Week 4 - RESP Flashcards
Pneumonia, COPD, Smoking
1
Q
What are the 2 main microscopic features of COPD?
A
- peribronchial chronic inflammation - CB (IL-8/LTB4)
2. loss of alveolar wall without inflammation - Emphysema (elastases/proteases)
2
Q
What is the pathogenesis of cavity formation in TB?
A
Due to drainage of caseous material through bronchus
3
Q
What are complications of TB?
A
- colonisation of cavities by fungus (aspergillosis)
- bronchiectasis
- empyema
- arterial pseudoaneurysm
- fibrothorax
- bronchopleural fistula
4
Q
What are the modes of spread of primary pulmonary TB?
A
- spread from primary focus –> hilar/mediastinal LNs to form the primary complex (Gohn complex)
- direct extension of primary focus –> progressive pulmonary TB
- spread to pleura –> TB pleurisy and pleural effusion
- blood-borne spread –> miliary TB + meningitis
5
Q
What are the factors in the pathogenesis of cavitary TB?
A
IFN-gamma + proteases
6
Q
What is the difference in pathogenesis of caseating vs. non-caseating granulomas in TB?
A
Caseating = M1 activation Non-caseating = M2 activation
7
Q
What is secondary TB?
A
- occurs in previously exposed host and classically involves lung apices
- re-activation usually occurs with decreased immunity
- sensitised T cells cause increased tissue damage, avitation and increased systemic manifestations
8
Q
What are CXR findings of TB?
A
- lower and middle lobe nodules of consolidation
- hilar adenopathy
- pleural effusion
- cavitation - RARE (increase in secondary TB in upper lobes)
9
Q
What is etiology of pleural effusions?
A
- transudate –> cardaic failure, nephrotic syndrome
- exudate –> infection, TB, bronchial carcinoma
- blood –> trauma
- chyle –> ruptured thoracic duct
10
Q
What is a:
- Ghon focus?
- Ghon complex?
- Ranke complex?
A
Manifestations of primary TB
Ghon focus –> pulmonary lesion
Ghon complex –> pulmonary lesion + draining lymph nodes
Ranke complex –> calcified parenchymal tuberculoma + ipsilateral calcified hilar node
11
Q
What is the clinical Dx. of COPD?
A
FEV1 < 80%
FEV1/FVC < 70%
12
Q
What is the cause of the slight airway obstruction in emphysema?
A
Loss of normal stretching of smaller airways by alveoli due to alveolar wall damage –> “broken alveoli”
13
Q
Why is Cor Pulmonale more common in CB than emphysema?
A
- inflammation and fibrosis of bronchial walls affects associated BVs
- therefore pulmonary HTN is more common in CB
- RVH –> RVF (Cor Pulmonale)
14
Q
What is BOOP?
A
Brochiolitis Obliterans Organising Pneumonia
- type of non-infective pneumonia
- ractive to irritants –> hyperplasia of type II pneumocytes
15
Q
What are the features of chronic pneumonia and what is the commonest cause?
A
- chronic, lymphoid infiltrate
- no classic stages
- lung destruction –> granuloma, cavity, abscess
- commonest cause = TB
16
Q
What is the pathogenesis of SOB, pain and high fever in pneumonia?
A
SOB
-endothelial leakage of plasma into alveolar lumen means less space for air to travel (dyspnoea)
HIGH FEVER
-release of inflammatory mediators
PAIN
-release of chemical mediators –> chest pain
17
Q
What are gross and microscopic features of emphysema?
A
Gross:
- distended lungs
- black spots all over (increase in upper zone)
Micro:
- loss of alveolar wall (bullae)
- carbon pigment in centrilobular area
18
Q
What are gross and microscopic features of bronchiectasis?
A
Gross:
-dilated irregular bronchi filled with pus (visible till pleural margin)
Micro:
-destruction of bronchial epithelium, replaced by acute/chronic inflammation, necrosis, pus.
19
Q
What is the common type of pneumonia in a chronic smoker?
A
Bronchopneumonia
20
Q
The 2 factors causing chronic bronchitis are?
A
IL-8 + LTB4
21
Q
What are the common pathogens seen in purulent sputum of patients with bronchiectasis?
A
Mixed normal flora
22
Q
What are the 2 main types of emphysema?
A
- Centrilobular
- commonest
- increase in smokers
- primarily upper lobes - Panlobular
- congenital
- alpha1-antitrypsin deficiency
- involves all lung fields particularly bases
23
Q
True or False?
Majority of primary TB cases are asymptomatic
A
True
-95%
24
Q
How is lung cancer classified?
A
Small cell lung cancer (SCLC)
Non Small cell lung cancer (NSCLC)
-squamous cell carcinoma (SCC)
-adenocarcinoma (glandular)
25
What is the characteristic CXR finding of pleural effusion?
Loss of costophrenic angle
26
What is the classification of pneumothorax?
Trauma --> e.g. rib fracture
| Spontaneous --> peripheral bullous rupture
27
What are complications of emphysema?
- pneumothorax
- pulmonary HTN (increase in CB)
- lung cancer
- consolidation/infective exacerbation (increase in CB)
28
What are CXR findings of emphysema?
- hyperinflation of lungs --> flattened diaphragm, >10 posterior ribs, >6 anterior ribs
- decreased peripheral vascularity
- increased size of central pulmonary arteries
- hyperlucency of lungs
29
What is atelectasis and bronchiectasis?
Atelectasis
- complete or partial collapse of a lung or lobe
- develops when alveoli become deflated --> impaired gas exchange
Bronchiectasis
- permanent dilatation and thickening of bronchi characterised by chronic cough and recurrent secondary infections
- cough, copious amounts of purulent, foul-smelling sputum
30
What is the definition of chronic bronchitis?
- chronic inflammation of bronchi
| - defined as a productive cough that occurs every day for 3 months in a row for 2 consecutive years
31
What is the definition of emphysema?
- pathological lung condition marked by increased size of air spaces --> laboured breathing
- caused by irreversible expansion of alveoli/destruction of alveolar walls (decreased surface area) --> loss of elastic recoil --> GAS TRAPPING
32
Alveolar damage in centrilobular emphysema is due to?
Proteases
33
What are some complications of COPD?
- secondary infections (mucous/irritant retention)
- pneumothorax/atelectasis
- bronchiectasis (secondary to CB)
- Cor Pulmonale (increased in CB)
- End-stage lung (honeycomb lung) --> marked scarring/fibrosis of the lungs
- lung cancer
34
What is the cause of the prominent black round markings on a smokers lungs and where are they located predominantly?
Centrilobular emphysema
- centrilobular alveolar destruction with carbon pigmentation
- increase in upper lobes due to rising of CO2 in lungs
35
Compare predominant CB to predominant emphysema
Chronic Bronchitis:
- 40-45yrs
- mild/late dyspnoea
- early cough with copious sputum
- infections common
- repeated resp. insufficiency
- cor pulmonale common
- increased airway resistance
- normal elastic recoil
- obese "blue bloater"
Emphysema:
- 50-75yrs
- severe/early dyspnoea
- late cough with scanty sputum
- occasional infections
- resp. insufficiency terminal
- cor pulmonale rare/terminal
- normal/slightly increased airway resistance
- low elastic recoil
- frail "pink puffer"
36
What is the pathogenesis of emphysema?
1. Neutrophils and macrophages
- damage alveolar walls
- irregular large sacs with decreased surface area
2. Proteases --> alveolar wall loss
3. Gas trapping, small airway obstruction
4. Loss of elastic recoil (functional obstruction)
- normal gas exchange --> "pink puffer"
37
Why are people with emphysema referred to as "pink puffers"?
no fibrosis --> no excess mucous
- normal gas exchange still occurs
- normal O2 levels
*SOB is due to lack of elastic recoil --> gas trapping
38
True or False?
| CB is a functional obstruction
False
| -physical obstruction due to narrowed bronchial lumen caused by excess mucous production
39
What is the pathogenesis of chronic bronchitis?
1. Smoke irritation --> cilia damage
2. Mucous + irritant retention --> inflammation
3. Mucous cell hyperplasia (caused by inflammation)
- narrowed lumen
4. Smooth muscle cell spasm (caused by inflammatory mediators)
40
What is a common congenital cause of COPD?
alpha1 anti-trypsin deficiency
- alpha1 anti-trypsin = protease inhibitor
- therefore decreased levels = increased protease activity and damage --> increased alveolar wall damage --> congenital emphysema (panlobular)
41
What are the proteases involved in the pathogenesis of COPD?
- neutrophil elastase
- cathepsins
- matrix metalloproteinases (MMPs)
42
What is the cause of the black pigment in smokers' lungs?
Carbon
| -not the cause of damage
43
What hemolysis does S. pneumoniae undergo?
alpha
44
Why are there maximal symptoms but minimal signs in atypical pneumonia?
- involvement is ONLY in the walls of alveoli
- lumen is reasonably empty
- walls are still very thick
- therefore no strong white areas of consolidation on CXR
- BUT, O2 not able to be taken in adequately due to thickening of alveolar walls --> interstitial pneumonia
45
What are the clinical features of atypical pneumonia?
MAXIMAL Sx. / MINIMAL signs
- slow, gradual onset malaise
- headache + fever >/= 3days to wks
- cough --> constant, harsh, DRY, hacking, non-productive
- NO physical findings of consolidation due to lack of alveolar exudate
46
Compare broncopneumonia vs. lobarpneumonia
Bronchopneumonia:
- extremes of age (young/old)
- secondary (in sick)
- both genders
- H. influenzae, staph, strep
- patchy consolidation
- around small bronchi
- not limited by anatomic boundaries
- usually bilateral
Lobarpneumonia:
- middle age (20-50)
- primarily in healthy adult
- male common
- 95% S. pneumoniae
- entire lobe consolidation
- diffuse
- limited by anatomic boundaries
- usually unilateral
47
True or False?
| Bronchopneumonias are limited to lower lobes (don't cross borders)
False
| -lobarpneumonias are limited by anatomic boundaries not bronchopneumonias
48
What are the complications of community-acquired pneumonia/typical pneumonia?
RARE - as bacteria usually less virulent and pts. generally have a good immune system
- lung abscess
- pleuritis
- pleural effusion
- pleural adhesions
- fibrosis
- emphysema
49
What are the complications of nosocomial (broncho) pneumonia?
COMMON
- lung abscess
- pleuritis
- pleural effusion
- pleural adhesions
- fibrosis
- emphysema
50
What type of pneumonia is nosocomial pneumonia?
bronchopneumonia
51
What are the 4 pathogenetic stages of community acquired/typical pneumonia?
1. CONGESTION - vasodilation/congestion (day 1)
2. RED HEPATISATION - exudation + RBCs (day 2)
3. GREY HEPATISATION - WBCs (day 4)
4. RESOLUTION - few macrophages/neutrophils (day 8)
52
What are the clinical features of community acquired/typical pneumonia?
- 1-->3 days
- high fever
- pleuritic chest pain
- rusty sputum
- unilateral; whole lobe or segment
53
What type of pneumonia is community acquired/typical pneumonia?
Lobarpneumonia
54
What is the pathogenesis of pneumonia?
1. Normal
- normal alveoli with alveolar capillaries + RBCs/WBCs + endothelial lining
2. Congestion
- bacteria enter
- severe inflammation + bacterial toxins
- increased vasodilation --> increased BVs/blood in alveolar wall causes thickening
- endothelial leakage into lumen
- no space for air to pass --> SOB
3. Red Hepatisation
- RBCs begin leaking out into lumen via diapedesis
- RBCs>WBCs --> lung appears reddish/solid (liver-like)
4. Grey Hepatisation
- increased neutrophils/macrophages (WBCs) enter lumen to remove dead debris/bacteria
* RESOLUTION occurs following this --> normal
55
What organisms are responsible for nosocomial pneumonia?
- H. influenzae
- Klebsiella
- Pseudomonas
- E. coli
- S. aureus
56
What are the commonest causative pathogens of community-acquired pneumonia?
- 90% S. pneumoniae
- H. influenzae
- Klebsiella in elderly, DM, alcoholics
57
True or False?
| Viral pneumonia is more common than bacterial pneumonia
False
58
What organisms are responsible for atypical pneumonia?
Mycoplasma pneumoniae
| -common in children (>3yrs) and young adults
59
What organisms are responsible for aspiration pneumonia?
Anaerobic oral flora (bacteroides)
60
What organisms are responsible for chronic pneumonia?
- TB*
- Atypical mycobacteria
- Fungi
61
What organisms are responsible for pneumonia in the immunocompromised?
- CMV
- pneumocytis (HIV)
- atypical mycobacterium
- candidiasis
- aspergillosis
