Respiratory Flashcards
COPD
Chronic bronchitis
Emphysema
COPD is a common respiratory condition involving the airways and characterised by airflow limitation
Exacerbations and comorbidities contribute to the overall severity in individual patients
Signs and symptoms of emphysema
Known as “pink puffer” due to difficulty reathing but are well perfused
Dyspnea
Productive cough
Wheezing
Chest tightness
Pure emphysema patients:
Barrel Chest
Muscle wasting
Pursed lips
Signs and symptoms of chronic bronchitis
“blue bloaters” because they are usually synosed
Dyspnea
Productive cough
Wheezing
Chest tightness
Pure chronic bronchitis:
Peripheral Oedema
Raised JVP due to potential right-sided heart failure
Pathophysiology of emphysema
Pure emphysema affects alveoli. Alveoli are covered in elastic fibers allowing alvoli to expand and recoil back pushing air out as we exhale
However in emphysema what we see is a loss of elastic fibers and decrease in surgace area of the alveoli, this could lead to collapsed alveoli
Can also get air trapping which is where air is still trapped in the alveoli as we exhale because the recoil mechanism isn’t working
Pathophysiology of chronic bronchitis
Problems along bronchioles. In chronic bronchitis you have smooth muscle hypertrophy and contraction as well as mucus hypersecretion. Leads to difficulty breathing
Risk Factors for COPD
Investigations for COPD
1.Spirometry: FEV1/FVC ratio >70%
When evaluationg a patient with possible COPD spirometry is performed. Spirometry is performed pre and post bronchodilator administration to determine whether airflow limitation is present, partial or fully restrictive
2.X-Ray:
-Flattened diaphragm
-Hyperexpansion -> Hyperinflation
- Pulse oximetry -> check for O2 sat
Decreased O2 -> Hypoxemia - FBC -> check for amaemia
- Arterial blood gas
Is it respiratory acidosis/alkalosis
Late Stage COPD usually decreased O2 and increased CO2 - ECG
Check for heart involvement
Rule out MI, heart Failure
Diagnosis of COPD
Management of COPD
- Smoking Cessation
- Vaccination
- Bronchodilators: B2 agonists/anticholinergic. Short/Long acting
- Corticosteroids: inhaled glucocorticosteroids used in combination with long acting bronchodilators -> corticosteroids are not used alone
- Pulmonary rehab
- Oxygen therapy: for chronic COPD who has hypoxemia
Classification of COPD
Assessment of severity of condition is based on three factors:
1.Severity of symtpoms
2.Spirometry
3.Risk of exacerbations
Using the three features -> COPD classification -> Gold guidelines for COPD management
What is asthma
Chronic inflammatory disease affecting the lower airway, characterised by hyperresponsiveness and bronchospasm leading to airway narrowing
Pathophysiology of asthma
Triggers:
Allergic: pollen, pets
Nonallergic: smoking, perfumes
Trigger taken by dendritic cell and presented to T-helper 2 cell. TH2 cells produce IL-4, IL-13 (cause plasma cells to release IgE. IgE activated mast cells to cause degranulation. Granules include histamine leukotriene, prostaglandin- type 1 hypersensitivty reaction -> bronchospasm, increased mucus production, oedema. This narrows airway and produces symptoms) and IL-5 (leads to activation of eosinophils which release more cytokines and leukotriene contibuting to symptoms as well.
Acute exacerbation of asthma vs long term
Acute: Reversible
Long term: remodelling. Irreversible
1. Subepithelial fibrosis
2. Smooth muscle hypertrophy
3. Increased mucus production
4. Increased vascuarity
Causes/Risk Factors of asthma
Signs and symptoms of asthma
Recurrent episodes:
1.Dyspnea
2.Wheezing
3.Chest tightness
4.Coughing
Often worse at night or in response to exercise/cold air
Associated:
Anxiety
Obstructive sleep apnea
GORD
Complications of asthma
Remodelling: COPD
Increased rates of anxiety and depression
Asthma can be lethal
Diagnosis of asthma
Acute Exacerbation severity (mnemonic)
A: Altered consciousness
Arrhythmia
C: Cyanosis. PaCO2
H: Hypotension/Hypoxia
E: Exhaustion
S: Silent chest
T: Threatening PEF (<=33% Of best)
Treatment for asthma
No definitve cure. Stepwise approach
Long term: Assess-> Adjust -> Review (Repeat)
1.Short acting B2 agonist (salbutamol). SABA used as a reliever in most steps
2.Low dose inhaled corticosteroids
3.Long acting B2 agonist (salmeterol) + increasing ICS doses
4.Leukotriene receptor antagonists (montelukast)
5.Long acting anti-muscarinic (tiotropium)
6.Targeted Therapy: Anti IgE (omalizumab). Anti IL4/IL5
Acute Exacerbations:
1. O2
2. Nebulisers: Salbutamol, ipratropium
3. Systemic corticosteroids: prednisolone
If unresolved:
4. Mechanical sulfate
5. Mechanical Ventilation
Viral infections are common triggers, antibiotics given if baterial
Lung Infections
TB
Pneumonia
What is tuberculosis
Bacterial infection caused by “mycobacterium tuberculosis complex”
Characterised by the presence of chronic granulomatous inflammatory reaction
99% Mycobacterium tuberculosis
Mycoacterium bovis: Oropharyngeal & Intestinal TB
Mycobacterium Tuberculosis
Obligate aerobe
Intracellular pathogen
Grow very slowly
Lipid rich cell wall - mycolic acid
Do not stain with gram stain
Mannose capped glycolipids to bind macrophages
Able to survive and multiply inside macrophages by avoiding lysosomal killing
Acid & alcohol fast bacilli - do not decolourise with acid or alcohol when stained with Ziehl Nielson stain
Sensitive to: Heat, UV light, alcohol fermaldehyde, gluteraldehyde
Primarily infects lungs, intestine, bone, liver, kidney, brain, eye
Risk Factors for TB
HIV infection: serious risk factor for TB
Alcoholism
Diabetes Mellitus
Recent surgery
Immunosuppressive therapy - corticosteroids
Workers in healthcare facilites
Types of TB
2 types:
1. Primary TB - in non-sensitised hosts
2. Post-Primary (secondary) TB - in sensitised hosts
Spectrum of disease based on the immune response of the host
- Active TB - multiplying bacilli
-Pulmonary TB
-Extra pulmonary TB
-Miliary TB - Blood stream spread wih high bacillary load
2.Latent TB -Dormant bacilli
Pathogenesis of Primary Pulmonary TB
Primary Pulmonary TB - In non sensitised hosts
Inhalation of M.tuberculosis -> Bacilli get lodged in the “upper part of the lower lobe, or lower part of the upper lobe sub pleurally” -> Bacteria are engulfed by the alveolar macrophages -> Survive inside the macrophage -> Unchecked bacillary proliferation (first 3 weeks) -> Bacgeria spread via lymphatics & blood stream to the other parts of the body -> Asymptomatic/Mild flu like illness
- Macrophage response -> Inflammation (Ghon’s focus)
- Bacilli are taken to the lymph nodes via lymphatics -> Inflammation at the lymph nodes
- Bacilli in lymph nodes -> Macrophage presents processed Mycobacterual antigens to CD4 T cells (> 3 weeks) -> T cells become T helper cells -> T helper cells secrete cytokines acivating macrophages
- Activated macrophages:
1: Kill the bacilli by varous mechanisms: ROS, RNS, proteases -> Most bacilli get killed, but some may remain dormant for several years.
2: Secrete cytokines (TNF) -> Recruit more macrophages/Macrophage activation/Differentiation of macrophages into epithelioid cells -> formuation of granulomas
Possible outcomes of Primary Pulmonary TB
Control of the infection in immunocompetent hosts with healed lesions
Granuloma -> Heals by fibrosis -> Dystrophic calcification -> Ossification
Some bacilli may remain dormant
In immunocompromised patients: Primary pulmonary TB -> Progressive pulmonary TB
Progressive Primary TB
Most often resembles an acute bacterial pneumonia
Pleural effusion
Lung collapse
Cavitation is rare
Lower and middle lobe consolidation
Dissemintation of bacilli via lymphatics & blood stream -> Miliary TB/TB meningitis/TB lymphadenitis/TB spine
Secondary (Post primary) Pulmonary TB - in sensitised hosts
Progression of secondary TB
Miliary TB
Systemic miliary TB
Extra pulmonary TB
Clinical Presentation of TB
Chronic cough (>2 weeks) - dry/productive
Low grade fever - remittent (appears late afternoon & fades out)
Anorexia
Weight Loss
Night Sweats
Progressive pulmonary involvement - increasing amounts of sputum
Haemoptysis (advanced) - agressive disease (invasion of blood vessels)
Pleuritic chest pain
Diagnosis of TB
Primarily based on history, signs and symptoms and radiographic findings
1.Sputum direct smear for acid fast bacilli
Stained in bright red with Ziehl Nielson stain
Need 3 sputum samples - early morning sample is best
Most commonly used method
Cannot differentiate between species
Cannot test antibiotic sensitivity
2.Mycobaterial culture
Need only 1 sputum sample
Can differentiate between species
Takes 4-12 weeks to bet result
- PCR
Rapid detection
Can detect antibiotic resistance genes - Mantoux test - screening method
Treatment for TB
Prevention of TB
What is pneumonia
Infection/Inflammation of the lungs
Signs and symtpoms of pneumonia
Risk Factors for pneumonia
Pulmonary Defences
Causes of pneumonia
Impaired pulmonary defence makes an individual more susceptible to getting pneumonia
Examples of impaired pulmonary defences
Pathophysiology of pneumonia
Bacteria “translocate” to normally sterile distal airway - bacteria from URT that has either came in quickly or colonised for a while are micro-aspirated into lower lung
Resident host cells become overwhelmed
Develop an inflammatory response – neutrophils and inflammatory exudate fill alveolar space
Resolution phase – when bacteria cleared
Inflammatory cells removed by apoptosis
Resolution phase leads to complete recovery
In pneumonia you see:
Fluid filled alveoli
Bronchoconstriction
Increase in mucus secretion
Consolidation: process that fills the alveoli with fluid, pus, blood, cells resulting in lobar diffuse opacities
Types of pneumonia based on areas of lung affected
Lobar pneumonia
Broncho pneumonia
Lobar pneumonia
Broncho pneumonia
Bronchopneumonia affects patches throughout both lungs
Infection spreads along airway and finally reaches distal areas
Tendency for secretion to graduate to longer lobes
When to hospitalise patients with pneumonia (community acquired pneumonia)
If greater than 2, needs to be hospitalised
Transmission of pneumonia
Types of pneumonia based on where infection was acquired and cause of infection
Community Acquired pneumonia
Hospital acquired pneumonia
Aspiration pneumonia
Chronic pneumonia
Community Acquired Pneumonia
Hospital Acquired Pneumonia
Aspiration pneumonia
Lung abscess complication:
Extention to pleural cavity
Haemorrhage
Brain abscess
Meningitis
Secondary amylodosis
Chronic pneumonia
Complication of pneumonia
Investigations for pneumonia
- Chest X Ray
Patchy “bronchopneumonia”
Consolidation “lobar” - Sputum testing (Gram Stain)
To identify bacteria
MCS - Urine antigen testing
Identify bacteria: strep pneumonia or legionella - Blood testing
FBC: WBC increase/decrease indicates severity. Neutrophilia indicates bacteria. Haemolytic anaemia suggests mycoplasma
EUC testing: Urea high indicates severity
LFT: Abnormal if basal pneumonia inflames liver
Pneumonia treatment
- Oxygen: All patients with tachypnoea, hypoxemia, hypotension or acidosis
Cardinal signs of Pneumonia:
Chest Pain
Dyspnoea
Exudate (sputum)
Fever
- Intravenous fluids: Severe patient, elerly. Increase in vomitng
- Pain: NSAIDs, opiods
- Antibiotics
What pneumonia is mot common in HIV patients
Pneumocystis pneumonia is most common in HIV patients
What is cystic fibrosis
One of the most common autosomal recessive disease
Cystic fibrosis is a disease resulting from abnormality in the cystic fibrosis conducting regulator
Clinical Manifestation: Pancreatic dysfunction, Lung disease, and salty sweat
Clinical Presentation of cystic fibrosis
The clinical presentation of cystic fibrosis defer in infants and children.
Infants
Meconium ileus (bowel obstruction due to poo)
Rectal prolapse
Children - Mainly failure to thrive and recurrent upper respiratory tract infection
Chronic cough and wheezing
FTT
Pancreatic insufficiency (symptoms of malabsorption such as steatorrhea)
Alkalosis and hypotonic dehydration
Neonatal intestinal obstruction (meconium ileus)/Nasal polyps
Clubbing of fingers/Chest radiograph with characteristic changes
Rectal prolapse
Electrolyte elevation in sweat, salty skin
Absence or congenital atresia of vas deferens
Sputum with S. aureus or P. aeruginosa (mucoid)
Remember Cystic Fibrosis usually presents in childhood as recurrent lung infections that become persistent and chronic
Differential diagnosis of cystic fibrosis
Failure to thrive
Asthma
Coeliac Disease
GORD
Immunodeficiency disorders
Investigations for cystic fibrosis
Infant have a Heel prick - Immunoreactive Trypsinogen (IRT) to detect cystic fibrosis
Side note Heel prick is performed to screen for metabolic disease of the newborn inlcuding: galactosemia, cystic fibrosis, phenylketouria, sickle-cell disease and congenital hypothyroidism
Sweat test - first line for diagnosis
>60mmol/L
Genetic screening - Type of CFTR mutation
Aetiology of cystic fibrosis
Aetiology A mutation of the CFTR gene on the long arm of chromosome 7 is the cause of cystic fibrosis. The mutation of the CTFR gene results in a mutated CFTR protein which is a transported for Cl- ions. The severity of cystic fibrosis depends on the type of mutation found on the CFTR gene.
Pathophysiology of cystic fibrosis
Pathophysiology Cystic Fibrosis is caused by mutated CTFR protein. The CFTR protein is found on the apical surface of many hollow tissues notably the lungs, pancreas, gastrointestinal tract and sweat glands.
The CTFR protein is a transporter for Cl-. A mutated CFTR protein can not transport Cl- properly and as a result this causes a disregulated ion distribution. Whereever Cl- exists Na+ will follow because of the electrochemical gradient. When Na+ move water tends to follow.
This basic principle is the cause of the signs and symptoms seen in Cystic Fibrosis
Remember Cystic Fibrosis is characterized by the triad of chronic obstructive pulmonary disease, pancreatic exocrine deficiency, and abnormally high sweat electrolyte concentrations.
Management of Cystic fibrosis
Management of meconium illeus performed after delivery.
General
High fat, high calorie diet
Pancreatic enzyme supplement
Vitamin supplementation (ADEK)
Salt supplementation
Pulmonary care
physiotherapy
shaking chest jackets
Long-term antibiotics (inhaler)
Bronchodilator
Ongoing management
Management of upper respiratory tract infection
Oral Antibiotics
IV antibiotics
Management of non-pulmonary complications
Remember patients with CF are at risk of having recurrent URTI which can be caused by S. aureus, H. Influenzae, P. aerugenosa.
Complications of cystic fibrosis
What is bronchiectasis
Irreversible dilation of the airways due to inflammatory destruction of airway walls resulting from persistently infected mucus
P.aureginosa is the most common pathogen
Clinical manifestations include: chronic cough copious mucopurelent expectoration
Common in patients with cystic fibrosis
Risk Factors of bronchiectasis
Cystic fibrosis
Host immunodeficiency
Previous infections
Congenital disorders of the bronchial airways
Primary ciliary dyskinesia
Alpha-1 antitrypisn deficiency
Connective tissue disease
Inflammatory bowel disease
Aspiration or inhalation
Clinical Presentation of bronchiectasis
Remember Massive haemoptysis is >500ml blood loss in 24hrs
Examination: Percussion resonant, mixed predominant coarse crackles, often additional polyphonic wheeze. Presence of of high pitch inspiratory squeals and rhonchi
Differential diagnosis of bronchiectasis
COPD
Asthma
Pneumonia
Chronic sinusitis
Investigations for bronchiectasis
Gold Standard - CT
Aetiology of bronchiectasis
Pathophysiology of bronchiectasis
Essentially the different causes of bronchiectasis with impaired respiratory defences/ immunodeficiency will trigger an inflammatory process, recurrent infections that will result in the pathological changes seen bronchiectasis. There will be bronchiole dilatation, immune cells infiltration into the tissue (lymphocytes), bronchial ulceration and oedema, smoother muscle hypertrophy and neovascularization.
Patients with bronchiectasis gets recurrent infection. Common causes of infections are p. aureginosa, s. pneumoniae, h. influenzae, s. aureus. Infection can trigger exacerbations.
Management of bronchiectasis
Remember to treat the underlying cause as well (ie. cystic fibrosis, Rheumatoid arthritis, Inflammatory bowel disease)
Complications of bronchiectasis
Massive haemoptysis
Respiratory failure
Cor pulmonale
What is pleural effusion
Accumulation of fluid in the pleural space
Pathophysiology of pleural effusion
Mechanisms:
Increase pleural fluid formation:
1. Increase in permeability (inflammation)
2. Increase venous pressure
3. Decrease plasma oncotic pressure (hypoproteinaemia)
4. Decrease pleural pressure
Pleural fluid protein is not altered by clearence of fluid of lymphatics
Decrease pleural fluid clearance
1. Cancer invasion
2. Blockage of lymphatic stoma
3. Mechanical compression (granuloma)
4. Injury from chemotherapy/radiation therapy
Clinical examination of pleural effusion
Investigations of pleural effusion
Gold Standard: Ultrasound
Lights Criteria
Used to differentiate exudative vs transudate pleural effusion
Diagnosis of pleural effusion
Ultrasound “gold standard” + thoracocentesis
thoracocentesis (pleural fluid analysis: lactate dehydrogenase. protein)
Light criteria
Causes of transudative vs exudative pleural effusion
Causes of transudative pleural effusion: Increase in peural BNP
1. Congestive Heart Failure
2. Liver Cirrhosis
3. Nephrotic syndrome
Causes of exudative pleural effusion: Pleural culture. pleural fluid cell differentiation + glucose
1. Infective
2. Malignancy
3. Pulmnary embolism
4. Gastrointestinal pathology
5. Connective tissue disease
Management of pleural effusion
Types of pleural effusion
What is a pneumothorax
Abnormal collection of air in pleural space
-Disrupts negative intrapleural pressure + presence in air and pressure -> Lung size will decrease and collapse
Pneumothorax Types & Classification
- Outside: through chest wall
- Inside: ruptured lung and pleura
Types:
1. Traumatic- cause by trauma
Blunt vs Penetrating
Iatrogenic (result of invasive procedure): result of positive pressure mechanical ventilation
- Non-traumatic - spontaneous
Primary Spontaneous Pneumothorax (PSP): Normal lung, no known cause
Secondary Spontaneous Pneumothorax (SSP): Lung with underlying disease (COPD, Asthma, TB, fibrosis, Cancer, pneumonia)
Classification:
Simple (No mediastinal shift) vs Tension (mediastinal shift)
Open (Open wound chest wall. Air in & out. “Sucking Chest wall”) vs Closed (Chest Wall intact)
Signs and symptoms of pneumothorax
Investigations of pneumothorax
Treatment for pneumothorax
What is idiopathic pulmonary fibrosis?
Chronic progressive fibrotic interstitial lung disease
Primarily occurs in older adults
Signs and symptoms of idiopathic pulmonary fibrosis
Differential diagnosis for idiopathic pulmonary fibrosis
Heart Failure
COPD
Risk Factors for Idiopathic Pulmonary Fibrosis
Pathphysiology of idiopathic pulmonary fibrosis
Patchy fibrosis of interstitium, minimal or absent inflammation, acute fibroblastic proliferation and collagen deposition.
Investigations for idiopathich pulmonary fibrosis
Pulmonary Function Test: Decreased FVC and TLC
Diffusing capacity of carbon monoxide: Decreased
Chest X-ray:
Bilateral reticular infiltrates
Hazy opacities
Decreased Inspiratory volume
High resolution CT chest: Gold Standard
Bilateral reticulation
Honeycombing: Changes are lower lobe predominant
Traction bronchiectasis
Differential diagnosis for idiopathic pulmonary fibrosis
Treatment for idiopathic pulmonary fibrosis
Complications and prognosis for idiopathic pulmonary fibrosis
What is sarcoidosis
Multisystem inflammatory disease of unknown aetiology
Predominantly affects: lungs, intrathoracic lymph nodes, non-caseating granulomas
Characterised by an exaggerated immune response against an unrecognised antigen
Causes of sarcoidosis
Symptoms of sarcoidosis
Pathophysiology of sarcoidosis
Non-caseating granulomata form at various sites in the body, particularly the thoracic cavity, skin and eyes. Bilateral hilar lymphadenopathy and/or pulmonary infiltrations.
Contain: Langhans giant cells and non-caseating granulomas
Diagnosis of sarcoidosis
Radiological stage by chest radiography at presentation inversely correlates with likelihood of spontaneous resolution.
Stage 0: normal
Stage I: bilateral hilar lymphadenopathy
Stage II: bilateral hilar lymphadenopathy plus pulmonary infiltrates
Stage III: pulmonary infiltrates without hilar lymphadenopathy
Stage IV: extensive fibrosis with distortion.
Typically shows bilateral hilar adenopathy.
Treatment of sarcoidosis
What is respiratory failure
Acute Respiratory failure causes hypoxia and/or impaired ventilation with hypercapnia, leading to severe hypoxemia and rapid deterioration. Two main types of respiratory failure
Types of respiratory failure
Type 1:Hypoxaemia (PaO2<60mmHg) without hypercapnia. Caused by conditions affecting oxygenation: right-to-left shunts or V/Q mismatch
Acute Respiratory Failure Type II: Chronic Respiratory Failure
Type I respiratory failure (non-hypercapniec respiratory failure)
Primarily from failure of oxygenation (PaO2 <60mmHg)
Normal or low CO2
pH 7.5
Usually responds to Oxygen therapy
Type II respiratory failure (hypercapniec respiratory failure): Hypoxaemia with hypercapnia (PaCO2>50mmHg).
Increased CO2 (PaCO2 >50mmHg)
Normal or low O2
pH <7.3
Failure of ventilation as well as oxygenation
Requires ventilator support as well as supplemtntal oxygen
Signs and symptoms of respiratory failure
Clinical Presentation
Increased work of breathing
Increased RR
Use of accessory muscles
Tracheal tug
Abdominal recession
Increased HR
Sweating or clammy skin
Anxiety or agitation
Exhaution and confusion
*Other signs and symptoms depending on cause
Signs of Hypoxia
Cyanosis
Low O2
Arrthymia (from hypoxia)
Anxiety, agitation
Acidosis (tissue hypoxia)
Hypoventilation
Vasodilation
Headache, fatigue
Asterixis
Acidosis
Obstruction
Inability to speak
Accumulation of secretion
Remember Use pulse oximetry, ECG, ABG and Chest X-ray in the initial assessment
Causes of respiratory failure
Type I Type II
Pneumonia COPD
ARDS Life-threatening asthma
Interstitial lung Disease Drug Intoxication (opioids)
Acute Pulmonary Oedema CVA/trauma
Asthma Primary muscles disorders
COPD Myasthenia gravis
Pneumothorax Poliomyelititis
Pulmonary Embolism Kyphoscoliosis
Obesity Polyneuropathies
Pulmonary hypertension Obesity
Pathophysiology of respiratory failure 1
V/Q mismatch
Pneumonia
ARDS
Interstitial Lung disease
PE
Pneumothorax
Right-to-left shunt
Physiological: Pneumonia, acute pulmonary oedema, atelectasis
Anatomical: intra-cardiac shunts (VSD, ASD), pulmonary AVM
Low inspired O2 partial pressure (FiO2)
High altitude
Diffusion impairment
Interstitial lung disease - Restrictive
Acute pulmonary oedema
ARDS
Hypoventilation
Obesity
Management of respiratory failure 1
Oxygenation (non-invasive)
Nasal prongs
Simple Mask
Venturi mask
Treat underlying cause
Ventalin - if asthma or COPD to reduce bronchoconstriction
Antibiotics – if infection
Diuretics – if fluid overload
Monitor clinically and with ABG
Non-invasive mechanical ventilation
CPAP/PEEP
Maintain recruitment of collapsed lung
Increased functional residual capacity
Minimise intrapulmonary shunt
BiPAP
Invasive mechanical ventilation - if not improving
Endotracheal Intubation
Tracheostomy Tube
Pathophysiology of respiratory failure type 2
Hypercapnia when alveolar ventilation insufficient to excrete volume of CO2 produced by tissue metabolism due to:
Decreased minute ventilation
COPD
Asthma
Heart failure
Neurological causes
Kyphoscoliosis
Obesity
Increase in dead space ventilation
Increased CO2 production
Fever, sepsis, seizure, acidosis, carbohydrate load
Treatment for respiratory failure type 2
Remember aims of treatment here is to achieving safe oxygen concentration without increasing CO2 and acidosis, while identifying precipitating condition
Oxygenation (non-invasive)
Nasal prongs
Simple Mask
Venturi mask
Treat underlying cause
Ventalin - if asthma or COPD to reduce bronchospasm
Antibiotics – if infection
Diuretics – if fluid overload
Monitor clinically and with ABG
Non-invasive mechanical ventilation
BiPAP
Invasive mechanical ventilation - if not improving
Intubation
Think Becareful using oxygen in COPD. Severe COPD hypoventilate and retain CO2. Giving uncontrolled O2 may increase CO2.
What is lung cancer
Leading cause of cancer related deaths
Cigarettes are the major cause of lung cancer
Risk Factors for lung cancer
Signs and symptoms of lung cancer
Differential diagnosis for lung cancer
Investigations for lung cancer
General
Chest X-Ray - opacity
Spirometry - if thinking of obstructive or restrictive lung disease
CT
Investigation Chest x-ray findings can vary in patients with lung cancer and can include pulmonary opacity, hilar enlargement, pleural effusion and collapsed lung.
Investigations for staging
CT
CT- Biopsy
PET scan
Pleural fluid aspiration
Lung biopsy with bronchoscopy
Endobronchial ultrasound
Sputum MCS
Lung Carcinoma classification
Lung cancer can be broadly divided into either small cell lung carcinoma or non-small cell carcinoma. Non small cell lung carcinoma making up the majority 80%
Small cell lung carcinoma (SCLC - 20%)
Non-small cell lung carcinoma ( NSCLC - 80%)
Adenocarcinoma
Squamous cell carcinoma
Large cell
Management and Staging of lung cancer
Once a patient presents with symptoms or radiographic findings suggestive of lung cancer, the next steps are as follows:
1.Tissue diagnosis to establish malignant diagnosis and histologic type
2.Staging to determine resectability or curative potential
3.Cancer treatment: surgery, radiotherapy, or chemotherapy
Complications on lung cancer
NSCLC
Post-obstructive pneumonia/hypoxia
Superior vena vaca syndrome
Paraneoplastic syndromes
SCLC
Post-obstructive pneumonia/hypoxia
Superior vena vaca syndrome
Paraneoplastic syndromes
Chemothreapy induced hematological toxicity
Radiation induced esophageal/lung injury
What is mesothelioma
Cancer arising from mesothelium
Types of mesothelioma
Pleural mesothelioma
Peritoneal mesothelioma
Pericardial mesothelioma
Cause of mesothelioma
exposure to asbestos
Signs and symptoms of mesothelioma
Shortness of breath, dull diffuse chest pain (occasionally pleuritic), weight loss, lethargy. Pleural effusion. History of asbestos exposure, sometimes. Potentially a palpable chest wall mass.
Pathophysiology of mesothelioma
Arises from mesothelial cells (80% pleura, rest are peritoneum and pericardium). Deposition of the asbestos fibres in parenchyma -> penetration of the visceral pleura -> transport of the fiber to the pleural surface -> Development of a malignant plaque (asbestos can apparently facilitate foreign DNA entering the cell -> messing with oncogenes etc)
Investigations for mesothelioma
CXR: Pleural effusion. Potentially rib destruction. Pleural aspiration: Straw coloured or blood stained.
Pleural biopsy: Gold standard
Treatment for mesothelioma
Surgical: Ressection (pleurectomy and decortication may relieve pain and effusions) Chemo: Improves survival of patients with unressectable mesothelioma. Radio: Mostly for pain control if at all
Causes of dyspnoea
COMMON CAUSES OF CHRONIC DYSPNOEA
Respiratory Disease Cardiovascular Disease
COPD Myocardial Dysfunction (Heart Failure)
Asthma Obesity/de-conditioning
Interstitial lung disease
Recognise the MRC dyspnoea scale
Classification of interstitial lung disease
interstitial lung disease: upper lobar predominance “BREASTS”
interstitial lung disease: lower lobar predominance “AIDS”
Clinical Presentation of Interstitial lung disease
Diagnosis of Interstital lung disease
High Res CT - gold standard
What is hypersensitivty pneumonitis
Inappropriate immune response to an antigen causing inflammation of the lung
extrinsic allergic alveolitis
Upper Lobe predominance
Types of hypersensitivity pneumonitis
Clinical Manifestation of hypersensitivity pneumonitis
Treatment of hypersensitivity pneumonitis
Differential diagnosis of hypersensitivity pneumonitis
Diagnosis of hypersensitivity pneumonitis
Pathophysiology of hypersensitivity pneumonitis
What is pulmonary hypertension
Increase in blood pressure in the pulmonary circulation
Mean arterial pressure >25mmHg
Causes of pulmonary hypertension
Diagnosis of pulmonary hypertension
Treatment for pulmonary hypertension
Complications of pulmonary hypertension
Right sided heart failure
Causes of croup
Parainfluenza 1 and 2
Respiratory syncytial virus (Common cause of bronchiolitis)
Remember Croup symptoms usually start with flu like symptoms. Croup is caused by viruses, with para-influenza virus (types 1 to 3) as the most common
Signs and symptoms for croup
Classic Tetrad: barking cough, stridor, hoarse voice, and respiratory distress
Agitation
Inspiratory stridor
Barking Cough
Hoarse voice
Male
Young age
Tracheal Tug
Lethargy
Abrupt onset of symptoms
Symptoms worse at night
Differential diagnosis for croup
Differentials for stridor
Croup (common)
Bacterial tracheitis (uncommon)
Foreign body
Epiglottitis (rare)
Investigations for croup
Croup is a clinical diagnosis based on early respiratory infections followed by a barking cough
Chest X-ray
Neck X-ray - steeple sign
Pathophysiology for croup
Classification of croup
Mild Airway Obstruction
Barking cough without inspiratory stridor
Moderate Airway Obstruction
Stridor at rest
Tracheal tug
Chest wall recession
Severe Airway Obstruction
Persisting stridor
Tracheal tug
Chest wall recession
Aaethetic/restless
Soft stridor, irritability, tachycardia, pallor indicates imminent airway obstruction
Management of croup
A single dose of dexamethasone is recommended in all patients with croup, including those with mild disease. Nebulized epinephrine is an accepted treatment in patients with moderate to severe croup.
Mild Airway Obstruction
No need for specific treatment
Moderate Airway Obstruction
Corticosteroids
Oral Prednisalone (1mg/kg)
Dexamethasone (0.3mg/kg)
+/- Nebulised Adrenaline - Budesonide (2mg)
Severe Airway Obstruction
Oxygen
Corticosteroids
Oral Prednisalone (1mg/kg)
Dexamethasone (0.3mg/kg)
+/- Nebulised Adrenaline - Budesonide (2mg)
Monitor
Remember Antibiotics have no role in uncomplicated croup as it has a viral aetiology
