Respiratory 2 Flashcards
What are the main risk factors of COPD?
Smoking
enviromental factors: •Climate, air pollution, urbanisation, social class and occupation (dust & silica) also play a role
alpha 1 antitrypsin deficiency
Infections
Low birth weight
What is the diseases within COPD?
CHronic bronchitis
Emphysema
Pathophysiology of chronic bronchitis breifly?
•Increased number of mucous secreting goblet cells in bronchial mucosa due to smoke irritation
- causes: narrowing of airway, hypertrophy (increase in the size of the mucous glands-bigger), hyperplasia (more mucous)
- Ciliary dysfunction: Globlet cells also have damage/motility in cilia so mucous build up more
- Air trapping: less oxygen getting in due to mucous block and less CO2 leaving body
•Hypersecretion à immobile cilia à mucous plugs à airflow obstruction à retention of CO2 and less O2 à hypoxia + acidosis à blue bloaters
- could lead to hypoxemia and hypercepnia
- risk of developing pneumonia because mucous plug might contain hemophilus influenza or moraxella which cause infection
-
Pathophysiology of emphysema?
- structural issue
- smoking and pollutants causes phagocytosis
- this releases cytokines
- cytokines activates neutrophils due to inflammation
- neutophils starts release specifc protease elastase which breaks down elastin
- macrophages to releases proteases and chemokines which attract neutrophils that release elastases, nicotine inhibits protease inhibitors (alpha 1 antitrypsin)
- since you dnt have much alpha 1 antitrypsin to oppose elastase, elastase causes damage to the alveoli.
Complications from chronic bronchitis?
- could lead to hypoxemia and hypercepnia
- risk of developing pneumonia because mucous plug might contain hemophilus influenza or moraxella which cause infection
Function of elastin?
Helps increase the recoil of the lungs
When you inhale it is a active process but when you exhale it is passive and so the lungs recoil and go back to its normal shape
What is the function of alpha 1 antityrpsin
What happens when you are deficient in it?
it is a protease inhibitor made in the liver.
it opposes elastase
•Alpha antitrypsin deficiency
- Protein accumulates in liver meaning low levels in the lungs à cant inhibit neutrophil elastases à destruction of alveolar wall connective tissue
- 2% of UK cases of emphysema
- Usually causes COPD in < 40 y/o
Complications from emphysema?
- damage to the alveoli
- airways will narrow and wont be able to keep open due to the lack of elastin
- start to lose sA from alveoli and blows up- Destruction of septa between alveoli creating distended bullae – deceased SA
- Enlarged air spaces distal to terminal bronchiolesalso build up of Co2 leads to hypoxia and hypercepnia
• loss of elastic recoil in lungs – hold more air (elastases > anti elastases)
What are the different types of emphysema?
centriacinar- dilated pockets of air in the proximal airway
panacinar- distal airways
Distal acinar-distal alveoli can cause spontaneous pneumothorax
Epidemiology of COPD?
Approximately 3 million people in the UK are diagnosed with COPD and a suspected 2 million more may be undiagnosed.
Clinical features of COPD?
Chronic productive cough and dyspnea are the hallmarks of COPD.
Symptoms:
- Chronic cough: usually productive
- Sputum production
- Breathlessness: usually on exertion in early stages
- Frequent episodes of ‘bronchitis’: usually in the winter
- Wheeze
- Pursed lip breathing: (prevents alveolar collapse by increasing the positive end expiratory pressure)
- Bronchial sounds
What does this scan show?
CXR demonstrating COPD with hyperinflation
Investigations for COPD?
Bedside
- Observations: including pulse oximetry
- Body mass index (BMI)
- Sputum culture (if purulent)
- Arterial blood gas (if hypoxia or hypercapnia is suspected): needed in acute exacerbations or work-up for long-term oxygen therapy
- ECG (if cor pulmonale suspected)
Bloods
- Full blood count: important to assess for anaemia and polycythaemia
- Alpha-1 antitrypsin levels
Imaging
Chest x-ray (CXR):
Hyperexpanded
Flattened hemidiaphragms
Hypodense
Saber-sheath trachea
CT scan: consider performing if
Symptoms disproportionate to spirometric assessment
Alternative diagnosis suspected (e.g. bronchiectasis, fibrosis)
Lung cancer suspected or to investigate abnormalities on chest x-ray
Echocardiogram: if cor pulmonale suspected.
Management for COPD patients?
All patients with COPD should be offered education, smoking cessation, vaccinations(influenza vaccine and pneumococcal), pulmonary rehabilitation (if indicated) and pharmacotherapy (e.g. inhalers).
Drugs for COPD
Beta-receptor agonists: bind to beta receptors of the sympathetic nervous system. Causes relaxation of airway smooth muscle and subsequent bronchodilation. May be short or long-acting.
Muscarinic receptor antagonists: these drugs prevent the activation of muscarinic receptors by acetylcholine. This prevents airway smooth muscle contraction and causes bronchodilation. Can be short or long-acting.
Corticosteroids: inhaled corticosteroids work by reducing inflammation within the lungs. They are thought to reduce the number of exacerbations, improve the efficacy of bronchodilators and decrease dyspnoea in stable COPD.
Inhaler types for COPD?
- Short-acting beta-agonists (SABA): Salbutamol
- Long-acting beta-agonists (LABA): Salmeterol
- Short-acting muscarinic antagonists (SAMA): Ipratropium
- Long-acting muscarinic antagonists (LAMA): Umeclidinium / tiotropium
- Inhaled corticosteroid (ICS): Beclomethasone
- LABA-ICS: Seretide (salmeterol/fluticasone)
- LABA-LAMA: Ultibro (indacaterol/glycopyrronium)
- LABA-LAMA-ICS: Trimbow (formoterol/glycopyrronium/beclometasone
What is Pulmonary embolism?
acute/chronic occlusion of pulmonary arteries. Clot breaks off and travels to the lungs (emboli).
Occlusion maybe due to a blood clot, fat, air or tumour
What is deep vein thrombosis?
acute/chronic occlusion of deep vein(s). Commonly affects the lower limbs through the formation of a clot forms (thrombus).
Venous thromboembolism (VTE) is a term that encompasses two conditions:
Pulmonary embolism
Deep vein thrombosis
What is incidence like with PE?
increases with age–doubles everydecade after 20 years
What is the aetiology of PE?
The typical cause of PE is an emboli that arises from a DVT. The DVT itself may be provoked or unprovoked based on the same risk factors of PE (it is also a thromboembolic disease). A history of unilateral leg swelling that precedes the onset of chest pain and dyspnoea is classical for the diagnosis of PE.
What are the major risk factors of PE?
- DVT
- Previous VTE
- Active cancer
- Recent surgery (e.g. within last 2-3 months)
- Significant immobility (e.g. hospitalisation, bed-rest)
- Lower limb trauma/fracture
- Pregnancy (+ 6 weeks postpartum)
What are additional risk factors to PE?
- Combined oral contraceptive pill
- Long-distance sedentary travel (e.g. long-haul flights)
- Thrombophilia
- Obesity
- Others
Due to the high risk of VTE in patients admitted to secondary care (i.e. hospital), a ____ ____ _________should be completed on admission. This assesses whether a patient is suitable to receive prophylactic blood thinning medication (e.g. low molecular weight heparin) to reduce the risk of VTE.
VTE risk assessment
What is VIrchow triad?
3 factors that are critically important in the development of venous thrombosis: a triad of venous stasis, endothelial injury, and a hypercoagulable state.
Staisis of venous circulation
What is meant by this
What are the conditons that lead to this
We want our blood to flow in our veins. THey do this by valves. So if valves are damaged or stop working properly then blood starts to gather and clot.
Conditons that lead to stasis of venous circulation:
- Varicose veins
- Surgery (especially hip or knees)
- Obstruction: late pregncancy, obesity
- Heart failure
- Atrial fibrillation
- Muscle weakness, leg injuryor trauma
Hypercoagulability
What is meant by this
What are the conditons that lead to this
high coagulation (rocess of a liquid, especially blood, changing to a solid or semi-solid state) of the blood
Conditons that cause this:
- Cancer
- Severe illness (sepsis)
- Dehyrdation
- Birth control (oestrogen)
- Postpartum Period
Endothelial Damage
What is meant by this
What are the conditons that lead to this
Damage to the endothelium
Conditons that lead to this are:
- IV drug usuage
- indwelling device
- medication
- trauma or injury to the vessel (surgeyr)
What is the pathophysilogy of PE?
The predominant theory for development of VTE is Virchow’s triad. This describes a triad of venous stasis, endothelial injury, and a hypercoagulable state. These are the three broad categories that contribute to the development of blood clots.
Natural history of PE
Occlusion of one or more of the pulmonary arteries leads to absence of perfusion to that area of the lung. There is said to be a ventilation/perfusion (V/Q) mismatch because ventilation is unaffected (i.e. the area of lung receives oxygen but not blood).
This V/Q mismatch may lead to hypoxia. The area of lung may undergo infarction (death from abnormal blood supply), but is usually prevented by the bronchial circulation. The V/Q mismatch can lead to elevated pulmonary arterial pressure, alveolar collapse, worsening hypoxaemia and reduction in cardiac output.
The sudden increase in pulmonary arterial pressure may rise to a level the right ventricle cannot overcome. This can lead to hypotension, syncope and in more serious circumstances shock and/or death due to acute right ventricular failure.
PE clinical features
- Dyspnoea
- Pleuritic pain
- Cough
- Leg swelling
- Leg pain
- Haemoptysis
- Palpitations
- Wheezing
- Angina-like pain
Scoring system for PE?
PE: scoring system
- WELLS–likelihood of PE
- GENEVA–likelihood of PE
- PERC-likelihood of PE
- PESI-severity of PE
Investigaions for PE
If Wells shows likely PE
- CTPA
- Parenteral anticoagulanttherapy
- Proximal deep vein legUSS
If Wells shows unlikely PE
- D-dimer→positive?→CTPA,Parenteralanticoagulant therapy
- D-dimer has highsensitivity (90%) but lowspecificity (can be raisedin many systemicillnesses)
- CXR
- V/Q scan
Management of PE
nitially = ABCDE-O2, fluids,ionotropes
- Risk assess-PE severity
- Give LMWH unless renalimpairment, risk ofbleeding,haemodynamically unstable
- Warfarin, NOAC and LMWHcontinuous
- Thrombolysis
- Embolectom
What is Bronchiectasis?
permanent, irreversible dilation of airways (chronic and obstructive)
Bronchiectasis is a long-term condition where the airways of the lungs become abnormally widened, leading to a build-up of excess mucus that can make the lungs more vulnerable to infection. The most common symptoms of bronchiectasis include: a persistent cough that usually brings up phlegm (sputum) breathlessness and chest pain
What disease can lead to bronchiectasis and how?
CF/TB
The defective gene and its protein causes the body to produce thick sticky mucous that clogs the lungs and leads to chronic life threatening lung infections with dilation and destruction of airways (bronchiectasis). Eventually it gets so thick that its consistently inflamed and infections that you cant clear ot so you get into chronic progressive pulmonary disease and respiratory failure
Pathophysiology of Bronchiectasis?
Chronic inflammation causes destruction of airway elastic tissue and ciliated epithelial cells
- Mucociliary stasis and increased mucous production
- Fibroblasts try to repair damage, deposits collagen, stiffens airways
SIgns and symptoms of Bronchiectasis?
ns and symptoms:•Purulent sputum, haemoptysis, suppuration,SoB, clubbing, crackles, wheeze
Investigations for Bronchiectasis?
•PFT= obstructive pattern→decreased FEV1/ FVC ratio
Imaging:
- HRCT/CT is better than CXR
- Dilation of bronchi and bronchioles
Management for Bronchiectasis?
•Clear mucus-percussion or postural drainage•Treat cause-Ab
Epidemiology of Lung cancer
3rdmost common malignancy in the UKand isthe leading cause of cancer relateddeath
- Itismorecommonaspeople get older ( around45% get diagnosed with lung cancer are aged 75years and older)
- Higherinmoredeprived areas, in terms ofethnicity and gender group more common inwhite males
Aetiology of Lung Cancer
- Smoking! (80%),including passive smoking•Increased risk in high pollution areas
- Family history
- Occupation; exposure to asbestosis ( carcinogenic building material,increases the risk of mesothelioma as well as other cancersieadenocarcinoma of the lung)
- Exposure to radon gas-increased risk to lung cancer
- Other comorbidities-pulmonary fibrosis, COPD, HIV infection
- Increasing age
- Previous history of malignanciesiehead and neck cancer
How is lung cancer categorised?
Small-cell (SCLC)
Non-small cell lung cancer (NSCLC): 85% of cancers
- Adenocarcinoma
- Squamous cell carcinoma
- Large cell
Pathology of lung cancer-Nonsmall cell types
adenocarcinoma
- Likely to become the common cell type in the UK in future(most common in US)
- Cancer of mucus secreting cells
- Appears more common in non smokers compared tosquamous cell carcinoma
- Asbestos and Smoking are risk factors
- Often causes peripheral lesions in Chest X ray/CT
- Metastases common-pleura, lymph nodes, brain, bone,adrenal gland
Pathology of lung cancer; Nonsmall cell types
squamous cell carinoma
- Remains the common type in Europe, main risk factor issmoking
- Arises from epithelial cells, associated with the productionofkeratin (‘keratin pearls’)
- Occasionally cavitates with central necrosis
- Causes obstructive lesions of the bronchus with postobstructiveinfection
- Paraneoplastic (‘hypercalcemia’)
- Local spread common-metastases relatively late
ClinicalManifestationsof Lung Cancer
signs
Symptoms of lung cancer?
Lung Cancer Treatment
Pathophysiology of IPF
Loss of structural integrity, loss of elasticity and restricted gas exchange leading to progressive respiratory failure
How do you know if it is non specific interstitial pneumonitis?
CT: Ground-glass opacities
Types of hypersensitivity pneumonitis related to occupation ?
Patho of hypersensitivity pneumonitis
Clinical features of hypersensitivity pneumonitis
Patho of sarcoidosis?
What is abestosis?
-Diffuse pulmonary fibrosis caused by inhalation of asbestos fibres, mostly affecting the lower lobes of the lung
