REsp Flashcards
Hospital acquired pneumonia - antibiotics to use
Ceftriaxone (low risk: HA from ward)
High risk: from ICU, ventilator etc (concern about pseudomonas)
Tazosin = piperacillin/tazobactram
Common causes of HA pneumonia
Gram neg: klebsiella, E coli, pseudomonas, bacteroides
MRSA
Common causes of community acquired pneumonia (typical)
Strep pneumonia (90% cases)
H influenzae
Moraxella
Staph aureus
Common causes of community acquired pneumonia (atypical)
Mycoplasma pneumonia
Chlamydia pneumoniae
Legionella
Pneumocystis Jiroveci
What is COPD characterised by?
airway inflammation and limitation that IS NOT FULLY reversible (asthma is fully reversible so is not COPD)
What medical conditions does COPD include? Define them
Emphysema - dilation and destruction of lung tissue distal to terminal bronchiole (alveolar wall destruction and overinflation)
Chronic bronchitis - persistent PRODUCTIVE cough for at least 3 consecutive months in at least 2 consecutive years (airway inflammation)
Risk factors/causes of COPD
Cigarette smoking Air pollution Occupational exposure Alpha1 antitrypsin deficiency Recurrent RTIs in childhood Genetics
What pattern would you see on respiratory function test with COPD?
Restrictive lung disease.
Forced expiratory ratio (FEV1/FVC) <70% indicating airflow obstruction.
FEV1 is reduced but FVC normal.
With no improvement with bronchodilator (ventolin).
Pathophysiology of emphysema
Noxious agent causes release of destructive cytokines and neutrophils, macrophages and CD8+ T cells which cause ongoing destruction of lung parenchyma - destruction of elastin and alveolar membranes -> reduced elastic coil - air trapping during expiration
Pathophysiology of chronic bronchitis
Noxious agent causes release of destructive cytokines and neutrophils, macrophages and CD8+ T cells which cause ongoing destruction of lung parenchyma and airway inflammation and remodelling
-> enlarged mucus secreting glands, goblet cell metaplasia, bronchial wall fibrosis, hyper secretion of mucus, inflammation
Clinical features of COPD
Chronic productive cough
Wheeze
SOB
HX smoking
What will you find on chest examination for COPD (Non-examination)
Auscultation - breath sounds reduced with prolonged expiratory phase, wheeze Percussion - normal/hyper-resonance Vocal resonance - normal or reduced Hyperinflation (barrel chest) Decr expansion
Classic CXR findings for COPD
hyperinflation (>6 ribs anterior ribs above diaphragm in mid-clavicular line)
Flat hemidiaphragms
Large central pulmonary arteries
Decr peripheral vascular markings
Management plan for COPD
CONFIRM diagnosis w pulmonary function tests
- smoking cessation
- influenza and pneumococcus vaccine (reduces risk of exacerbations)
- pulmonary rehab
- medications (depend on stage of disease)
- Long-term o2 therapy if chronic resp failure (Stage 4) - must be non-smokers
Pharmacological treatment of COPD
Stage 1: Short acting bronchodilators when needed
- Short acting beta 2 agonists (Salbutamol/Ventolin)
- SAMAR (ipratropium)
Stage 2: regular treatment with one or more long acting bronchodilators
- LABAs (Salmeterol/Serevent)
- LAMAR (Tiotropium/Spiriva)
Stage 3/4: Inhaled glucocorticosteroids if repeated exacerbations
Complications of COPD
CHRONIC BRONCHITIS COMPLICAITONS:
- SCC of lung resulting from squamous metaplasia
- Infective exacerbations
- Hypoxia -> pulmonary HTN -> cor pulmonale
EMPHESEMA COMPLCIATIONS
- Loss of diffusion capacity
- pneumothorax
- hypoxia -> pulmonary HTN -> cor pulmonale
Management of exacerbation of COPD
Give O2
Bronchodilators
Corticosteroids
Antibiotics
Mobilisation
Non-invasive ventilation - BiPap, VPAP
Why don’t you give high flow O2 with COPD?
Don’t give too much too quickly though, may be in chronic resp failure where their drive to breathe is low O2.
If you increase O2 then you decrease their drive to breathe which leads to hypercapnoea
Definition of bronchiectasis
Chronic infection of bronchi and bronchioles leads to permanent dilation of bronchi, as well as inflammatory changes in airway walls and neighbouring parenchyma
Pathophys of bronchiectasis
Recurrent inflammation of bronchial walls weakens walls
Fibrosis of surrounding parenchyma puts traction on and weakens walls, causes dilation
Symptoms of bronchiectasis
Signs
Cough
Copious purulent foul smelling sputum
intermittent haemoptysis
Signs:
- Clubbing
- Exp wheeze
- Coarse insp crepitations
Causes of bronchiectasis
Obstructive
- tumour
- foreign body
- thickened mucus (asthma)
Post-inflammation
- pneumonia
- Tb
- measles etc
Weakened defences
-CF
Common causes of lung abscesses
- Most commonly a complication of aspiration pneumonia (aspirated objects accompanied by bacteria -> inflammation secondary to inflammation -> localised consolidation)
- Pulmonary infarct
- malignancy
- Penetrating trauma
- Bronchial obstruction
Management of lung abscess
Empiracle antibiotics
If non-resolving, surgical intervention
+/- postural drainage
+/- chest physiotherapy
What is the histopath pattern of Tb?
Caseating granulomatous inflammation with epithelial cells, giant cells and lymphocytes and central caseating necrosis.
Tests for DIAGNOSIS OF Tb
Quantiferon GOLD test or Mantoux test
Ziel-nelson stain
When does primary vs progressive vs secondary occur?
Primary Tb is what occurs following first exposure to M. Tb
Progressive Tb occurs in less than 10% patients, mostly immunocompromised/malnourished. Rapid spread through lungs/body
Secondary: reactivation of a dormant focus of primary infection, often with immunosuppression (steroids and HIV)
Possible sequelae of progressive Tb
Caveatting fibrocaseous Tb (erosion of ghon complex into bronchiole)
Miliary Tb (haematogenous dissemination)
Tuberculous bronchopneumonia (infection spreads rapidly -> diffuse bronchopneumonia or lobar exudative consolidation)
Gohn complex vs focus in Tb
Occurs in primary Tb
GHON focus - small area of encapsulated granulomatous inflammation (central cassation)
GHON complex - involves adjacent lymphatics and lymph nodes
What area of lungs do Tb GHON focuses in primary Tb occur in?
Mid zone sub-pleural
At what stage in Tb do patients become symptomatic and what are those SX?
Primary Tb usually asymptomatic
Progressive- have pulmonary and systemic SX
Secondary Tb - systemic symptoms (cough, fever, malaise, weight loss)
What area of lungs does secondary tb affect?
Upper lobes
Causes of granulomatous inflammation in the lung
Tb Sarcoid (non-caseating) Hypersensitivity pneumonitis Wegener's granulomatosis vasculitis Aspiration pneumonia Rheumatoid nodules
Treatment of Sarcoidosis
Immunosuppression
What is sarcoidosis?
Non-caseating granulomatous inflammation
- affects lungs, skin
- common in young adults 20-40
Asthma
- 3 characteristics
1. reversible airflow limitation
2. airway hyperresponsiveness to a variety of stimuli
3. bronchial inflammation (T lypmphocytes, mast cells, eosinophils)
Asthma symptoms
Wheeze (exp if mild; exp and insp if severe)
Cough
Chest tightness
SOB
Often worse at night
Why might asthma become associated with irreversible airflow limitation?
Chronic inflammation leading to airway remodeling (smooth and goblet cell hyperplasia with incr mucus secretion) in chronic asthma patients (60-70)
Triggers for asthma
Cold Exercise Pollen, dust, pollution Tobacco smoke Animals - cat, dog, birds URTI Medications (NSAIDs, beta blocers) Emotion, stress
Investigations for asthma
CXR and ABG
Lung function tests (forced peak expiratory flow) - decr
Spirometry - >15% improvement in FEV1 or peak exp flow rate following bronchodilator
Blood or sputum test - large eosinophil titre and IgA/IgE levels
Skin prick tests to help identify allergic causes
Histamine or methacholine bronchial provocation testing (measures airway hyperresponsiveness). Note: can provoke resp arrest so dont do in individuals w FEV1<1.5L or w brittle asthma
Management of chronic asthma
Intermittent asthma
§ Inhaled SABA (beta 2 agonist) as needed
Mild persistent
§ Use low potency inhaled GC
Moderate persistent
§ Mild dose of inhaled GC + LABA (or leukotriene antagonist)
§ OR moderate dose of inhaled GC
Severe persistent
§ Med-high dose of inhaled GC + LABA +/- leukotriene antagonist
+ SABA as needed Salbutamol
Management of acute asthma attack (in ED) = status asthmaticus
O2
Nebulise bronchodilators on O2, not air
CXR
Large dose oral prednisilone or IV hydrocortisone
+/- IV Mg (vasodilator/dilates airway)
ICU assessment if no improvement in 1 hour
DO NOT give IV beta agonists - toxic.
Medications used for asthma
Beta 2 agonists - SABA Salbutamol; LABA Salmeterol (SX relief)
Inhaled corticosteroids -fluticasone (preventer)
Oral coritcosteroids in ED only
Combination inhaleds - Seretide (ICS/LABA = fluticasone/salmeterol)
Leukotriene R antagonists (oral montelukast)
Anti IgE (omalizumab) - SC inj every 2-4 weeks w persistent allergic asthma
SE of Inhaled corticosteroids in treatment of asthma
Thrush, hoarse voice
Cushingoid syndrome w v high doses
Features of life threatening asthma (status asthmaticus)
silent chest cyanosis feeble resp effort exhaustion, confusion, coma bradycardia or hypotension peak exp flow rate <30% of predicted normal
hypercalaemia, hypoxaemia
Low/falling arterial pH
Treatment of pulmonary oedema
LMNOPP
Lasix (frusemide) Morphine Nitroglycerin (GTN) O2 (hypoxemic) Position (sit upright) Positive airway (CPAP, BiPAP)
Causes of viral pneumonia . is this a typical or atypical pneumonia ?
Influenza
Parainfluenza
RSV
Atypical presentation
Atypical vs typical pneumonia
Who does it affect? Time course Pattern Degree of rise - WCC SX
Typical (bacterial):
- Older people
- Sudden onset, lasts 7-10days
- Lobar consolidation
- High rise WCC
- Fatigue, high fever, productive cough (resp Sx only)
Atypical:
- Younger people
- Gradual onset over 2-3 weeks
- Diffuse, bilateral
- No consolidation; mild incr WCC
- SX not as severe - cough w minimal sputum; low grade fever + extrapulm SX (muscle aches, headache, nausea, vomiting diarrhoea, abdo pain)
Acute bronchopneumonia vs acute lobar pneumonia
Acute bronchopneumonia
- Patchy bilateral distribution involving multiple lobes, multiple foci of inflammation
- Bug w low virulence
Acute lobar pneumonia
-Inflammation of an entire lobe w no part spared
-Bug w high virulence
+Pleural pain (inflame of pleura)
Consolidation - findings on chest examination
Decr expansion Dull percussion note Incr vocal resonance Bronchial breathing Pleural rub
Investigations for suspected pneumonia
Bloods: FBE, U&E (renal baseline), CRP, blood culture
CXR
Pulse oximetry
Sputum sample for MCS
If suspected atypical infection:
Urine test - legionella and pneumococcal Ag
Viral serology
Nasopharyngeal swab for influenza PCR
Treatment for CA atypical pneumonia
Doxycycline + macrolide
Treatment CA typical pneumonia
Augmentin (Strep)
Azithromycin (H infl, moraxella)
Doxycycline (H infl)
What agents, in what context, might cause lung abscess
Strep pygenes, staph aureus, Klebsiella
Secondary to bacterial pneumonia
Complications of pneumonia
Empyema Pleural effusion Lung abscess Respiratory failure Sepsis
What is cor pulmonale?
Cor pulmonale is RV enlargement and eventually failure secondary to a lung disorder that causes pulmonary artery hypertension.
Causes of pulmonary HTN
Primary pull artery HTN
Increased LA pressure
- Mitral Stenosis
- LV failure
- Diastolic dysfunction
Increased pulmonary blood flow
- L-R shunts
- high flow states
- Fluids overload
Increased pulmonary vascular resistance
- Vasoconstriction secondary to hypoxia (COPD, bronchiectasis)
- Obstruction (PE)
- Obliteration (emphysema, pulmonary fibrosis, arteritis)
Signs of pulmonary HTN (without R heart failure)
RV (L parasternal) heave
Prominent “v” wave in JVP
Cyanosis, tachypnoea
How does pulm HTN lead to RV hypertrophy (what sort) and Cor pulmonale?
Pulmonary HTN leads to incr afterload on R ventricle -> R ventricular concentric hypertrophy
- > decr CO -> RH failure - > incr systemic venous pressure -> extravasation of fluid into interstitial tissues and peritoneal and/or pleural spaces
Type 1 vs Type 2 resp failure
Type 1: Hypoxaemia WITHOUT Co2 in blood. caused by VQ mismatch (failure of blood oxygenation)
Type 2: Hypoxaemia WITH hypercapnoea; low pH . caused by inadequate alveolar ventilation or high inspired CO2 or high CO2 production (fever, sepsis, acidosis etc)
What is Mesothelioma strongly associated with, in terms of social history?
Asbestos
Workers: miners, dockers, masons, plumbers, welders, installation
What is the most frequent initial presentation of mesothelioma?
Pleural effusion
What is mesothelioma?
What is the life expectancy?
Primary malignancy of pleura, usually occurring 20-30 years after asbestos exposure
<1 year after symptom onset
Investigations/diagnosis of mesothelioma
CXR/chest CT
Biopsy of pleura with histological confirmation and biomarker staining
What are benign manifestations of asbestos exposure?
Pleural plaques (asymptomatic radiological finding) Pleural effusion - Self-resolving and exudative
How do you characterise pleural effusions are what are possible causes under each category?
- Transudative:
- High hydrostatic pressures or low oncotic pressure
- Low protein content)
- CCF, cirrhosis, renal failure
- Hypoproteinemia (nephrotic syndrome, cirrhosis, malabsorption)
- Exudative:
- Incr vasc permeability/damage to vessels
- High protein content
- Infectious: Pneumonia, Tb
- Malignant: Primary cancer, mets
- Inflammatory: RA, SLE, PE-> Pulm Infarct
- Haemothorax (blood, traumatic )
- Chylous effusion (lymph in pleural space)
- Empyema (pus)
Signs of a pleural effusion on chest examination
Chest expansion: decr
Percussion: stony dull
Vocal resonance: decr
Breath sounds: decr
If severe, tracheal deviation away from effusion
Investigations for pleural effusion
CXR (blunting of costophenic angle +/- meniscus)
Pleural tap (diagnostic or therapeutic)
-> Protein and LDH
-> MCS
-> Tb stain
-> Cytology
-> Immunology if indicated (Rh factor; ANA, C’ for SLE)
+/- biopsy (if malignancy, Tb suspected)
+/- US (locate pleural fluid and guide diagnostic or therapeutic aspiration)
Management of pleural effusion
Pleural tap to drain the effusion if symptomatic
PLeurodesis for recurrent effusions
What is an empyema?
Pus in pleural space or pleural effusion with purulent bacteria seen on Gram stain or culture
Causes of empyema?
Complication of pneumonia (contiguous spread)
Infection through chest wall (trauma, surgery)
definition of Sarcoidosis
Multisystem granulomatous disease of unknown cause, commonly affecting lungs, and skin (but also lymph nodes, liver, spleen, eyes, heart, brain)
Diagnosis of Sarcoidosis
Tissue Biopsy showing non-caseating granulomatous inflammation (lung, liver, lymph nodes, skin nodules, lacrimal glands)
Bloods: raised serum ACE (60%), +/- hypercalcaemia, raised ESR, incr LFTs
CXR: 90% peripheral pulmonary infiltrates +/- bilatera hilar lymphadenopathy
Management of Sarcoidosis
- Bilateral hilar lymphadenopathy alone: no treatment, spontaneous recovery
- Acute sarcoidosis: bed rest and NSAIDS
- Pulmonary disease, uveitis, hypercalcaemia, cardiac or neuro involvement
- Oral prednisilone
- IV steroids or immunosuppressants if severe
- Anti TNF alpha or lung transplant if refractory
What are the presenting features of acute sarcoidosis?
Treatment?
Erythema Nodosum
+/- polyarthralgia
Treatment: bed rest and NSAIDs
What is Cystic Fibrosis? and how does it present?
Autosomal recessive condition (mutation in Cl channel)
Chloride transport dysfunction
-> defective Cl secretion and increased Na absorption across airway epithelium.
This Cl channel involved in fluid production
In lungs -> leads to thicker secretions of airway mucus which clogs airways and predisposes to pulm infection and bronchiectasis
Also affects pancreas, skin, reproductive organs
How does CF usually present?
What else happens w time?
Presenting in childhood with recurrent lung infections that become persistent and chronic.
Results in
- severe lung disease
- pancreatic insufficiency
- diabetes
- azoospermia
Signs on examination of CF (lung disease)
Clubbing
Bilateral coarse crackles
Cyanosis
How do you diagnose CF?
Sweat chloride test (incr [NaCl and K in sweat)
Pulmonary function tests (reduced FEV1 - obstructive pattern)
ABGs - hypoxaemia, w hypercapnoea later on
CXR: hyperinflation, incr pulmonary markings
What diseases are associated with industrial dust
Coal Worker’s Pneumoconiosis (inhalation of coal dust), can progress to ‘Progressive Massive Fibrosis’
Silicosis (inhalation of silica which is fibrogenic)
Asbestosis (inhalation of asbestos which is fibrogenic), assoc w Mesothelioma
Mesothelioma
Definition of Interstitial Lung Disease
Inflammatory and/or fibrosing process in the alveolar walls causing distortion and destruction of normal alveoli and microvasculature . Generally BILATERAL.
Common causes of interstitial lung disease
Rheumatic
- RA, SLE, Scleroderma
Drugs
-Methotrexate, amiodarone, bleomycin, nitrofurantoin
Radiation
Environmental/Occupational
- Silicosis, asbestosis, coal worker’s pneumoconiosis
Pulmonary Vasculitis
Inherited
Sarcoidosis
What pattern do you get on spirometry w ILD?
Restrictive due to decr lung compliance (TLC and VC reduced; FEV1/FVC incr/normal)
Common causes of acute bronchitis
Mostly viral.
Influenza when + fever.
Definition of acute bronchitis
Acute bronchitis is suggested by the persistence of cough for more than five days.
Cough generally persists two to three weeks, and airway hyperreactivity may last five to six weeks.
Fever uncommon and suggests influenza or pneumonia.
What are the indications for CXR in patients w acute cough?
To exclude pneumonia:
Tachypnoea
Tachycardia
Fever
Chest exam: signs of consolidation, rales
Hypoxaemia (pulse oximetry)
Altered mental state
Treatment of acute bronchitis
Reassurance and symptomatic treatment (NSAIDs, aspirin and/or ipratropium)
NOT ANTIBIOTICS.
Classifying lung tumours
Benign or malignant
Primary or secondary
Endobronchial or parencymal
What is the most common type of primary lung tumour?
Bronchogenic carcinoma
- small cell
- non-small cell (SCC, adenocarcinoma, large cell undifferentiated)
-Adenocarcinoma the most common overall
Which type of lung cancer is most common in NON SMOKERS
non small cell adenocarcinoma
Where are bronchogenic non small cell SCCs found in lungs
centrally
Where are bronchogenic small cell carcinomas found?
centrally
Where are bronchogenic non-small cell adenocarcinomas found?
Peripherally
Which type of lung cancer is most aggressive?
Small cell - disseminated at presentation.
What are the histological features of :
SCC
adenocarcinoma
SCC: keratin pearls and intercellular bridges
Adenocarcinoma: glandular, mucin-producing
What are apical lung tumours called and what are common SX?
Pan coast tumour .
Horner Syndrome
Brachial plexus palsy (C8, T1 nerve roots -> weak intrinsic hand muscles)
What are distant met sites for lung cancer?
Brain
Bone
Liver
What are local sites of spread/obstruction for lung cancer?
Hilum, mediastinum, pleura Pericardium Oesophagus Phrenic nerve Recurrent laryngeal nerve SVC Rib and vertebrae
Investigations for lung cancer
Bloods: UEC, LFTs, Ca
CXR, CT chest and abdo
+/- PET and bone scan
Sputum sample cytology
Bronchoscopy -> biopsy
Horner’s syndrome
Mitosis
ANhydrosis
Ptosis
Treatment for lung cancer
Combination treatment
surgery (not for small cell and CI with spread to lymph nodes or distant sites or poor pulm function)
radiotherapy
chemotherapy
palliation
Causes of pneumothorax
- Traumatic - penetrating or non-penetrating injuries
- Iatrogenic
- Spontaneous (no HX trauma)
○ Primary (no underlying lung disease)
§ Generally due to spontaneous rupture of subpleural bleb of lung into pleural space
§ Common in tall, healthy young males
○ Secondary (underlying lung disease)
§ Rupture of subpleural bleb
§ Necrosis of lung tissue adjacent to pleural space (Often w pneumonia, abscess, PCP, lung CA, emphysema )
Treatment for pneumothorax
○ Give 100% O2 in all cases
Small pneumothoraxes (haem stable) resolve spontaneously
Small intercostal tube for spontaneous pneumothoraces
Large pneumothoraces or those w secondary causes
○ Chest tube connected to underwater seal +/- suction
○ Treat underlying causes (ex: antibiotic for PCP)
Signs on examination of pneumothorax
- Tracheal deviation (if tension -> deviates AWAY from pneumothorax)
- Unilateral reduced chest expansion
- Decr vocal/tactile fremitus
- Hyper-resonant
- Unilateral reduced breath sounds
What signs make you think that a person might have a tension pneumothorax rather than a simple one and how does this change your management?
- Severe resp distress
- Tracheal deviation away from affected lung
- Distended neck veins (incr JVP)
- Hypotension
In this case, do NOT perform CXR -> needs immediate MX
Treatment for resp failure.. what investigations would you do?
Investigations: serial ABGs, CXR, chest CT (for underlying cause)
- Give O2
- Positive pressure ventilation: BiPAP, CPAP
- Reverse/manage underlying pathology and/or exacerbators
NOTE: in COPD patients w chronic hypercapnoea, give low-flow O2 to achieve target SaO2 of 88-92%
What is the different in definition between OSA and central sleep apnea?
OSA: Transient, episodic obstruction of upper airway with reduced or absent airflow despite persistent respiratory effort.
CSA: Transient, episodic decreases in CNS drive to breathe with no airflow because no resp effort.
Signs and symptoms of sleep apnea
• Due to fragmented sleep: ○ Daytime somnolence ○ Personality and cognitive changes ○ Snoring • Due to hypoxemia and hypercapnia ○ Morning headache ○ Polycythemia ○ Pulmonary/systemic HTN ○ Cor pulmonale/CHF ○ Nocturnal angina ○ Arrhythmias
Investigations and treatment for OSA
Investigate w sleep study
Treatment
- manage risk factors (weight loss, decr alch and sedatives, nasal decongestion, treat underlying medical conditions)
- nasal CPAP
- no supine sleeping
- dental appliance
- surgery (tonsillectomy. uvulopalatopharyngoplasty)
