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Pathology Term 1 > Week 4 - RESP > Flashcards

Week 4 - RESP Flashcards

Pneumonia, COPD, Smoking

1
Q

What are the 2 main microscopic features of COPD?

A
  1. peribronchial chronic inflammation - CB (IL-8/LTB4)

2. loss of alveolar wall without inflammation - Emphysema (elastases/proteases)

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2
Q

What is the pathogenesis of cavity formation in TB?

A

Due to drainage of caseous material through bronchus

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3
Q

What are complications of TB?

A
  • colonisation of cavities by fungus (aspergillosis)
  • bronchiectasis
  • empyema
  • arterial pseudoaneurysm
  • fibrothorax
  • bronchopleural fistula
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4
Q

What are the modes of spread of primary pulmonary TB?

A
  1. spread from primary focus –> hilar/mediastinal LNs to form the primary complex (Gohn complex)
  2. direct extension of primary focus –> progressive pulmonary TB
  3. spread to pleura –> TB pleurisy and pleural effusion
  4. blood-borne spread –> miliary TB + meningitis
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5
Q

What are the factors in the pathogenesis of cavitary TB?

A

IFN-gamma + proteases

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6
Q

What is the difference in pathogenesis of caseating vs. non-caseating granulomas in TB?

A 
Caseating = M1 activation
Non-caseating = M2 activation
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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
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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)
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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
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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

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11
Q

What is the clinical Dx. of COPD?

A

FEV1 < 80%

FEV1/FVC < 70%

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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”

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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)
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14
Q

What is BOOP?

A

Brochiolitis Obliterans Organising Pneumonia

  • type of non-infective pneumonia
  • ractive to irritants –> hyperplasia of type II pneumocytes
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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
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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

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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
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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.

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19
Q

What is the common type of pneumonia in a chronic smoker?

A

Bronchopneumonia

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20
Q

The 2 factors causing chronic bronchitis are?

A

IL-8 + LTB4

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21
Q

What are the common pathogens seen in purulent sputum of patients with bronchiectasis?

A

Mixed normal flora

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22
Q

What are the 2 main types of emphysema?

A
  1. Centrilobular
    - commonest
    - increase in smokers
    - primarily upper lobes
  2. Panlobular
    - congenital
    - alpha1-antitrypsin deficiency
    - involves all lung fields particularly bases
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23
Q

True or False?

Majority of primary TB cases are asymptomatic

A

True

-95%

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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)

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25
Q

What is the characteristic CXR finding of pleural effusion?

A

Loss of costophrenic angle

26
Q

What is the classification of pneumothorax?

A

Trauma –> e.g. rib fracture

Spontaneous –> peripheral bullous rupture

27
Q

What are complications of emphysema?

A
  • pneumothorax
  • pulmonary HTN (increase in CB)
  • lung cancer
  • consolidation/infective exacerbation (increase in CB)
28
Q

What are CXR findings of emphysema?

A
  • hyperinflation of lungs –> flattened diaphragm, >10 posterior ribs, >6 anterior ribs
  • decreased peripheral vascularity
  • increased size of central pulmonary arteries
  • hyperlucency of lungs
29
Q

What is atelectasis and bronchiectasis?

A

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
Q

What is the definition of chronic bronchitis?

A
  • chronic inflammation of bronchi

- defined as a productive cough that occurs every day for 3 months in a row for 2 consecutive years

31
Q

What is the definition of emphysema?

A
  • 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
Q

Alveolar damage in centrilobular emphysema is due to?

A

Proteases

33
Q

What are some complications of COPD?

A
  • 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
Q

What is the cause of the prominent black round markings on a smokers lungs and where are they located predominantly?

A

Centrilobular emphysema

  • centrilobular alveolar destruction with carbon pigmentation
  • increase in upper lobes due to rising of CO2 in lungs
35
Q

Compare predominant CB to predominant emphysema

A

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
Q

What is the pathogenesis of emphysema?

A
  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
Q

Why are people with emphysema referred to as “pink puffers”?

A

no fibrosis –> no excess mucous

  • normal gas exchange still occurs
  • normal O2 levels

*SOB is due to lack of elastic recoil –> gas trapping

38
Q

True or False?

CB is a functional obstruction

A

False

-physical obstruction due to narrowed bronchial lumen caused by excess mucous production

39
Q

What is the pathogenesis of chronic bronchitis?

A
  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
Q

What is a common congenital cause of COPD?

A

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
Q

What are the proteases involved in the pathogenesis of COPD?

A
  • neutrophil elastase
  • cathepsins
  • matrix metalloproteinases (MMPs)
42
Q

What is the cause of the black pigment in smokers’ lungs?

A

Carbon

-not the cause of damage

43
Q

What hemolysis does S. pneumoniae undergo?

A

alpha

44
Q

Why are there maximal symptoms but minimal signs in atypical pneumonia?

A
  • 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
Q

What are the clinical features of atypical pneumonia?

A

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
Q

Compare broncopneumonia vs. lobarpneumonia

A

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
Q

True or False?

Bronchopneumonias are limited to lower lobes (don’t cross borders)

A

False

-lobarpneumonias are limited by anatomic boundaries not bronchopneumonias

48
Q

What are the complications of community-acquired pneumonia/typical pneumonia?

A

RARE - as bacteria usually less virulent and pts. generally have a good immune system

  • lung abscess
  • pleuritis
  • pleural effusion
  • pleural adhesions
  • fibrosis
  • emphysema
49
Q

What are the complications of nosocomial (broncho) pneumonia?

A

COMMON

  • lung abscess
  • pleuritis
  • pleural effusion
  • pleural adhesions
  • fibrosis
  • emphysema
50
Q

What type of pneumonia is nosocomial pneumonia?

A

bronchopneumonia

51
Q

What are the 4 pathogenetic stages of community acquired/typical pneumonia?

A
  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
Q

What are the clinical features of community acquired/typical pneumonia?

A
  • 1–>3 days
  • high fever
  • pleuritic chest pain
  • rusty sputum
  • unilateral; whole lobe or segment
53
Q

What type of pneumonia is community acquired/typical pneumonia?

A

Lobarpneumonia

54
Q

What is the pathogenesis of pneumonia?

A
  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
Q

What organisms are responsible for nosocomial pneumonia?

A
  • H. influenzae
  • Klebsiella
  • Pseudomonas
  • E. coli
  • S. aureus
56
Q

What are the commonest causative pathogens of community-acquired pneumonia?

A
  • 90% S. pneumoniae
  • H. influenzae
  • Klebsiella in elderly, DM, alcoholics
57
Q

True or False?

Viral pneumonia is more common than bacterial pneumonia

A

False

58
Q

What organisms are responsible for atypical pneumonia?

A

Mycoplasma pneumoniae

-common in children (>3yrs) and young adults

59
Q

What organisms are responsible for aspiration pneumonia?

A

Anaerobic oral flora (bacteroides)

60
Q

What organisms are responsible for chronic pneumonia?

A
  • TB*
  • Atypical mycobacteria
  • Fungi
61
Q

What organisms are responsible for pneumonia in the immunocompromised?

A
  • CMV
  • pneumocytis (HIV)
  • atypical mycobacterium
  • candidiasis
  • aspergillosis

Pathology Term 1 (6 decks)

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