Pathologies and Treatment Flashcards
What is asthma?
What occurs during an asthma attack?
- A chronic, inflammatory, obstructive disease of the airways.
- Inflammatory mediators induce changes in the airways. They cause smooth muscle contraction, ↑mucous secretion, oedema. These changes ↓airway lumen, ↑resistance = ↓airflow.
Explain the 2 stages of the allergic response?
- Allergen sensation: APC engulfs allergen, presents its antigens (MHC II) for CD4 cells. Th1→Th2, which eventually stimulates eosinophil proliferation and activates B cells→IgE production, which bind to mast cell receptors.
- Allergen response: Allergen binds to IgE on mast cells to induce degranulation. Inflammatory mediators then bind to receptors for more degranulation, bronchoconstriction, ↑mucous secretion, oedema.
What is airway remodelling and what causes it?
Chronic asthma = tissue damage over time, leading to airway remodelling.
Airway remodelling includes fibrosis, smooth muscle hypertrophy, epithelium disruption, and goblet cell hyperplasia. This will lead to poor airway function.
What is COPD?
What are its clinical features?
Chronic, accelerated decline in respiratory function. It includes Chronic bronchitis and Emphysema.
Chronic Bronchitis: long term bronchi inflammation, cilia damage, ↑mucous secretion, and weakened airway structure. The damaged cilia ↑resp. infections, irritation = coughing, and ↓lumen = ↑airway resistance.
Emphysema: enlargement of alveoli and loss of elastin fibres. ↓surface area and perfusion so less gas exchange. Loss of elastin = ↑compliance; expiration is no longer passive.
How does tobacco smoke lead to pathological changes in the respiratory system?
Tobacco smoke has harmful contents, like nicotine and benzene, which damage respiratory tissue = inflammation. With repeated exposure, the inflammation will become chronic, pathological, and irreversible.
Cilia damage will also increase likelihood of infections. Long term damage will lead to airway remodelling and ↓respiratory function.
How does COPD affect cardiovascular function?
Chronic alveolar hypoxia leads to hypoxic vasoconstriction = ↑pulmonary resistance. This will lead to pulmonary hypertension, RV hypertrophy (RV works harder), and R-sided heart failure.
How do the B2 agonists work?
What are the side-effects?
- Can be SABA (short-acting) e.g. Salbutamol, LABA (long-acting) e.g. Salmeterol, Ultra LABA.
Bind to B2 receptors on smooth muscle cells to induce the cascade leading to relaxation. ↑cAMP = ↑PKA = ↓Ca2+ mobilisation/sensitivity = relaxation
- They may activate B2 receptors on SAN and myocardium, leading to tachycardia, and palpitations. Binding to B2 receptors on skeletal muscle can cause tremors, and muscle growth.
How do muscarinic antagonists work?
How do Phosphodiesterase (PDE) inhibitors work?
- Block ACh from binding at m3 receptors, so no contraction occurs.
- Inhibits Phosphodiesterase, which breaks down cAMP→AMP. Therefore, its inhibition ↑cAMP = relaxation
How do Corticosteroids work?
How do Leukotriene antagonists work?
How is asthma therapy administered?
- • Can be inhaled or oral
• Binds to intracellular (nuclear) steroid receptor then goes into nucleus to alter gene expression - ↓pro-inflammatory gene expression and ↑anti-inflammatory gene expression = ↓inflammation. - Leukotrienes are inflammatory mediators from mast cells.
- In a step-wise manner to control improvement and avoid adverse effects.
LOOK AT NOTES FOR GRAPH!
Describe the graph of Airway Function and define FEV1, FVC, and explain how its used to measure lung function.
What do the % represent?
- FEV1 (Forced expiratory volume) - how much air forced out in 1 second.
FVC (Forced vital capacity) - max amount of air exhaled in 1 breath.
100 x FEV1/FVC gives the % of the lung capacity that can be exhaled in one second.
- FEV1/FVC < 70% and FVC normal = Obstructive respiratory diseases - e.g. asthma = ↑resistance
FVC < 80% and FEV1/FVC normal = Restrictive respiratory diseases - e.g. fibrosis = ↓compliance
LOOK AT NOTES FOR GRAPH!
Describe the graph of Compliance and the difference between static and dynamic compliance
What does the internal area and gradient represent on the dynamic compliance graph?
= Volume diff./pressure diff., using transplumonary pressure and lung volume.
With Static compliance, measurements are taken when airflow is 0 - gradient of steepest part is used.
With DYNAMIC compliance, measurements are taken when airflow > 0 - gradient between first and last point is used. Uses INTRAPLEURAL pressure on the x-axis, instead of transplumonary pressure
Lung resistance and compliance, respectively:
↑InTernal area = ↑resisTance
↑Gradient = ↑compliance
What is the alveolar gas equation (AGE)?
What is RER?
What is the A-a O2 gradient?
- PaO2 = FiO2 x (Patm - PH2O) - PCO2/RER
- Respiratory change ratio - relationship between CO2 produced and O2 consumed by metabolism.
- The different between alveolar and arterial pressure. Normally its 2kPa. If it’s > 2kPa = less O2 moving into blood due to V/Q inequality or diffusion defect.
LOOK AT NOTES FOR TREE DIAGRAM!
Explain respiratory/metabolic compensation.
What is Mixed acidosis/alkalosis?
- ↑pCO2 during Alkalosis or ↓pCO2 during Acidosis = Respiratory compensation
↑[HCO3-] during Acidosis or ↓[HCO3-] during Alkalosis = Metabolic compensation
*Compensation can be full or partial, depending on if PH has been restored.
- It occurs when both respiratory and metabolic systems are dysfunctional.
Mixed acidosis = ↑pCO2 and ↓[HCO3-]
Mixed alkalosis = ↓pCO2 and ↑[HCO3-]
Define Hypoxaemia and Hypercapnia and what causes them?
What are the consequences of acute/chronic hypoxaemia and hypercapnia?
- Hypoxaemia - low blood pO2 - due to asthma, pneumonia, and COPD
Hypercapnia - High blood pCO2 - due to hypoventilation and lung disease
- Hypoxaemia causes Type 1 respiratory failure
Hypercapnia causes Type 2 respiratory failure
