Lecture 2 Flashcards
(41 cards)
What is agenisis, Aplasia and hyperplasia
Agenisis: complete absence of a lung or lobe with absent bronchi
Aplasia: absence of lung tissue but presence of rudimentary bronchus
Hypoplasia: presence of both bronchi and alveoli in an underdeveloped lobe
What are obstructive lung diseases
OLD: obstruction of air flow, air trapping in lungs, due to premature airway closure includes COPD, asthma and bronchiectasis.
Chronic obstructive pulmonary disease: often due to tobacco use or allergens often associated with viral or bacterial upper respiratory tract infection.
Chronic bronchitis: productive cough for more than 3 months. We have hypertrophy and hyperplasia of mucus secreting glands in bronchi
What are some disorders associated with airflow obstruction
- chronic bronchitis ( mucous gland hyperplasia)
- bronchiectasis ( airway dilation or scarring)
- asthma ( smooth muscle hyperplasia excess mucous, inflammation
- emphysema ( air space enlargement, wall destruction)
- small airways disease ( inflammatory scarring)
What is emphysema and DLCO
Alveolar wall destruction -> damage to alveolar capillary membrane
Centriacinar - associated with tobacco smoking and seen in upper lobes
Panacinar - effects lower lobes and associated with alpha 1 antitrypsin deficiency
DLCO: lung diffusion test, used asses lungs ability to transfer gas from inspired air to blood stream
What are the types of emphysema
1) centracinar
2) panacinar
3) paraseptal
4) mixed and unclassified
Symptoms of emphysema
Coughing without phlegm
Fatigue
Wheezing
Barrel like chest
Difficulty sleeping
Chronic bronchitis
Chronic airway inflammation
Bronchial tubes in lungs inflamed causing productive cough
If we have exposure to irritants then it can cause the hypertrophy of bronchial mucous glands causing more mucous production
Risk factors are: smoking, cystic fibrosis and genetics
Complication: pulmonary hypertension, right ventricle increased load
Symptoms: wheezing and hypoxemia
Diagnosis: chest X ray, ABGs
What is asthma
Coughing, tight chest, difficulty breathing.
It is triggered by allergens, associated with atopy, type 1 hypersensitivity, smooth muscle hypertrophy and hyperplasia
ACUTE: Allergen -> production of CD4 and Th2 then we have the release of IL4 and IL5 then esinophils and mass cells release inflammatory mediators
CHRONIC: scarring, fibrosis causing thickness of the epithelial basement membrane, permanent narrowing causing Th2 cells to release IL5.
COPD VS ASTHMA
COPD: not fully reversible, mostly causing be smoking, symptoms are often constant and progressive, productive cough higher neutrophil level
ASTHMA: fully reversible, not really caused by smoking , symptoms are recurrent episodes, dry cough, higher esinophil level
Asthma and COPD
COPD: not fully reversible, mostly causing be smoking, symptoms are often constant and progressive, productive cough higher neutrophil level
ASTHMA: fully reversible, not really caused by smoking , symptoms are recurrent episodes, dry cough, higher esinophil level
What is bronchiectasis
Pulmonary infection combined with obstruction or impaired clearance causing permanently dilated airways: Chronic cough,
Caused by airway obstruction, cystic fibrosis,
What are some characteristics of Kartageners syndrome
- bronchiectasis
- chronic sinusitis
- situs inversus totalis
This is the triad
Infertility is a diagnosis
What is idiopathic pulmonary fibrosis
Abnormal pulmonary healing process causing excess deposits of collagen -> progressive scarring of lung tissue-> lung function declines
Also we could have over proliferated type 2 pneumonocytes -> excess collagen and it accumulates-> restriction of lung expansion
Digital clubbing, crackles
What is sarcoidosis
Widespread of non caseating granulomas, elevatedACE and CD4 and CD8
Associated with bell palsy
SCHAUMANN & ASTEROID bodies, RHEUMATOID arthritis, high CALCIUM, OCULAR uveitis, INTERSTITIAL fibrosis, vitamin D activation, SKIN changes
How do we diagnose sarcoidosis
Ct scan
Non caseating granulommas disorder
Panda sign: in Ga scan, in bilateral and paratoid gland
Lambda sign: increased uptake of radionuclide right paratracheal lymph nodes
What is hypersensitivity pneumonitis
Mixed type III/ IV HS reaction to environmental triggers like actinomyces and aspergillus, seen in farmers, chronically leads to irreversible fibrosis
What is pneumoconiosis
ASBESTOS RELATED DISEASE: like pulmonary fibrosis associated w pleural plaques, increased risk of caplan syndrome, effects the lower lobes
BERYLILOSIS: associated w exposure to beryllium we see granulomas so it it responsive to glucocorticoids, affects upper lobes
COAL WORKERS: prolonged coal dust exposure, increased risk of caplan syndrome, affects upper lobes. Anthracosis ( asymptotic, found when there is exposure to sooty air)
SILICOSIS: associated w sandblasting and foundries mines macrophages respond to silica and release fibrogenic factors leading to fibrosis. We can see eggshell calcification on lymph nodes
What is pneumonia
Infection of one of both of the lungs, characterised by inflammation of alveoli
Types of pneumonia
Lobular: S pneumoniae, legionella and Klebsiella and it make involve the entire lobe or the whole lung
Bronchopneumonia: S pneumoniae, S aureus, H influenza, klebsiella- acute inflammatory infiltrates from bronchus into alveoli
Interstitial: mycoplasma, chlamydia etc. diffuse patchy inflammation to interstitial areas at alveolar walls
Cryptogenic organising: does not respond to antibiotic but responds to glucocorticoids- noninfectious, inflammation of bronchioles
Aspiration: aspiration of oropharyngeal or gastric contents it can progress to abscess
Aspiration (chemical) - hours after aspiration event due to gastric acid inflammation
What is the natural history of lobular pneumonia
Day 1-2: congestion ( red purple parenchyma)
Day 3-4: red hepatization ( red brown consolidation, exudate with fibrin, bacteria, RBCs and WBCs
Day 5-7: gray hepatizaton, exudate filled with WBCs RBCs and fibrin
Day 8+: resolution, enzymatic digestion of exudate by macrophages
What is community acquired pneumonia
Acquired outside hospital setting caused by S pneumoniae, S areus, H influenza etc
Risk: advanced age, low immunity, smoking, malnutrition
High fever, cough, dullness on percussion
What is pulmonary hypertension and the etiologies
Definition: Elevated mean pulmonary artery pressure > 20 mm Hg at rest.
• Results in:
• Arteriosclerosis
• Medial hypertrophy
• Intimal fibrosis
• Plexiform lesions
• ↑ Pulmonary vascular resistance → ↑ RV pressure → RVH → RV failure
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Etiologies (Groups 1–5):
1. Group 1: Pulmonary Arterial Hypertension (PAH)
• Often idiopathic; more common in females.
• May involve BMPR2 gene mutation → abnormal smooth muscle proliferation.
• Endothelial dysfunction → ↑ vasoconstrictors (e.g., endothelin), ↓ vasodilators (NO, prostacyclins).
• Causes: drugs (e.g., cocaine), connective tissue disease, HIV, portal HTN, congenital heart disease, schistosomiasis.
2. Group 2: Left Heart Disease
• Due to systolic/diastolic dysfunction or valvular disease.
3. Group 3: Lung Diseases or Hypoxia
• From lung parenchymal destruction (e.g., COPD), fibrosis, hypoxic vasoconstriction (e.g., OSA, high altitude).
4. Group 4: Chronic Thromboembolic
• Recurrent microthrombi → ↓ cross-sectional area of pulmonary vascular bed.
5. Group 5: Multifactorial
• Due to hematologic, systemic, or metabolic disorders, or tumor compression.
What is lung abscess
Localised collection of puss within parenchyma, caused by aspiration of oropharyngeal contents
What is acute respiratory distress syndrome
Alveolar insult (e.g. infection, trauma, etc.) triggers the immune system.
2. This causes release of pro-inflammatory cytokines, which attract and activate neutrophils.
3. Neutrophils release toxic substances (like reactive oxygen species and proteases).
4. These substances damage the capillary endothelium, increasing blood vessel permeability.
5. Protein-rich fluid leaks into the alveoli, leading to:
• Hyaline membrane formation (from fluid and dead cells)
• Noncardiogenic pulmonary edema (fluid buildup not due to heart failure; PCWP is normal)
6. This results in:
• ↓ Lung compliance (lungs become stiff)
• Ventilation-perfusion (V/Q) mismatch (oxygen can’t pass into the blood properly)
7. Hypoxic vasoconstriction occurs (body tries to redirect blood to better-ventilated areas), which increases pulmonary vascular resistance.
8. Loss of surfactant (a substance that keeps alveoli open) worsens alveolar collapse, especially in:
• Preterm infants
• Drowning victims
Cause is sepsis, consequences is low like compliance and pulmonary hypertension