasopharyngeal epithelium and tonsillar B lymphocytes.

A

Subclinical in childhood (but Infection in adolescence more likely to be symptomatic (infectious mononucleosis or ‘glandular fever’))

Nasopharyngeal carcinoma

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16
Q

True or false:
In Singapore, annual screening (EBV IgA antibody test and nasoendoscopy) is recommended in people with strong family history (2 close family members with NPC).

A

True

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17
Q

What are the 2 screening tests for NPC?

A

1) EBV IgA
2) Nasoendoscopy

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18
Q

What are 3 symptoms of NPC?

A

1) Diplopia
- invasion of CN6

2) Hearing loss and tinnitus
- obstruction to eustachian tube/secretory otitis media

3) Nasal obstruction, epistaxis, serous nasal discharge

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19
Q

What is the most common cause of epiglottitis in children?

A

Haemophilus influenzae

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20
Q

What are 2 childhood disease that (i) cause airway obstruction (ii) largely eradicated by vaccination in SG?

A

1) Corynebacterium diphtheriae
- exotoxin → epithelial necrosis → pseudomembrane → aspirated → airway obstruction
- DTaP vax

2) Haemophilus influenzae
- acute epiglottis → airway obstruction
- HiB vax

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21
Q

Acute pharyngitis and laryngitis is usually caused by (bacterial/viral) infection

A

Viral

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22
Q

What are 3 symptoms of Acute pharyngitis and laryngitis?

A

1) Sore throat (supraglottic)
2) Hoarseness (glottic)
3) Cough
4) Tracheal soreness (subglottic/trachea)

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23
Q

What is stridor?

A

breathing sound due to large airway obstruction,
usually worse in inspiration

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24
Q

What is croup?

A

In children, cough + stridor due to infection = croup

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25
Q

What is the common complication of URTIs in elderly/ debilitated/ unconscious individuals?

A

Bronchopneumonia
- cough reflex is poor and infected material may not be coughed up but pass into the smaller airways and rest of lung

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26
Q

What is Allergic pharyngolaryngeal oedema?

A

Life-threatening Type I hypersensitivity reaction

a/w: facial oedema and bronchospasm

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27
Q

Acute toxic laryngitis is an important cause of death in _______.

A

Fires

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28
Q

Chronic laryngitis is common in what population, leading to increased risk of _________________.

A

Heavy smokers

↑risk of SCC
- chronic irritation of epithelium → squamous metaplasia → ↑ risk of dysplasia

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29
Q

What is 1 example of a benign lesion of the larynx?

A

“Singer’s nodules” (vocal cord nodules
- reactive nodular thickenings of vocal cords seen in singers and chronic smokers

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30
Q

Laryngeal carcinomas are most commonly what type?

A

Squamous cell carcinoma (95%)

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31
Q

Glottic squamous cell carcinomas present earlier and often lower stage at presentation than supraglottic and subglottis tumours because ___________________.

A

Poor lymphatic supply of glottic region

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32
Q

SCC of the larynx can occur in __________________ regions and is locally invasive, spreading first to _______________.
They have ___________ growth patterns.

A
  • supraglottic, glottic or subglottic regions
  • regional lymph nodes
  • polyploid/ulcerative
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33
Q

What is atelectasis?

A

Collapsed lung

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34
Q

What are 3 etiologies of atelectasis?

A

1) Resorption: airway obstruction

2) Compression: pneumothorax, pleural effusion or post-op poor lung expansion

3) Contraction: scarring of lung/pleura, loss of surfactant

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35
Q

What are 2 normal defences of the lungs against infection?

A

1) Mucocilliary ladder
2) Cough reflex
3) Phagocytosis by alveolar macrophages

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36
Q

What are 3 factors that may increase the risk of LRTIs?

A

1) Poor swallowing
2) ↓cough reflex
3) Smoking
4) Intubation
5) Prior infection

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37
Q

Bronchitis and bronchiolitis is common and usually due to (bacteria/viruses).

A

Viruses
eg. Influenza tracheobronchitis, Respiratory syncitial virus bronchiolitis, systemic (eg. measles, VSV)

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38
Q

What is pneumonia?

A

Infective inflammation and consolidation of lung
(filling of airspaces by inflammatory exudate which renders affected area solid and airless)

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39
Q

How are bacterial pneumonia and viral pneumonitis differentiated on CXR?

A

Bacterial: air space spread
- consolidation
- bronchopneumonia
- lobar pneumonia

Viral: interstitial spread
- no consolidation but interstitial markings

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40
Q

What is pneumonitis?

A

Inflammatory disease dominated by interstitial inflammation

Apart from infection, many other causes (e.g. inhaled toxins and allergens, drug reactions, irradiation, connective tissue disease)

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41
Q

Bronchopneumonia vs Lobar pneumonia

A

Broncho:
- bronchi → alveoli
- “tree trunk appearance”
- common in infancy, old age, debilitated
- usually affects lower lobes more

Lobar
- alveoli and bronchioles → whole lobe
- well confined infection
- > virulent pathogens (eg. Klebsiella, Strep pneumo)

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42
Q

Community-acquired pneumonia is usually caused by (gram stain) bacteria.
Most common: __________
Others: ____________(3)

A

CAP usually gram positive:
#1: Strep pneumo
Others:
1) H. influenzae
2) Legionella
3) Mycoplasma
4) M. TB
5) Viral

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43
Q

Hospital-acquired pneumonia is usually caused by (gram stain) bacteria.
eg. (3)

A

HAP usually gram-negative
eg. Klebsiella, E. coli, Pseudomonas

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44
Q

Microbiological investigation of sputum in intubated patients often a problem because of _________, may require direct sampling of affected lung by __________.

A

Colonisation
so need Bronchoalveolar lavage (BAL)

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45
Q

Atypical/Non-tuberculous mycobacteria are (more/less) virulent than TB and cause disease mainly in____________.

A

Less virulent
- mainly in immunocompromised or pre-existing lung disease

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46
Q

What is tuberculosis?

A

A chronic pneumonia which is communicable, granulomatous, caused by Mycobacterium tuberculosis.
- usually affects lungs (90%) but can affect any organ or tissue

High prevalence where there is poverty, crowding and chronic
debilitating illness
Certain disease states also increase the risk: Diabetes, chronic
lung disease, alcoholism, HIV infection

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47
Q

TB often spreads via _____________, but if it enters the blood supply, the px will develop __________.

A

Usually spread via bronchi/lymphatics into pleural space

Hematogenous spread: Miliary TB

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48
Q

In which condition is “Ghon focus” seen?

A

Primary pulmonary tuberculosis

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49
Q

Primary TB occurs in (sensitised/unsensitised) hosts.

Lung lesion often (small/big) just beneath pleura “___________”, lymph node involvement more
evident.

A

Unsensitised
- small lung lesion
- form “Ghon focus”

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50
Q

95% of primary TB cases are self-resolving via CD4+ cell mediated immunity leaving ______________________.

A

Area of healed caseation → small calcified nodule @ infection site

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51
Q

True or false:
In self-resolved primary TB, viable organisms may lie dormant for decades as latent TB and may not by symptomatic but can spread the disease to immunocompromised individuals.

A

False:
Latent TB → no active disease → non-transmittable

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52
Q

Uncommonly, in progressive primary TB, there is continuing enlargement of the caseating granulomas in lymph nodes. These can spread by:
i) ___________________
ii) __________________

A

Spread occurs by the enlarging nodes eroding either through:

i) the wall of a bronchus (tuberculous bronchopneumonia)
ii) into a thin-walled blood vessel (miliary TB)

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53
Q

What is the CXR presentation of miliary TB?

A

many tiny spots distributed throughout the lung fields with the appearance similar to millet seed

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54
Q

Secondary TB occurs in (sensitised/unsensitised) individuals and commonly presents in (immunocompromised/immunocompetent) individuals?

A

Sensitised

Immunocompetent adults

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55
Q

In secondary TB there is (more/less) lymph node involvement than primary TB.

A

Less

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56
Q

In which condition is “Assmann focus” seen?

A

Secondary pulmonary TB

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57
Q

In secondary TB, healing of the apical lesion usually occurs, leaving a central area of caseous necrotic material (may still contain bacteria) surrounded by a thick, dense collagenous wall, which often calcifies (__________ TB)

A

Fibrocaseous TB

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58
Q

What is aspiration pneumonia?

A

Aspiration of mixed organism ± gastric acid ± food → infective pneumonia + chemical damage

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59
Q

Aspiration pneumonia most commonly occurs in what type of px? Thus, what type of organisms are usually found in aspiration pneumonia? They frequently lead to lung __________.

A

Unconscious/impaired swallowing → Anaerobes and oropharyngeal bacteria → lung abscesses

60
Q

What is atypical pneumonia?

A

Symptoms of pneumonia but there is absence of consolidation on Xray.

  • characterised by minimal airspace exudate, instead there is marked infiltration of the alveolar septa/interstitium by chronic inflammatory cells (pneumonitis)
61
Q

What are 3 causative organism of atypical pneumonia?

A

1) Mycoplasma
2) Chlamydia
3) Rickettsia
4) Some viruses

62
Q

What are 2 viral causative organisms for viral pneumonia?

A

1) Influenza (eg. H5N1)
2) COVID-19 (SARS-CoV2)
3) SARS-CoV1

63
Q

In severe cases, viral pneumonia can lead to _______________________.

A

Acute respiratory distress syndrome

64
Q

What are 3 causative organisms of opportunistic pneumonia?

A

1) Mycobacterium (TB/atypical)

2) Viruses (usually systemic reactivation eg. CMV, HSV)

3) Fungi (eg. Candida, Aspergillus, Pneuomocystis jirovecii)

65
Q

What is bronchiectasis?

A

Permanent abnormal dilatation of the main bronchi
- may contain purulent secretions, chronic inflammation of wall with loss of normal epithelium

66
Q

What is the common presentation of bronchiectasis?

A

Recurrent infection and hemoptysis

67
Q

What are 2 main factors predisposing a px to bronchiectasis?

A

1) Interference with drainage of secretions e.g. :
a) obstruction of proximal airway
b) abnormality in viscosity of mucus (cystic fibrosis)
c) immotile cilia syndrome

2) Recurrent and persistent infection

68
Q

What are 3 complications of bronchiectasis?

A

1) Chronic suppuration
2) Spread of infection beyond lung
3) Massive hemoptysis
4) Loss of normal lung parenchyma → respi failure, cor pulmonale

69
Q

What is a lung abscess?

A

Localised area of suppurative necrosis, usually forming large
cavities

70
Q

What are 3 common causes of infection and thus lung abscess?

A

1) Pulmonary infarction
2) Aspiration
3) Bronchial obstruction
4) Bronchiectasis
5) Staph aureus

71
Q

Multiple lung abscesses suggest (intra/extrapulmonary spread)?

A

Multiple lung abscesses commonly septic emboli (extra pulmonary)

72
Q

What are 3 complications of lung abscesses?

A

1) Rupture into pleura → empyema and pneumothorax

2) Haemorrhage into pulmonary vessel

3) Bacteraemia

73
Q

Obstructive lung disease:
- problem with (ventilation/perfusion)
- usually at level of __________-
- (exhalation/inhalation) more effected and requires more effort
- (wheeze/stridor) may be heard

A

Ventilation issue
- usually at level of small branches of bronchial tree
- exhalation more affected
- wheeze heard

74
Q

What is obstructive sleep apnoea?

A

Episodes of partial or complete closing of the upper airways during sleep → wake repeated to gasp for air

  • More common in men, obesity. The jaw and tongue fall backwards and obstruct the airway.
75
Q

What are 2 presentations of obstructive sleep apnea?

A

1) Hypoxemia
2) Poor sleep (fatigue, daytime somnolence)

76
Q

What is asthma?

A

Chronic disease affecting bronchioles:
- recurring episodes of bronchospasm and excessive production of mucus
- can be precipitated by atopic or non-atopic (airways are hypersensitive)

77
Q

What happens in severe and progressive asthma?

A

Status asthmaticus:
prolonged bronchospasm and mucus plugging results in respiratory failure

78
Q

What is the pathogenesis of allergic asthma?

A

1) Previous sensitisation causes IgE mediated response → activate mast cells + direct stimulation of nerve receptors

2) Mast cells release chemical mediators →
i) recruitment of eosinophils
ii) bronchoconstriction
iii) ↑ vascular permeability
iv) ↑ mucus secretion

3)Recruited eosinophils and Th cells release further mediators → amplify and sustain inflammatory response

79
Q

What are the structural changes in asthma (5)?

A

1) Hyperactivity and hypertrophy of smooth muscle of bronchus

2) Hypersecretion of mucus

3) Mucosal oedema

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

5) Deposition of collagen beneath bronchial epithelium in longstanding cases

80
Q

In asthma, the restricted airlow is (reversible/irreversible) whereas in COPD it is (reversible/irreversible)

A

Asthma: reversible
COPD: not fully reversible

81
Q

What are 3 main pathologies contributing to COPD?

A

1) Emphysema
- destruction of airspaces + loss of elastic recoil

2) Chronic bronchitis
- mucus hypersecretion and luminal narrowing

3) Bronchiolitis
- narrowing of smaller airways by inflammation and scarring

82
Q

What is emphysema?

A

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

  • Destruction of alveolar walls → loss of elastic recoil in lungs → ↓ gas exchange capacity
83
Q

In which condition are bullas seen?

A

Emphysema

84
Q

How does smoking cause emphysema?

A

1) Inhibits effect of protease inhibitors, potentiating tissue destruction (proteases normally inactivated by extracellular protease inhibitors)

2) contains abundant free radicals → tissue damage

3) Persistent irritation→ ↑ inflammatory cells in the lungs which themselves release mediators and enzymes

85
Q

Why are px with congenital α-1-antitrypsin deficiency at high risk of developing emphysema?

A

Normally, proteases secreted by inflammatory cells are inactivated by extracellular protease inhibitors in the lung e.g. alpha-1-antitrypsin.

Deficiency
→ Imbalance in activity of proteases and protease inhibitors

→ parenchymal destruction by extracellular proteases/elastases

86
Q

What is chronic bronchitis?

A

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

  • luminal obstruction + luminal narrowing → alveolar hypoventilation
87
Q

What is bronchiolitis?

A

Inflammation of airways <2mm in diameter:
- Macrophages and lymphoid cells infiltrate airway wall
- May progress and lead to scarring and narrowing of airways, contributing to functional airways obstruction

88
Q

What are 2 risk factors for COPD?

A

1) Lifetime smoking exposure
2) Recurrent childhood infections
3) Occupational exposure to dust

89
Q

Exacerbations of COPD are usually _________ or _____________

A

Infective or due to poor air quality

90
Q

Death related to COPD is usually due to ______________ or ______________.

A

Respiratory failure or 2° heart failure (cor pulmonale)

91
Q

What are Diffuse parenchymal lung diseases?

A

Group of lung diseases characterised by widespread inflammatory pathology, predominantly in the interstitium.

  • ↓ compliance of lungs. Oedema (in acute form) and fibrosis (in chronic form) of alveolar walls renders them rigid.
  • Thickening of alveolar walls → ↓ gas exchange
92
Q

What are 3 main histological patterns of reaction in lung following damage?

A

1) Haemorrhage and fibrin exudation into alveoli (hyaline membranes)

2) Oedema and inflammation of interstitium

3) Macrophage accumulation in alveolar spaces

4) Fibrosis in interstitium or alveolar spaces

93
Q

What is Acute Respiratory Distress Syndrome (ARDS)?

A

A severe form of acute lung injury (acute form of diffuse parenchymal lung disease) caused by diffuse alveolar and capillary damage.

  • high mortaliity, others left with sig. ↓lung f(x)
94
Q

What are 3 common causes of ARDS?

A

1) Systemic sepsis
2) Severe trauma/burns
3) Inhalation of toxic fumes

95
Q

What are the 2 phases of ARDS?

A

1) Acute exudative
- interstitial edema + high protein exudation into alveoli (hyaline membranes)

2) Late organisation
- regeneration of type 2 pneumocytes
- organisation of hyaline membranes w fibrosis

96
Q

What are 5 causes of diffuse parenchymal lung diseases?

A

1) ARDs
2) Atypical pneumonias
3) Connective tissue diseases
4) Sarcoidosis
5) Drug-induced
6) Radiation damage
7) Pneumoconiosis (caused by inhaling inorganic dusts)
8) Extrinsic allergic alveolitis/hypersensitivity pneumonitis (caused by immune reactions to inhaled organic dusts)
9) Smoking-related
10) ‘Idiopathic’

97
Q

What is end stage pulmonary fibrosis?

A

“Honeycomb lung”
Chronic respiratory impairment and reduced diffusion capacity
- death due to combination of respi and cardiac failure

98
Q

In what condition is “honeycomb lung” seen?

A

End stage pulmonary fibrosis

99
Q

What is the commonest chronic diffuse parenchymal lung disease?

A

Idiopathic pulmonary fibrosis/ Cryptogenic fibrosing alveolitis

  • lung biopsy shows “usual interstitial pneumonia” pattern
100
Q

What is hypersensitivity pneuomonitis?

A

Lung disease due to hypersensitivity to inhaled organic antigens

  • most commonly due to:
    1) Animal proteins
    2) Microbial agents
  • can be acute or chronic
101
Q

What is pneumoconiosis?

A

Disease of lungs caused by inhalation of dust (eg. silica, coal dust, asbestos)
- Interaction of dust with defence mechanisms of lung, leading to inflammation, release of cytokines and stimulation of fibrosis

102
Q

What are 3 diseases associated with asbestos?

A

1) Pleural plaques
2) Pleural effusions and thickening
3) Asbestosis (progressive chronic lung fibrosis)
4) Malignant mesothelioma
5) Lung carcinoma

103
Q

What are 3 causes of granulomas in the lung?

A

1) Infection (TB, fungal)
2) Foreign material (eg. pneumoconiosis, hypersensitivity pneumonitis)
3) Sarcoidosis

104
Q

What is sarcoidosis?

A

Systemic disease of unknown cause characterised by non-necrotising granulomas in many tissues and organs

105
Q

True or false:
80% of lung cancer (worldwide) occurs in active or recent smokers.

Risk of cancer increases with number of cigarettes smoked and age at which smoking was started (‘pack years’)

Stopping smoking reduces risk of lung cancer (never returns to normal if >20/d)

Passive smokers have double risk compared to those not exposed

A

True, just read

106
Q

What are the 2 main histological types of lung cancer?

A

1) Small cell carcinoma (20%)
2) Non-small cell carcinoma
- Squamous cell carcinoma
- Adenocarcinoma
- Others (eg. large cell carcinoma)

107
Q

What are 3 methods of spread in lung cancer?

A

1) Local
- lungs, pleura, mediastinal structures, chest wall

2) Lymphatic

3) Transcoelomic
- pleural and pericardial effusion

4) Hematogenous

108
Q

Squamous cell lung carcinoma:
- highly a/w _________
- Commoner in _________
- Often undergoes __________
- Often preceded by __________

A

Squamous cell carcinoma:
- highly a/w smoking
- Commoner in M (often central)
- Often undergoes central cavitation
- Often preceded by squamous meta/dysplasia

109
Q

Lung adenocarcinoma:
- equal gender incidence
- most as closely a/w smoking compared to _______
- special type _______________

A

Lung adenocarcinoma:
- equal gender incidence
- most as closely a/w smoking compared to squamous cell/small cell lung carcinoma

  • special type: minimally invasive carcinoma (bronchioalveolar carcinoma)
    →spreads along alveolar septa → looks like consolidation rather than mass on CXR
110
Q

Small cell lung carcinoma:
- high a/w ______
- tumour cells show __________
- usually central (slow/rapid) rate of growth
- (few/most) metastasised by time of diagnosis

A

Small cell lung carcinoma:
- high a/w smoking
- tumour cells show neuroendocrine differentiation
- usually central rapid rate of growth
- most metastasised by time of diagnosis

111
Q

True or false:
All subtypes of lung cancer have absolutely dismal prognosis as most diagnosed are like stage 4.

A

True :(

112
Q

Why can lung cancer not just be routinely screen for with CXR?

A

1) no early symptoms (until metastasis)
2) many lesions found on chest XRay screening have already spread
3) only way to pick up small lesions is by CT scan

113
Q

What are 3 paraneoplastic syndromes caused by lung cancer?

A

1) Endocrine disturbances (esp small cell lung cancer)
- SIADH, ectopic ACTH secretion, hyperCa

2) Neurological syndromes
3) Hypertrophic pulmonary osteoarthropathy

114
Q

How do SCLC and NSCLC differ in their treatment options?

A

NSCLC: if haven’t spread out of lung can resect (but most inoperable)

SCLC: sensitive to radio and chemo but most survival poor despite local control

115
Q

Which of the lung cancer subtypes have recently been found to be effective treated using EGFR TKIs?

A

Adenocarcinoma in non smoking women with EGFR mutation (L858R)

116
Q

The pleura is lined by _____________

A

Mesothelial cells

117
Q

There is a constant generation of fluid from the _____________ which is resorbed by the _____________.

A

Fluid from parietal pleura → resorbed by visceral

118
Q

What are 4 types of abnormal accumulations in the pleura?

A

1) Empyema (pus)
2) Hemothorax (blood)
3) Chylothorax (chyle from thoracic duct)
4) Pneuomothorax (air)
5) Fluid effusion
- transudate: CHF, hypoalbuminemia
- exudate: infection, neoplasm

119
Q

How do pleural effusions appear on CXR?

A

Loss of costophrenic angle

120
Q

What is pleurisy?

A

Acute inflammation of the pleura, usually due to infection
- Fibrinous or purulent exudate is seen on the pleural surface
- can be organised to form fibrous pleural adhesions

121
Q

What are 3 causes of pneumothorax?

A

1) Trauma
2) Iatrogenic
3) Primary spontaneous pneumothorax (thin young men/rupture of congenital subpleural apical bleb)
4) Rupture of emphysematous bulla
5) Asthmatics

122
Q

What is the most common tumour of the pleura?

A

Metastatic carcinoma

123
Q

What is the no. 1 primary neoplasm of the pleura?

A

Malignant mesothelioma
- a/w asbestos exposure
- spread around lungs and mediastinal structures
- poor prognosis

124
Q

What are 2 histological features of mesotheliomas?

A

1) tubular (‘epithelioid’)
2) spindle cell (‘sarcomatoid’) patterns

125
Q

What are 2 common mediastinal mass lesions in children?

A

1) Lymphoma/leukemia
2) Neuroblastoma/other neural tumours

126
Q

What are 4 common mediastinal mass lesions in adults?

A

1) Metastases/direct invasion from lung cancer

2) Primary TB

3) Thymoma

4) Lymphoma
- Specific types arise in mediastinum: T cell lymphoblastic lymphoma (adolescent/young adult males), Primary mediastinal large B cell lymphoma (young adult females), Hodgkin lymphoma

5) Germ cell tumours (adolescent/young adult males)

127
Q

How do thymic tumours present?

A

Anterior mediastinal masses

128
Q

What are 3 main tumours of the thymus?

A

1) Thymoma
2) Lymphoma
3) Germ cell tumour

129
Q

What is a thymoma?

A

Neoplasm derived from thymic epithelial cells (lymphocytes are present but are non-neoplastic)
- a/w myasthenia gravis
- encapsulation/invasion of local structures is main determinant of operability and hence prognosis

130
Q

What are 3 common developmental lung abnormalities?

A

1) Bronchia atresia

2) Bronchogenic cysts
- accessory bronchial buds sealed off from rest of airway

3) Bronchopulmonary sequestration
- area of lung that has no respiratory function and no connection w bronchial tree, only systemic blood supply

131
Q

What is neonatal respiratory distress syndrome?

A

Premature babies → deficiency of surfactant
→ alveolar collapse
→ hypoxia and damage to alveoli/endothelium → hyaline membranes

132
Q

How does immotile cilia syndrome result in recurrent infections?

A

Cilia have abnormal structure or are unable to beat in coordinated fashion → ↓mucociliary clearance

133
Q

How does cystic fibrosis affect the lung?

A

Symptoms due to production of abnormally viscous mucus that cannot be cleared from lungs, pancreas, intestines

→ Stagnant mucus → repeated infections and
bronchiectasis

→ death by infection or respiratory failure in early adulthood

134
Q

What is the main cause of pulmonary capillary congestion?

A

Left heart failure

135
Q

In which condition are hemosiderin-laden macrophages seen?

A

“Heart failure” cells
- pulmonary edema 2° to left heart failure

136
Q

What are 4 causes of pulmonary hypertension?

A

1) Left heart disease (esp mitral valve → P transmitted to pulmonary system)

2) Shunts from L → R heart (eg. ASD, VSD)

3) Chronic lung disease (loss of normal capillaries + hypoxic vasoconstriction of arterioles)

4) Sequelae of pulmonary emboli

5) Idiopathic

137
Q

How does pulmonary hypertension worsen in a cycle?

A

Sustained ↑ pulmonary arterial P
→ Medial hypertrophy in muscular arteries and intimal proliferation
→ narrowing/occlusion, ↓ cross-sectional area

→ further ↑ pressure

138
Q

What is cor pulmonale?

A

Heart failure secondary to lung disease
- Long term need to pump at higher pressures eventually causes the right heart to fail.

139
Q

The outcome of pulmonary emboli depend on (i)______ and (ii)___________.

A

Size and local haemodynamics

140
Q

How can pulmonary emboli lead to pulmonary hypertension?

A

Recurrent small thromboemboli
→ organisation of thrombi in small arteries
→ permanent occlusion
→ progressive ↓ in pulmonary vasculature
→ pulmonary HTN

141
Q

What is pulmonary vasculitis?

A

Inflammatory destruction of blood vessels results in bleeding into lungs.
- Repeated episodes → vessel damage → pulmonary hypertension
- eg. Granulomatosis w poly angiitis (Wegener granulomatosis), Eosinophilic granulomatosis w polyangiitis (Churg-Strauss syndrome)

142
Q

What are 2 ways oxygenation is measured?

A

1) Pulse oximeter
2) Arterial blood gas

143
Q

What are 2 main symptoms of respiratory failure?

A

1) Breathlessness/ air hunger
2) Hypoxia sequelae (eg. fatigue, cyanosis)

144
Q

What are 2 sequelae of longstanding hypoxia?

A

1) Pulmonary HTN and 2° right heart strain
2) Polycythemia (2° to EPO↑)

145
Q

What is the difference between type 1 and type 2 respiratory failure?

A

Type 1: Hypoxemia w/o hypercapnia
- poor gas exchange
- eg. alveolar edema, pulmonary embolism, atelectasis, emphysema
- often progress to type 2

Type 2: Hypoxemia w hypercapnia
- poor ventilation
- eg. airway obstruction, failure of neuromuscular ventilation

146
Q

What is the difference between “pink puffers” and “blue bloaters” in COPD?

A

Pink puffers:
- pink complexion, obvious breathing effort
- emphysema is 1° pathology
- less SA for gas exchange compensated by hyperventilation (few unventilated areas → CO2 retention not an issue)

Blue bloaters:
- poor ventilation → hypoxemia + hypercapnia (type 2 respi failure)
- chronic bronchitis is 1° pathology
- might have RHF (heart tries to compensate)
- cannot give too much O2

Respiratory System (10 decks)

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