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
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
Investigations for bronchiectasis
Gold Standard - CT
Aetiology of bronchiectasis
Management of bronchiectasis
Remember to treat the underlying cause as well (ie. cystic fibrosis, Rheumatoid arthritis, Inflammatory bowel disease)
Clinical examination of pleural effusion
Investigations of pleural effusion
Gold Standard: Ultrasound
Lights Criteria
Used to differentiate exudative vs transudate pleural effusion
Management of pleural effusion
Types of pleural effusion
Signs and symptoms of pneumothorax
Investigations of pneumothorax
Treatment for pneumothorax
Signs and symptoms of idiopathic pulmonary fibrosis
Risk Factors for Idiopathic Pulmonary Fibrosis
Differential diagnosis for idiopathic pulmonary fibrosis
Treatment for idiopathic pulmonary fibrosis
Complications and prognosis for idiopathic pulmonary fibrosis
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
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
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
Cause of mesothelioma
exposure to asbestos
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
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
Causes of pulmonary hypertension
Diagnosis of pulmonary hypertension
Treatment for pulmonary hypertension
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
