Week 4 - RESP Flashcards
Pneumonia, COPD, Smoking
What are the 2 main microscopic features of COPD?
- peribronchial chronic inflammation - CB (IL-8/LTB4)
2. loss of alveolar wall without inflammation - Emphysema (elastases/proteases)
What is the pathogenesis of cavity formation in TB?
Due to drainage of caseous material through bronchus
What are complications of TB?
- colonisation of cavities by fungus (aspergillosis)
- bronchiectasis
- empyema
- arterial pseudoaneurysm
- fibrothorax
- bronchopleural fistula
What are the modes of spread of primary pulmonary TB?
- 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
What are the factors in the pathogenesis of cavitary TB?
IFN-gamma + proteases
What is the difference in pathogenesis of caseating vs. non-caseating granulomas in TB?
Caseating = M1 activation Non-caseating = M2 activation
What is secondary TB?
- 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
What are CXR findings of TB?
- lower and middle lobe nodules of consolidation
- hilar adenopathy
- pleural effusion
- cavitation - RARE (increase in secondary TB in upper lobes)
What is etiology of pleural effusions?
- transudate –> cardaic failure, nephrotic syndrome
- exudate –> infection, TB, bronchial carcinoma
- blood –> trauma
- chyle –> ruptured thoracic duct
What is a:
- Ghon focus?
- Ghon complex?
- Ranke complex?
Manifestations of primary TB
Ghon focus –> pulmonary lesion
Ghon complex –> pulmonary lesion + draining lymph nodes
Ranke complex –> calcified parenchymal tuberculoma + ipsilateral calcified hilar node
What is the clinical Dx. of COPD?
FEV1 < 80%
FEV1/FVC < 70%
What is the cause of the slight airway obstruction in emphysema?
Loss of normal stretching of smaller airways by alveoli due to alveolar wall damage –> “broken alveoli”
Why is Cor Pulmonale more common in CB than emphysema?
- inflammation and fibrosis of bronchial walls affects associated BVs
- therefore pulmonary HTN is more common in CB
- RVH –> RVF (Cor Pulmonale)
What is BOOP?
Brochiolitis Obliterans Organising Pneumonia
- type of non-infective pneumonia
- ractive to irritants –> hyperplasia of type II pneumocytes
What are the features of chronic pneumonia and what is the commonest cause?
- chronic, lymphoid infiltrate
- no classic stages
- lung destruction –> granuloma, cavity, abscess
- commonest cause = TB
What is the pathogenesis of SOB, pain and high fever in pneumonia?
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
What are gross and microscopic features of emphysema?
Gross:
- distended lungs
- black spots all over (increase in upper zone)
Micro:
- loss of alveolar wall (bullae)
- carbon pigment in centrilobular area
What are gross and microscopic features of bronchiectasis?
Gross:
-dilated irregular bronchi filled with pus (visible till pleural margin)
Micro:
-destruction of bronchial epithelium, replaced by acute/chronic inflammation, necrosis, pus.
What is the common type of pneumonia in a chronic smoker?
Bronchopneumonia
The 2 factors causing chronic bronchitis are?
IL-8 + LTB4
What are the common pathogens seen in purulent sputum of patients with bronchiectasis?
Mixed normal flora
What are the 2 main types of emphysema?
- Centrilobular
- commonest
- increase in smokers
- primarily upper lobes - Panlobular
- congenital
- alpha1-antitrypsin deficiency
- involves all lung fields particularly bases
True or False?
Majority of primary TB cases are asymptomatic
True
-95%
How is lung cancer classified?
Small cell lung cancer (SCLC)
Non Small cell lung cancer (NSCLC)
-squamous cell carcinoma (SCC)
-adenocarcinoma (glandular)
What is the characteristic CXR finding of pleural effusion?
Loss of costophrenic angle
What is the classification of pneumothorax?
Trauma –> e.g. rib fracture
Spontaneous –> peripheral bullous rupture
What are complications of emphysema?
- pneumothorax
- pulmonary HTN (increase in CB)
- lung cancer
- consolidation/infective exacerbation (increase in CB)
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
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
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
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
Alveolar damage in centrilobular emphysema is due to?
Proteases
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
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
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”
What is the pathogenesis of emphysema?
- Neutrophils and macrophages
- damage alveolar walls
- irregular large sacs with decreased surface area - Proteases –> alveolar wall loss
- Gas trapping, small airway obstruction
- Loss of elastic recoil (functional obstruction)
- normal gas exchange –> “pink puffer”
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
True or False?
CB is a functional obstruction
False
-physical obstruction due to narrowed bronchial lumen caused by excess mucous production
What is the pathogenesis of chronic bronchitis?
- Smoke irritation –> cilia damage
- Mucous + irritant retention –> inflammation
- Mucous cell hyperplasia (caused by inflammation)
- narrowed lumen - Smooth muscle cell spasm (caused by inflammatory mediators)
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)
What are the proteases involved in the pathogenesis of COPD?
- neutrophil elastase
- cathepsins
- matrix metalloproteinases (MMPs)
What is the cause of the black pigment in smokers’ lungs?
Carbon
-not the cause of damage
What hemolysis does S. pneumoniae undergo?
alpha
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
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
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
True or False?
Bronchopneumonias are limited to lower lobes (don’t cross borders)
False
-lobarpneumonias are limited by anatomic boundaries not bronchopneumonias
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
What are the complications of nosocomial (broncho) pneumonia?
COMMON
- lung abscess
- pleuritis
- pleural effusion
- pleural adhesions
- fibrosis
- emphysema
What type of pneumonia is nosocomial pneumonia?
bronchopneumonia
What are the 4 pathogenetic stages of community acquired/typical pneumonia?
- CONGESTION - vasodilation/congestion (day 1)
- RED HEPATISATION - exudation + RBCs (day 2)
- GREY HEPATISATION - WBCs (day 4)
- RESOLUTION - few macrophages/neutrophils (day 8)
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
What type of pneumonia is community acquired/typical pneumonia?
Lobarpneumonia
What is the pathogenesis of pneumonia?
- Normal
- normal alveoli with alveolar capillaries + RBCs/WBCs + endothelial lining - 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 - Red Hepatisation
- RBCs begin leaking out into lumen via diapedesis
- RBCs>WBCs –> lung appears reddish/solid (liver-like) - Grey Hepatisation
- increased neutrophils/macrophages (WBCs) enter lumen to remove dead debris/bacteria
* RESOLUTION occurs following this –> normal
What organisms are responsible for nosocomial pneumonia?
- H. influenzae
- Klebsiella
- Pseudomonas
- E. coli
- S. aureus
What are the commonest causative pathogens of community-acquired pneumonia?
- 90% S. pneumoniae
- H. influenzae
- Klebsiella in elderly, DM, alcoholics
True or False?
Viral pneumonia is more common than bacterial pneumonia
False
What organisms are responsible for atypical pneumonia?
Mycoplasma pneumoniae
-common in children (>3yrs) and young adults
What organisms are responsible for aspiration pneumonia?
Anaerobic oral flora (bacteroides)
What organisms are responsible for chronic pneumonia?
- TB*
- Atypical mycobacteria
- Fungi
What organisms are responsible for pneumonia in the immunocompromised?
- CMV
- pneumocytis (HIV)
- atypical mycobacterium
- candidiasis
- aspergillosis
