Patho Flashcards
1
Q
What are 2 etiologies of rhinitis?
A
1) Allergic (type 1 to allergens in atopic individual)
2) Infective (usually viral)
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
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
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
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
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
7
Q
What is sinusitis?
A
Inflammation of the paranasal sinus linings of the maxillary, ethmoid and frontal sinuses
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
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
10
Q
True or false.
Nasopharyngeal carcinoma is rare throughout most of the world but is endemic/common in SG.
A
True
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
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
13
Q
What are 3 main risk factors for NPC?
A
1) EBV infection @ young age
2) Salt-preserved food
3) FHx
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
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
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
17
Q
What are the 2 screening tests for NPC?
A
1) EBV IgA
2) Nasoendoscopy
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
19
Q
What is the most common cause of epiglottitis in children?
A
Haemophilus influenzae
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
21
Q
Acute pharyngitis and laryngitis is usually caused by (bacterial/viral) infection
A
Viral
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)
23
Q
What is stridor?
A
breathing sound due to large airway obstruction,
usually worse in inspiration
24
Q
What is croup?
A
In children, cough + stridor due to infection = croup
25
What is the common complication of URTIs in elderly/ debilitated/ unconscious individuals?
Bronchopneumonia
- cough reflex is poor and infected material may not be coughed up but pass into the smaller airways and rest of lung
26
What is Allergic pharyngolaryngeal oedema?
Life-threatening Type I hypersensitivity reaction
a/w: facial oedema and bronchospasm
27
Acute toxic laryngitis is an important cause of death in _______.
Fires
28
Chronic laryngitis is common in what population, leading to increased risk of _________________.
Heavy smokers
↑risk of SCC
- chronic irritation of epithelium → squamous metaplasia → ↑ risk of dysplasia
29
What is 1 example of a benign lesion of the larynx?
"Singer's nodules" (vocal cord nodules
- reactive nodular thickenings of vocal cords seen in singers and chronic smokers
30
Laryngeal carcinomas are most commonly what type?
Squamous cell carcinoma (95%)
31
Glottic squamous cell carcinomas present earlier and often lower stage at presentation than supraglottic and subglottis tumours because ___________________.
Poor lymphatic supply of glottic region
32
SCC of the larynx can occur in __________________ regions and is locally invasive, spreading first to _______________.
They have ___________ growth patterns.
- supraglottic, glottic or subglottic regions
- regional lymph nodes
- polyploid/ulcerative
33
What is atelectasis?
Collapsed lung
34
What are 3 etiologies of atelectasis?
1) Resorption: airway obstruction
2) Compression: pneumothorax, pleural effusion or post-op poor lung expansion
3) Contraction: scarring of lung/pleura, loss of surfactant
35
What are 2 normal defences of the lungs against infection?
1) Mucocilliary ladder
2) Cough reflex
3) Phagocytosis by alveolar macrophages
36
What are 3 factors that may increase the risk of LRTIs?
1) Poor swallowing
2) ↓cough reflex
3) Smoking
4) Intubation
5) Prior infection
37
Bronchitis and bronchiolitis is common and usually due to (bacteria/viruses).
Viruses
eg. Influenza tracheobronchitis, Respiratory syncitial virus bronchiolitis, systemic (eg. measles, VSV)
38
What is pneumonia?
Infective inflammation and consolidation of lung
(filling of airspaces by inflammatory exudate which renders affected area solid and airless)
39
How are bacterial pneumonia and viral pneumonitis differentiated on CXR?
Bacterial: air space spread
- consolidation
- bronchopneumonia
- lobar pneumonia
Viral: interstitial spread
- no consolidation but interstitial markings
40
What is pneumonitis?
Inflammatory disease dominated by interstitial inflammation
Apart from infection, many other causes (e.g. inhaled toxins and allergens, drug reactions, irradiation, connective tissue disease)
41
Bronchopneumonia vs Lobar pneumonia
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)
42
Community-acquired pneumonia is usually caused by (gram stain) bacteria.
Most common: __________
Others: ____________(3)
CAP usually gram positive:
#1: Strep pneumo
Others:
1) H. influenzae
2) Legionella
3) Mycoplasma
4) M. TB
5) Viral
43
Hospital-acquired pneumonia is usually caused by (gram stain) bacteria.
eg. (3)
HAP usually gram-negative
eg. Klebsiella, E. coli, Pseudomonas
44
Microbiological investigation of sputum in intubated patients often a problem because of _________, may require direct sampling of affected lung by __________.
Colonisation
so need Bronchoalveolar lavage (BAL)
45
Atypical/Non-tuberculous mycobacteria are (more/less) virulent than TB and cause disease mainly in____________.
Less virulent
- mainly in immunocompromised or pre-existing lung disease
46
What is tuberculosis?
A chronic pneumonia which is communicable, granulomatous, caused by Mycobacterium tuberculosis.
- usually affects lungs (90%) but can affect any organ or tissue
## Footnote
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
47
TB often spreads via _____________, but if it enters the blood supply, the px will develop __________.
Usually spread via bronchi/lymphatics into pleural space
Hematogenous spread: Miliary TB
48
In which condition is "Ghon focus" seen?
Primary pulmonary tuberculosis
49
Primary TB occurs in (sensitised/unsensitised) hosts.
Lung lesion often (small/big) just beneath pleura "___________", lymph node involvement more
evident.
Unsensitised
- small lung lesion
- form "Ghon focus"
50
95% of primary TB cases are self-resolving via CD4+ cell mediated immunity leaving ______________________.
Area of healed caseation → small calcified nodule @ infection site
51
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.
False:
Latent TB → no active disease → non-transmittable
52
Uncommonly, in progressive primary TB, there is continuing enlargement of the caseating granulomas in lymph nodes. These can spread by:
i) ___________________
ii) __________________
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)
53
What is the CXR presentation of miliary TB?
many tiny spots distributed throughout the lung fields with the appearance similar to millet seed
54
Secondary TB occurs in (sensitised/unsensitised) individuals and commonly presents in (immunocompromised/immunocompetent) individuals?
Sensitised
Immunocompetent adults
55
In secondary TB there is (more/less) lymph node involvement than primary TB.
Less
56
In which condition is "Assmann focus" seen?
Secondary pulmonary TB
57
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)
Fibrocaseous TB
58
What is aspiration pneumonia?
Aspiration of mixed organism ± gastric acid ± food → infective pneumonia + chemical damage
59
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 __________.
Unconscious/impaired swallowing → Anaerobes and oropharyngeal bacteria → lung abscesses
60
What is atypical pneumonia?
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
What are 3 causative organism of atypical pneumonia?
1) Mycoplasma
2) Chlamydia
3) Rickettsia
4) Some viruses
62
What are 2 viral causative organisms for viral pneumonia?
1) Influenza (eg. H5N1)
2) COVID-19 (SARS-CoV2)
3) SARS-CoV1
63
In severe cases, viral pneumonia can lead to _______________________.
Acute respiratory distress syndrome
64
What are 3 causative organisms of opportunistic pneumonia?
1) Mycobacterium (TB/atypical)
2) Viruses (usually systemic reactivation eg. CMV, HSV)
3) Fungi (eg. Candida, Aspergillus, Pneuomocystis jirovecii)
65
What is bronchiectasis?
Permanent abnormal dilatation of the main bronchi
- may contain purulent secretions, chronic inflammation of wall with loss of normal epithelium
66
What is the common presentation of bronchiectasis?
Recurrent infection and hemoptysis
67
What are 2 main factors predisposing a px to bronchiectasis?
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
What are 3 complications of bronchiectasis?
1) Chronic suppuration
2) Spread of infection beyond lung
3) Massive hemoptysis
4) Loss of normal lung parenchyma → respi failure, cor pulmonale
69
What is a lung abscess?
Localised area of suppurative necrosis, usually forming large
cavities
70
What are 3 common causes of infection and thus lung abscess?
1) Pulmonary infarction
2) Aspiration
3) Bronchial obstruction
4) Bronchiectasis
5) Staph aureus
71
Multiple lung abscesses suggest (intra/extrapulmonary spread)?
Multiple lung abscesses commonly septic emboli (extra pulmonary)
72
What are 3 complications of lung abscesses?
1) Rupture into pleura → empyema and pneumothorax
2) Haemorrhage into pulmonary vessel
3) Bacteraemia
73
Obstructive lung disease:
- problem with (ventilation/perfusion)
- usually at level of __________-
- (exhalation/inhalation) more effected and requires more effort
- (wheeze/stridor) may be heard
Ventilation issue
- usually at level of small branches of bronchial tree
- exhalation more affected
- wheeze heard
74
What is obstructive sleep apnoea?
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
What are 2 presentations of obstructive sleep apnea?
1) Hypoxemia
2) Poor sleep (fatigue, daytime somnolence)
76
What is asthma?
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
What happens in severe and progressive asthma?
Status asthmaticus:
prolonged bronchospasm and mucus plugging results in respiratory failure
78
What is the pathogenesis of allergic asthma?
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
What are the structural changes in asthma (5)?
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
In asthma, the restricted airlow is (reversible/irreversible) whereas in COPD it is (reversible/irreversible)
Asthma: reversible
COPD: not fully reversible
81
What are 3 main pathologies contributing to COPD?
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
What is emphysema?
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
In which condition are bullas seen?
Emphysema
84
How does smoking cause emphysema?
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
Why are px with congenital α-1-antitrypsin deficiency at high risk of developing emphysema?
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
What is chronic bronchitis?
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
What is bronchiolitis?
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
What are 2 risk factors for COPD?
1) Lifetime smoking exposure
2) Recurrent childhood infections
3) Occupational exposure to dust
89
Exacerbations of COPD are usually _________ or _____________
Infective or due to poor air quality
90
Death related to COPD is usually due to ______________ or ______________.
Respiratory failure or 2° heart failure (cor pulmonale)
91
What are Diffuse parenchymal lung diseases?
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
What are 3 main histological patterns of reaction in lung following damage?
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
What is Acute Respiratory Distress Syndrome (ARDS)?
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
What are 3 common causes of ARDS?
1) Systemic sepsis
2) Severe trauma/burns
3) Inhalation of toxic fumes
95
What are the 2 phases of ARDS?
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
What are 5 causes of diffuse parenchymal lung diseases?
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
What is end stage pulmonary fibrosis?
"Honeycomb lung"
Chronic respiratory impairment and reduced diffusion capacity
- death due to combination of respi and cardiac failure
98
In what condition is "honeycomb lung" seen?
End stage pulmonary fibrosis
99
What is the commonest chronic diffuse parenchymal lung disease?
Idiopathic pulmonary fibrosis/ Cryptogenic fibrosing alveolitis
- lung biopsy shows "usual interstitial pneumonia" pattern
100
What is hypersensitivity pneuomonitis?
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
What is pneumoconiosis?
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
What are 3 diseases associated with asbestos?
1) Pleural plaques
2) Pleural effusions and thickening
3) Asbestosis (progressive chronic lung fibrosis)
4) Malignant mesothelioma
5) Lung carcinoma
103
What are 3 causes of granulomas in the lung?
1) Infection (TB, fungal)
2) Foreign material (eg. pneumoconiosis, hypersensitivity pneumonitis)
3) Sarcoidosis
104
What is sarcoidosis?
Systemic disease of unknown cause characterised by non-necrotising granulomas in many tissues and organs
105
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
True, just read
106
What are the 2 main histological types of lung cancer?
1) Small cell carcinoma (20%)
2) Non-small cell carcinoma
- Squamous cell carcinoma
- Adenocarcinoma
- Others (eg. large cell carcinoma)
107
What are 3 methods of spread in lung cancer?
1) Local
- lungs, pleura, mediastinal structures, chest wall
2) Lymphatic
3) Transcoelomic
- pleural and pericardial effusion
4) Hematogenous
108
Squamous cell lung carcinoma:
- highly a/w _________
- Commoner in _________
- Often undergoes __________
- Often preceded by __________
Squamous cell carcinoma:
- highly a/w smoking
- Commoner in M (often central)
- Often undergoes central cavitation
- Often preceded by squamous meta/dysplasia
109
Lung adenocarcinoma:
- equal gender incidence
- most as closely a/w smoking compared to _______
- special type _______________
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
Small cell lung carcinoma:
- high a/w ______
- tumour cells show __________
- usually central (slow/rapid) rate of growth
- (few/most) metastasised by time of diagnosis
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
True or false:
All subtypes of lung cancer have absolutely dismal prognosis as most diagnosed are like stage 4.
True :(
112
Why can lung cancer not just be routinely screen for with CXR?
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
What are 3 paraneoplastic syndromes caused by lung cancer?
1) Endocrine disturbances (esp small cell lung cancer)
- SIADH, ectopic ACTH secretion, hyperCa
2) Neurological syndromes
3) Hypertrophic pulmonary osteoarthropathy
114
How do SCLC and NSCLC differ in their treatment options?
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
Which of the lung cancer subtypes have recently been found to be effective treated using EGFR TKIs?
Adenocarcinoma in non smoking women with EGFR mutation (L858R)
116
The pleura is lined by _____________
Mesothelial cells
117
There is a constant generation of fluid from the _____________ which is resorbed by the _____________.
Fluid from parietal pleura → resorbed by visceral
118
What are 4 types of abnormal accumulations in the pleura?
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
How do pleural effusions appear on CXR?
Loss of costophrenic angle
120
What is pleurisy?
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
What are 3 causes of pneumothorax?
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
What is the most common tumour of the pleura?
Metastatic carcinoma
123
What is the no. 1 primary neoplasm of the pleura?
Malignant mesothelioma
- a/w asbestos exposure
- spread around lungs and mediastinal structures
- poor prognosis
124
What are 2 histological features of mesotheliomas?
1) tubular (‘epithelioid’)
2) spindle cell (‘sarcomatoid’) patterns
125
What are 2 common mediastinal mass lesions in children?
1) Lymphoma/leukemia
2) Neuroblastoma/other neural tumours
126
What are 4 common mediastinal mass lesions in adults?
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
How do thymic tumours present?
Anterior mediastinal masses
128
What are 3 main tumours of the thymus?
1) Thymoma
2) Lymphoma
3) Germ cell tumour
129
What is a thymoma?
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
What are 3 common developmental lung abnormalities?
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
What is neonatal respiratory distress syndrome?
Premature babies → deficiency of surfactant
→ alveolar collapse
→ hypoxia and damage to alveoli/endothelium → hyaline membranes
132
How does immotile cilia syndrome result in recurrent infections?
Cilia have abnormal structure or are unable to beat in coordinated fashion → ↓mucociliary clearance
133
How does cystic fibrosis affect the lung?
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
What is the main cause of pulmonary capillary congestion?
Left heart failure
135
In which condition are hemosiderin-laden macrophages seen?
"Heart failure" cells
- pulmonary edema 2° to left heart failure
136
What are 4 causes of pulmonary hypertension?
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
How does pulmonary hypertension worsen in a cycle?
Sustained ↑ pulmonary arterial P
→ Medial hypertrophy in muscular arteries and intimal proliferation
→ narrowing/occlusion, ↓ cross-sectional area
→ further ↑ pressure
138
What is cor pulmonale?
Heart failure secondary to lung disease
- Long term need to pump at higher pressures eventually causes the right heart to fail.
139
The outcome of pulmonary emboli depend on (i)______ and (ii)___________.
Size and local haemodynamics
140
How can pulmonary emboli lead to pulmonary hypertension?
Recurrent small thromboemboli
→ organisation of thrombi in small arteries
→ permanent occlusion
→ progressive ↓ in pulmonary vasculature
→ pulmonary HTN
141
What is pulmonary vasculitis?
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
What are 2 ways oxygenation is measured?
1) Pulse oximeter
2) Arterial blood gas
143
What are 2 main symptoms of respiratory failure?
1) Breathlessness/ air hunger
2) Hypoxia sequelae (eg. fatigue, cyanosis)
144
What are 2 sequelae of longstanding hypoxia?
1) Pulmonary HTN and 2° right heart strain
2) Polycythemia (2° to EPO↑)
145
What is the difference between type 1 and type 2 respiratory failure?
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
What is the difference between "pink puffers" and "blue bloaters" in COPD?
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
