Week 3-resp: d&D

COPD

100

What spirometry criterion defines airflow obstruction in COPD?

POST-bronchodilator FEV1/FV, <70% ratio

200

What would classic symptoms of emphysema present as?

SOB, cachectic, barrel chest (AP diameter increase), pursed lips, accessory muscle use, 

300

Why can patients develop secondary polycythaemia? and is this associated more with chronic bronchitis or emphysema?

Chronic hypoxaemia stimulates erythropoietin release from the kidneys, increasing red blood cell production.

400

COPD treatment: How do we do it? Why? Name the medication

*Looking for 4+ types of treatment

• CONTROLLED OXYGEN ADMINISTRATION  →alleviate hypoxia-induced pulmonary vasoconstriction & cor pulmonale
• BONCHODILATORY DRUGS open up airways to facilitate alveolar ventilation
• CORTICOSTEROIDS →minimise any inflammatory component and reduce mucosal oedema
• ANTIBIOTICS → treat bacterial infection
• CHEST PHYSIOTHERAPY → encourage expectoration of mucus secretions/plugging to open up peripheral airways

500

Why can high-flow oxygen worsen hypercapnia in patients with severe COPD?

rimarily due to worsening V/Q mismatch from reversal of hypoxic pulmonary vasoconstriction, with additional contribution from the Haldane effect (reduced CO₂ binding to haemoglobin).

Histology and pathology

100

What can be seen on this histology?

Fibroblastic foci

Type II pneumoctye

200

Whats this?

CURSCHMANN SPIRALS = composed of mucus plugs from small airways

300

What disease is present?

bronchiectasis

400

Disease and describe some features?

Silicotic nodule: central collagen bands

500

*Bonus point up for grabs*

*What disease is this

Name 5-7 features you would expect to see?

Angiogenesis 

altered epithelial barrier

mucus plug

thickened reticular basement membrane 

goblet cell hyperplasia 

sub-epithelial fibrosis 

physiology

100

In COPD why does decrease in work of airway resistance by slow and deep breathes help the patient?

• Decrease in turbulent flow= decrease in resistance 
• when patients take VERY deep breathes, expands lungs= pulls airways open through radial traction 
• when airways open lower resistance 

200

What is a complication of late stage emphysema that you will not see in chronic bronchitis?

Pneumothorax. Bullae ruptures= spontaneous pneumothorax 

300

What lab values on ABG would be most consistent with chronic bronchitis?

*PaO2, PaCO2, pH, HCO3-

decreased PaO2

decreased pH

increased PaCO2

Increased HCO3-

400

Explain cor pulmonale

Chronic alveolar hypoxia in COPD leads to increased pulmonary vascular resistance via what physiological mechanism = Hypoxic pulmonary vasoconstriction.

500

Draw the pathway of COPD tissue destruction 

Nicotine use (or other noxious stimuli) inactivates protease inhibitors (especially α1-antitrypsin) → imbalance of protease and antiprotease → 

↑ elastase activity → loss of elastic tissue and lung parenchyma (via destruction of the alveolar walls), which causes:

• Enlargement of airspaces → ↓ elastic recoil and ↑ compliance of the lung → ↓ tethering of small airways → expiratory airway collapse and obstruction → air trapping and hyperinflation → ↓ ventilation (due to air-trapping) and ↑ dead space → ↓ DLCOand ↑ ventilation-perfusion mismatch (V/Q) → hypoxemia and hypercapnia 
• Pulmonary shunt and ↓ blood volume in pulmonary capillaries → ↑ number of alveoli that are ventilated but not perfused (↑ dead space) → ↓ DLCO and ↑ V/Q → hypoxemia and hypercapnia
• Imbalance of oxidants and anti-oxidants and an overabundance of free radicals → chronic inflammation and inactivation of anti-elastase → breakdown of elastic tissue.

Diseases

100

Which type of pneumonia presents with dry cough and diffuse interstitial infiltrates?

Name two pathogens that cause it?

Atypical pneumonia

- mycoplasma

- Pneumoniae 

200

What immune mechanism causes tissue destruction in TB?

What immune mechanism causes tissue destruction in TB?

300

Clinical scenario time!!

pneumothorax 

400

Macroscopic and histopathology of honeycomb lung 

Honeycomb lung: 

macroscopically (a) & (b) • The lung appears as large cystically dilated air spaces surrounded by fibrosis • The pleural surface has a bosselated leathery surface

Histopathology (c): • Coalescence of bronchiolar & alveolar airspaces to form cysts lined by cuboidal epithelium • Focal squamous metaplasia is frequently seen • Proliferation of smooth muscle around terminal bronchioles

500

diffuse alveolar damage leads to:

*walk through two (maybe three depending on how you see it) phases

Tissue damage (pulmonary or extrapulmonary) → release of inflammatory mediators (e.g., interleukin-1) → inflammatory reaction → migration of neutrophils into alveoli → excessive release of neutrophilic mediators (e.g., cytokines, proteases, reactive oxygen species) → injury to alveolar capillaries and endothelial

• Exudative phase: excess fluid in interstitium and on alveolar surface → pulmonary edema with normal pulmonary capillary wedge pressure (noncardiogenic pulmonary edema) → decreased lung compliance and respiratory distress 
• Hyaline membrane formation: exudation of neutrophils and protein-rich fluid into the alveolar space → formation of alveolar hyaline membranes → impaired gas exchange → hypoxemia 
  • Hypoxemia → compensation through hyperventilation → respiratory alkalosis
  • Hypoxemia → chronic hypoxic pulmonary vasoconstriction → pulmonary hypertension and right-to-left pulmonary shunt (increased shunt fraction) 
  • Damage to type I and type II pneumocytes → decrease in surfactant → alveolar collapse → intrapulmonary shunting
• Organizing phase (late stage): proliferation of type II pneumocytes and infiltration of fibroblasts → progressive interstitial fibrosis

Rebecca's Random Resp

100

Classic histological finding in ARDS?

Diffuse alveolar damage with hyaline membrane formation.

200

5 diseases asbestos causes?

1. ASBESTOSIS = progressive chronic fibrosis of the lungs

2. PLEURAL PLAQUES = benign plaques of collagenous fibrosis on pleural surfaces

3. PLEURAL EFFUSIONS and pleural thickening → formation in the absence of obvious other cause → both may compress the lungs

4. CARCINOMA of the LUNG

5. MALIGNANT MESOTHELIOMA = a highly malignant tumour of the mesothelium lining the pleura

300

Clinical scenario time! 

decreased ratio of ventilated alveoli 

400

4 histological reaction patterns that occur in diffuse interstitial lung diseases

1. HAEMORRHAGE and FIBRIN EXUDATION in alveoli forming ‘HYALINE MEMBRANES’
2. OEDEMA and INFLAMMATION of the INTERSTITIUM
3. MACROPHAGE ACCUMMULATION in alveolar spaces
4. FIBROSIS in the interstitium and alveolar spaces

500

6-7 major Structural changes in asthma and implications

• BRONCHOCONSTRICTION from heightened bronchial smooth muscle reactivity
• MUCUS HYPERSECRETION →plugging of airways
• MUCOSAL OEDEMA →narrowing of airway lumen
• PLASMA EXTRAVASATION in SUBMUCOSAL TISSUES
• BRONCHITIS from complex inflammatory reaction: eosinophils, mast cells, lymphocytes (T and B) & macrophages
• COLLAGEN PLATE THICKENING beneath bronchial epithelium in longstanding cases
• FOCAL NECROSIS of airway epithelium→mucus