Clinical Respiratory Medicine Flashcards
embryonic stage of devlelopment
trachea and main bronchi appear
pseudoglandular stage of development
all conducting airways form
epithelial cells differentiate
canalicular stage of development
respiratory airways form
blood-gas barrier thins
surfactant appears
saccular stage of development
saccules (terminal sacs) appear
alveolar stage of development
saccules form alveoli
lung development into childhood
alveoli continue to multiply
stages of lung morphogenesis
- Embryonic
- Pseudo-glandular
- Canalicular
- Saccular
- Alveolar
stage of lung development at which extra-uterine life is possible
late canalicular / early saccular
Tracheo-bronchomalacia pathophysiology
Cartilage in airways doesn’t form properly in early development.
leads to “floppy” airways that are only held open by muscle
usually resolves naturally without treatment
Symptoms of tracheo-bronchomalacia
Barking cough
Dyspnoea on exertion
Recurrent /early croup
Frequent infections
Congenital Pulmonary Airway Malformation (CPAM)
aka Pulmonary adenomatoid malformation
overgrowth of terminal bronchioles creates areas of cystic tissue that cannot function normally
may resolve spontaneously in utero.
most cases are asymptomatic.
sometimes other areas of the lung are compressed (causing difficulty breathing) or other organs are compressed.
surgery may be required
Infant respiratory distress syndrome/ Surfactant Deficiency Disorder/ Hyaline Membrane Disease
surfactant deficiency
treated with surfactant replacement
fetal origins of COPD
in utero nicotine exposure
fetal infection
poor maternal nutrition
Low birth weight/ prematurity
pediatric origins of COPD
infection
growth
environmental pollutants
Remodelling
definition + examples
The alteration of structure following external influence
e.g lung hypoplasia caused by pre-natal nicotine exposure.
chronic inflammation in asthma causing airway narrowing
Specific features to be included in the clinical history of asthma
childhood asthma inhalers taken (+ doses) occupation (past and present) smoking - pack year history eczema hayfever atopic disease in family pets phycosocial aspects - stress
Specific features to be included in the clinical history of COPD
childhood asthma inhalers taken (+ doses) occupation (past and present) smoking - pack year history past respiratory diseases Ischaemic heart diease
assessing the severity of acute COPD
Uses FEV1/FVC
> 80% = mild
50 - 79% = moderate
30 - 49% = severe
<30% = very severe
assessing the severity of acute severe asthma
can be: moderate, severe, life threatening or near fatal. objectively measured using:- - ability to speak - heart rate - respiratory rate - peak expiratory flow - O2 saturation and PaO2
near fatal = raised PaCO2
nebulisers
used if a patient cannot use an inhaler
proven aetiological factors of asthma
Atopy - tendency for IgE response to allergens
Smoking
maternal smoking during pregnancy
occupational factors - spray paint, rodent urinary protein, grains, crustacean
putative aetiological factors for asthma
obesity diet reduced exposure to microbes pollution cleaning sprays
The British Thoracic Society’s “Stepwise” approach to management of asthma
There are different steps for different intensities of treatment
Patients should try to be on the lowest step on which they can maintain control of their asthma
This reduces cost and adverse effects
Epidemiology
The incidence, distribution and determinants of disease in a population
Atopy
a (genetic) predisposition toward developing type I hypersensitivity reactions (excessive IgE production)
Hyperplasia
increased proliferation
Emphysema pathophysiology
increase in size of air spaces (hyperinflation) due to destruction of elastin causing dilatation and destruction of alveolar cell walls
Airways collapse due to pressure in chest cavity on expiration, no elastin to hold them open
Air becomes trapped
Centriacinar emphysema
smoke particles get trapped in the airspaces of the bronchioles causing inflammation.
neutrophils make elastase which destroys elastin
Panacinar emphysema
a-1 antitrypsin (a protein which destroys elastase) deficiency.
leads to elastin destruction in bronchioles and alveoli
Periacinar (bullous) emphysema
alveoli expand to form large (>1cm) air spaces called bulla.
rupture can leak air into the pleural cavity causing pneumothorax
Clinical definition of chronic bronchitis
a cough lasting for at least 3 consecutive months of the year for at least 2 consecutive years
Morphological changes of large airways in chronic bronchitis
- mucous gland hyperplasia
- goblet cell hyperplasia
- some inflammation and fibrosis
morphological changes of small airways in chronic bronchitis
- goblet cells appear
- inflammation and fibrosis (in long standing disease)
cause of obstruction in chronic bronchitis
airways obstructed by thick mucous and fibrosis
Causes of hypoxaemia in COPD
- Airway obstruction
- loss of alveolar surface area for gas exchange
- reduced respiratory drive (central chemoreceptors get used to high [H+] in CSF
These all cause low ventilation
Hypoxic cor pulmonale
enlargement of the right ventricle of the heart.
because higher blood pressure is needed in the lungs due to vasoconstriction due to shunt
Asthma mechanism
Type I hypersensitivity in the airways.
IgE is produced in response to stress, chemicals cold, etc…
IgE triggers mast cell degranulation which causes:-
1. Bronchial smooth muscle contraction (immediate response)
2. Chronic inflammation of airways
This narrows the airways
Clinical definition of asthma
Chronic airflow obstruction causing WHEEZE which is VARIABLE and REVERSIBLE with asthma treatment
Symptoms of asthma
Wheeze
Dry cough
Dyspnoea (at rest)
Chest tightness
Investigations used for diagnosis of asthma
Spirometry: Low FEV1/FVC
Peak-flow monitoring: Variable obstruction
reversibility with bronchodilator/ oral corticosteroids
Skin prick test: proves atopy
Bronchial provocation: response to lower loses of bronchial constrictors (methacholine etc.)
Fractional exhaled NO: ↑ due to inflammation in airways
CXR: Hyperinflation
FBC: Eosinophillia = atopy
Definition of COPD
airway obstruction (chronic bronchitis) and hyperinflation (emphysema). Constant and not fully reversible
Symptoms of COPD
Breathlessness on exertion chronic cough with sputum recurrent chest infections wheeze/ chest tightness weight loss
Investigations used for diagnosis of COPD
Spirometry: low FEV1/FVC = fixed airflow obstruction
Reversibility: Minimal w/ bronchodilators and oral corticosteroids
CXR: Hyperinflated lungs, compressed diaphragm and heart
Full pulmonary function testing: ↑RV, ↑TLC and RV/TLC> 30% = emphysema
Blood gases: ↓PaO2, ↑PaCO2
Management strategies for COPD
smoking cessation!
vaccinations (increased risk of respiratory infection)
long term oxygen therapy
pulmonary rehabilitation (exercise, support, etc.)
Inhaled therapy
characteristics of obstructive lung diseases
airflow limitation
reduced peak expiratory flow rate
reduced FEV1
pathogenesis
the development of a disease from the causes and origin to the end stages
Pulmonary embolism deffinition
a thrombus (blood clot) formed in the venous system that embolises to the pulmonary arteries
pulmonary embolism symptoms
pleuritic chest pain
cough + haemoptysis
dyspnoea
MASSIVE PE:
syncope
cardiac arrest
pulmonary embolism investigations
Pre-test probability: Wells/ Geneva score
V/Q scan: Low perfusion
CT pulmonary angiogram: Shows occlusion of pulmonary artery
D-dimer: High
ECG: Tachycardia
Blood Gases: ↓PCO2 + Hypoxia
Pulmonary embolism management
Immediate oxygen for resuscitation
Anticoagulation:
Heparin, Warfarin, DOACs
Massive PE: Thrombolysis Pulmonary embolectomy
pulmonary infarction definition
local necrosis of lung tissue caused by obstruction of arterial blood (usually due to PE)
most common in people with underlying lung disease (e.g. COPD) as well tissue is well oxygenated from multiple sources
pulmonary infarction management
100% oxygen (for initial resuscitation)
mechanical ventilation
ultimately depends on cause
pulmonary hypertension definition
elevated blood pressure (>25mmHg) in pulmonary arteries
causes of pulmonary hypertension
Idiopathic Secondary to chronic respiratory disease Secondary to left heart disease Artery Occlusion (Chronic thromboembolic PH /CTEPH) Collagen vascular disease Portal hypertension Congenital HD (L -> R shunt) HIV
symptoms of pulmonary hypertension
exertional dyspnoea
exertional presyncope/ syncope
chest tightness
pulmonary hypertension investigations
Doppler echo: Estimates pulmonary artery systolic pressure
V/Q scan: CTEPH
CT(PA)/ CXR: Enlarged pulmonary arteries
Right heart catheterisation: Direct measurement of pulmonary artery pressure
management of pulmonary hypertension
Treatment of underlying condition Oxygen Anticoagulation Diuretics Lung/ Heart transplant Thromboendarterectomy (CTEPH)
PULMONARY VASODILATORS: CCBs
Endothelin receptor antagonists
Phosphodiesterase inhibitors
Prostacyclin
theophyllines
IV/ oral bronchodilator used in asthma
venography
x-ray of the veins using an IV contrast. used to identify DVT and PE
Pleural effusion definition
an abnormal collection of fluid in the pleural space
Transudates
caused by an imbalance of hydrostatic forces influencing formation and absorption of pleural fluid
usually bilateral
pleural fluid protein <30g/l
Exudates
caused by an increase in the permeability of the pleural surface and/or local capillaries.
usually unilateral
pleural fluid protein >30g/l
Causes of transudates
left ventricular failure
liver cirrhosis
hypoalbuminaemia
peritoneal dialysis
hypothyroidism
nephrotic syndrome
mitral stenosis
pulmonary embolism
constrictive pericarditis
ovarian hyperstimulation syndrome
meig’s syndrome
Causes of exudates
malignancy
parapneumonic
pulmonary embolism/ infarction rheumatoid arthritis autoimmune diseases benign asbestos effusion pancreatitis post myocardial infarction
yellow nail syndrome
Drugs: amiodarome, nitrofuratoin, phenytoin, methotrexate, carbamazapine……
Symptoms of pleural effusion
- asyptomatic (if small and accumulates slowly)
- increasing breathlessness
- pleuritic chest pain ( improves if inflammatory, worsens w/ malignancy)
- dull ache
- dry couch
- weight loss, malaise, fevers, night sweats…
Signs of pleural effusion
On affected side of chest:
- decreased expansion
- stony dullness to percussion
- bronchial breathing sounds
- decreased vocal resonance
clubbing increased JVP trachea moved away from large effusion cervical lymphadenopathy peripheral oedema
when to investigate pleural effusion
clinical picture is usually characteristic for bilateral transudate. investigate if…
-is unilateral
unusual features
fails to respond to appropriate treatment
Investigations for pleural effusion
- CXR (confirms presence)
- CT (differentiates malignant from benign)
- Pleural aspiration
- Pleural biopsy
- Thoracoscopy
Management of pleural effusion
Treatment of cause
Pleurodhesis (drain) Chemical pleurodhesis (e.g. talc slurry) Surgical pleurodhesis (performed at time of thoracoscopy)
Palliative (e.g. if due to malignancy) = repeated pleural aspiration
Malignant mesothelioma defnition
pleural malignanct caused by exposure to aasbestos (occurs 20-40yrs after exposure)
Malignant mesothelioma clinical presentations
breathlessness
chest wall pain
radiology = usually unilateral pleural thickening
Malignant mesothelioma treatment
pleuropneumonectomy (remova of entire lung and parietal pleura) if very fit
otherwise, palliative treatment
pleural fibrosis
caused by inflammation, surgical trauma, pleural effusion, asbestos etc.
pleura develops fibrous tissue and loses elastic properties which impairs lung function
pleural plaques
Benign plaques of the pleura caused by asbestos exposure. Can become calcified but rarely inhibit lung function.
almost always asymptomatic
Empyema
collection of pus in the pleural cavity which can eventually form fibrous scar tissue and inhibit lung function.
caused by pneumonia, trauma, surgery…
Symptoms: chest pain, fever, NO cough.
Diagnosed by pleural aspiration
appearance of tuberculous granuloma in TB
Rounded outline,
Epithelioid and langhan’s giant cells (transformed macrophages),
Lymphocytes, plasma cell and fibroblasts,
(Central caseous necrosis)
symptoms of primary TB
Usually asymptomatic,
Sometimes fever and malaise
Symptoms of post-primary TB
May be asymptomatic for months, Cough w/ sputum and haemoptysis, Pleuritic pain, Breathlessness, (Malaise, fever, weight loss, night sweats)
CXR of post-primary TB
Patchy, often bilateral shadowing in upper zones/ upper lower lobe,
Cavitation if advanced,
Calcification if chronic or healed
Anti-tuberculous drug therapy
For 2 months: Rifampicin, Isoniazid, Ethambutol, Pyrazinamide
Then For 4 months: Rifampicin, Isoniazid
DOT
Directly Observed Therapy
needed to make sure TB patients take medication as multi-drug resistant organisms pose a world issue
Public health duties of doctors managing TB
Legal requirement to report all cases to public health,
Should ensure patients take drugs,
TB contact tracing: must screen close household contacts and, if they are infected, casual contacts.
HIV screening in patients from areas with high HIV prevalence.
Pathogenesis of primary TB
Inhaled mycobacteria implant in distal airspaces,
No preceding exposure or immunity (usually in children),
Usually no symptoms
Can be cleared, become latent, or progress
Pathogenesis of post-primary TB
Caused by reactivation of latent mycobacteria or new re-infection from an outside source.
May progress to:
- TB caseous pneumonia (when lesions coalesce)
- Miliary TB
- Fibrocaseous TB
Fibrocaseous Tuberculosis
Large areas of fibrosis and caseous necrosis (cell death in which the dead tissue maintains a “cheese-like” appearance)
Miliary TB
TB that has disseminated throughout the body, characterised by minute tubercles
Caseating granuloma
A granuloma that shows caseous necrosis
Pharmacology of anti-tuberculous drugs
Rifampicin - inhibits mycobacterial RNA synthesis.
Isonazid - inhibits mycobacterial cell wall synthesis.
Ethambutol - inhibits mycobacterial cell wall synthesis
Pyrazinamide - inhibits mycobacterial growth.
CFTCR
Cystic Fibrosis Transmembrane Conductance Regulator
An active transport chloride channel found in many organs of the body
Mutations causing CF
There are ~30 mutations in the gene for CFTCR that cause cyctic fibrosis. Different mutations result in different phenotypes of the disease
Most common CFTCR gene mutation
Delta F508 - responsible for 2/3 cases worldwide.
A deletion of 3 nucleotides resulting in the loss of phenylalanine, producing a CFTCR protein with abnormal folding
Respiratory effects of CF
very thick secretions cause cillia collapse and excessive inflammation
Respiratory symptoms of CF
Progressive bronchiestasis (inflammation causing airway widening) Recurrent LRTIs Airflow obstruction - low FEV1 Cough w/ sputum production Haemoptysis - due to infection
GI effects of CF
digestive enzymes can’t leave pancreas, bile can’t leave liver
inhibits digestion, fat soluble vitamins and minerals not absorbed
GI presentations of CF
Meconeum ileus/ DIOS
Diarrhoea
Malnutrition
Diabetes
Possible complications of CF
Infertility, Osteoporosis, Diabetes Distal intestinal obstruction Hepatopathy
Reasons for infertility in CF
MALES:
vas deferens don’t develop in >95%
FEMALES:
fertile but malnutrition affects chances of conception
Reasons for osteoporosis in CF
Vitamin D needed for bone development, but is a fat soluble vitamin so not absorbed as bile ducts are blocked. (bile needed to break down fat to be absorbed)
Reasons for hepatopathy in CF
Bile produced is thick so blocks bile ducts. The surrounding liver becomes scarred, this fibrosis eventually spreads throughout the liver
Management of pancreatic insufficiency in CF
Enteric coated enzyme pellets
High energy, high fat diet
Fat soluble vitamin and mineral supplements
Management of chest infection in CF
Segregation of patients to prevent cross-infection
Prophylactic antibiotics
Annual influenza vaccination
Mucolytics (thin sputum)
Anti-inflammatory drugs (ibuprofen, azithromycin, prednisolone)
Physiotherapy - breathing techniques
- airway clearance devices
Antenatal screening for CF
Chorionic Villous Sampling (CVS)
- performed when parents have CF gene or foetus has echogenic (bright on ultrasound) bowel
- 1% risk to baby
- performed at ~11 weeks
Neonatal screening for CF
Newborn blood spot (guthrie test) at 5 days
-measures immunoreactive trypsinogen (a pancreatic enzyme precursor found in neonates w/ CF)
If positive…
- mutation analysis
- sweat test
Role of transplantation
Last resort treatment,
Not a miracle cure
Decision made by a multidisciplinary team
For a transplant a patient should have…
FEV1 of <30%
hypoxia at rest,
hypercapnia,
worsening quality of life
For a transplant a patient must/ should NOT have…
Other organ failure/ dysfunction, Malignancty within 5 years, Drug, nicotine or alcohol dependency, Non-compliance, Low BMI
Symptoms of primary lung cancer
Chronic cough Haemoptysis Wheeze Chest pain Recurrent LRTIs Difficulty swallowing Hoarse voice Dyspnoea Weight loss
Signs of primary lung cancer
Finger clubbing,
Lymphadenopathy,
Hepatomegaly (liver enlargement)
HPOA
Coin lesion
a mass <3cm in diameter seen on CXR
Causes of coin lesion on CXR
Primary lung cancer, Metastasis, Benign lung neoplasm, Infection (e.g. TB) Vascular haematoma (collection of blood)
4 Types of lung carcinoma
Small cell lung cancer,
Adenocarcinoma,
Squamous cell carcinoma,
Large cell carcinoma
Spread of lung cancer within the thorax
Lymph node metastasis,
Direct chest wall invasion
Direct invasion of nerves
Direct invasion of blood vessels (e.g. Superior vena cava)
Horner’s syndrome
cause + symptoms
Caused by direct invasion of the sympathetic chain.
Causes a constricted pupil, droopy eyelid and decreased sweating on the same side as the invasion.
Superior Vena Cava Obstruction Symptoms
Dyspnoea
Cough
Swelling of face, neck and arms
Hypertrophic Pulmonary Osteoarthropathy (HPOA)
painful inflammation of the periosteum around ankles and wrists + finger clubbing
Common distant metastases of lung cancer
Bone,
Brain,
Liver,
Adrenal glands
- Lungs are the only organ that receives the entire body’s blood flow, so metastases to and from them are common
Investigations for staging of lung cancer
Clinical history/ examination
(ECOG) Performance status
Pulmonary function
CXR
CT/PET
Bronchoscopy Image guided biopsy Mediastinoscopy/otomy Surgical excision biopsy Sputum cytology (rarely done)
TNM staging
T = size and position of tumour
N = lymph node metastases
M = distant metastases
Staging for SCLC
Limited disease (LD) = contained in thorax
Extensive disease (ED) = extrathoracic metastases
Principles for surgical treatment of lung cancer
Remove all of tumour + minimum amount of lung tissue = curative resection
Lung cancer surgeries
Wedge resection,
Segmental resection,
Lobectomy,
Pneumonectomy
Thoracotomy
An incision into the pleural space to gain access to the thoracic organs
Reasons for perioperative (after surgery) death
after lung cancer surgery
ARDS Bronchopneumonia MI Pneumothorax Intrathoracic bleeding
Non-fatal complication of lung cancer surgery
Post thoracotomy wound pain Empyema Bronchopleural fistula Wound infection Post-Op respiratory insufficiency
Radiotherapy side effects
Fibrosis - lung function tests essential,
Fatigue,
Dyspnoea + cough
loss of chest and neck hair
Management of LD SCLC
Combination chemotherapy,
Early thoracic radiotherapy,
Prophylactic Cranial Irradiation (PCI)
Management of ED SCLC
4 cycles combination chemotherapy,
PCI
Palliative RT (if not fit for chemo)
RT and steroids for brain mets
Programmed Cell Death Pathway (Nivolumab)
Nivolumab blocks the binding of PDL1 (on cancer cells) to PD1 (on T-cells).
This precents T-cell inactivation
Increases 1yr survival from 24% to 42%
Tyrosine Kinase Inhibitors
Inhibit transduction cascades + shrink solid tumours.
Well tolerated, tumour responses in many tumour types
Monoclonal antibodies
e.g. Herceptin
Mab binds to cancer cell antigens, allows immune cells to recognise the cancer cells
Chimeric Antigen Receptor (CAR) T-cell therapy
T-cells are induced to produce CARs which can recognise cancer cells
Targeted drugs for adenocarcinoma with driver mutation
Approved drugs for 4 mutations/ rearrangements:
- EGFR
- ALK
- ROS1
- BRAF
Bronchodilators for asthma management
B2 agonists
Anti-muscarinics
Theophylines (oral/IV)
Magnesium
Anti-inflammatory asthma management
Inhaled corticosteroids - chronic
Oral steroids - acute
Leukotriene receptor antagonists (oral) - chronic
Monoclonal antibodies - anti IgE - chronic
Types of inhalers
Pressurised Metered Dose Inhalers (pMDI) - can be with spacers
Dry Powder Inhalers (DPI)
Benefit of inhalers
Direct delivery to target organ,
Small dosage,
Fast onset of effect,
Minimal systemic exposure
Clinical management of acute, life threatening asthma
IV salbutamol
IV theophylline
IV/ nebulised magnesium
IV hydrocortisone
Intubate + ventilate
Non-pharmacological management of asthma
Exercise Smoking cessation Weight management Flu vaccinations Asthma action plans Inhaler technique Allergen avoidance Bronchial thermoplasty
consolidation
pus in alveoli
Symptoms of tonsillitis/ pharyngitis
Red, swollen tonsils, White/ yellow coating/patches Sore throat, Difficult/ painful swallowing, Lymphadenopathy, Sneezing, Runny nose, Cough, Fever
Symptoms of the common cold
Runny/ blocked nose, Sore throat, Cough, Sneezing, Fever, Malaise
Epstein Barr Virus (glandular fever/ mononucleosis) Symptoms
Sore throat, Lymphadenopathy, Fever, Fatigue, Malaise, Rash, Lack of appetite
Otitis Media Symptoms
Earache, Hearing problems, Ear discharge (if eardrum perforation), Pink, bulging eardrum, Fever
Sinusitis Symptoms
Facial pain,
Nasal discharge,
Blocked nose,
Fever
Common bacteria causing URTIs
Streptococcus pyogenes
Common viruses causing URTIs
Rhinovirus, Adenovirus, Parainfluenza, Influenza, Epstein Barr Virus
Symptoms + Signs of Acute Bronchitis
Hacking cough + yellow/green sputum, Painful/ difficult breathing Sore throat, Headache, Runny/ blocked nose, Fatigue + Malaise
Wheeze
Crackles
Symptoms of pneumonia
BRONCHOPNEUMONIA:
Cough + purulent sputum
LOBAR PNEUMONIA:
Cough + rusty sputum,
Haemoptysis,
Rigors
GENERAL: Malaise, Fever, Chest pain (pleuritic), Dyspnoea
Signs of pneumonia
Pyrexia, tachypnoea, Central cyanosis, Dullness on percussion, Bronchial breath sounds, Inspiratory crackles, Increased vocal resonance
Bronchiectasis
A permanent dilation of bronchi causing a build-up of sputum
Symptoms and signs of bronchiectasis
*Chronic cough + sputum Wheeze, Dyspnoea, Flitting chest pains, Haemoptysis, Fatigue
Finger clubbing,
Coarse inspiratory crackles
Lung abscess
A pus filled cavity that often follows pneumonia
Lung abscess symptoms and signs
Cough + purulent sputum Haemoptysis, Dyspnoea, Fever, Night sweats, Weight loss, Fatigue
Finger clubbing,
Bronchial breath sounds,
Localised dullness on percussion,
Pathogenesis of bronchopneumonia
Patchy inflammation + consolidation in bronchioles.
Common in infants, elderly and immunocompromised patients.
Most commonly caused by Staph. aureus and H. influenzae
Pathogenesis of lobar pneumonia
Inflammation + consolidation of alveoli in a whole lobe.
Common in healthy adults
Most commonly caused by strep. pneumoniae
Complications and consequences of LRTIs
Pleurisy, Pleural effusion, Empyema, Fibrosis, Lung abscess, Bronchiectasis, Septicaemia, Metastatic infection, ARDS
- Most resolve
Common organisms causing LRTIs
Strep. pneumoniae,
Haemophilus influenzae,
Moraxella catarrhalis,
Staph. aureus
ATYPICAL PATHOGENS: Mycoplasma, Chlamydia, Coxiella, Legionella
Viruses
Causes of recurrent Pneumonia
Local bronchial obstruction (tumour, foreign body etc),
Generalised lung disease (e.g. COPD, CF)
Non-respiratory disease (e.g. HIV)
Local pulmonary damage (e.g. bronchiectasis)
Differential spectrum of hospital acquired (nosocomial) vs. community acquired pneumonia
NOSOCOMIAL:
Staph. aureus,
Antibiotic resistant organisms
COMMUNITY ACQUIRED:
Strep. pneumoniae,
Haemophilus influenzae,
Viruses
Usual antimicrobial therapy of LRTIs
LOW RISK, TREATED IN COMMUNITY:
-amoxycillin or clarithromycin/ doxycyclin
HOSPITAL TREATMENT REQUIRED:
-amoxycillin or levofloxacin (penicillin allergy) AND clarithromycin
HIGH RISK OF DEATH, ITU:
-co-amoxiclav or levofloxacin (penicillin allergy) AND clarithromycin
Specialist antimicrobial therapy of LRTIs
ASPIRATION PNEUMONIA:
-metronidazole + amoxycillin (anaerobes)
MRSA:
- vancomycin
- OR linezolid
Supportive therapy of LRTIs
in addition to antimicrobial therapy
Oxygen,
IV fluids,
Continuous Positive Airway Pressure (CPAP),
Intubation + ventilation
Management of bronchiectasis
Chest physiotherapy,
Prompt antibiotic treatment of infections,
May need inhaled B2 agonists or corticosteroids
Management of lung abscess
Prolonged antibiotics,
Occasionally percutaneous drainage
Management of empyema
Chest drain,
IV antibiotics (sometimes prolonged),
Surgery (if above methods fail)
Common clinical symptoms of restrictive lung diseases
Dyspnoea,
Cough,
Chest pain
Diffuse Alveolar Damage Syndrome (DADS) definition
An acute interstitial syndrome characterised by:
Widespread inflammation and fibrosis in the alveoli
(Not an individual disease)
Causes of DADS
Major trauma, Infection, Chemical injury (toxic inhalation), Drugs, Radiation (sometimes idiopathic)
Sarcoidosis
A multi-system granulomatous disease
(non-caseating granulomas form in many organs)
Most commonly affects lymph nodes and lungs
also called “Granulomatous lung disease”
Cause of sarcoidosis
idiopathic
Sarcoidosis investigations
CXR: Hilar lymphadenopathy + fibrosis, Honeycombing in later stages
Bronchoscopy: Hilar lymphadenopathy
Pulmonary function tests: Forced vital capacity <80% of predicted normal
Biopsy: Non-caseating granulomas (can be from any affected area)
Sarcoidosis management
No treatment - if mild and few symptoms
Anti-inflammatories (NSAIDs)
Topical steroids - for skin lesions
Only some patients will progress, careful monitoring needed
Idiopathic pulmonary fibrosis definition
Fibrotic scarring of lung tissue
Idiopathic pulmonary fibrosis investigations
CXR: Basal/ posterior ground glass opacities, Honeycombing in later stages
Pulmonary function tests: Forced vital capacity <80% of predicted normal
Surgical biopsy: shows fibrosis
Signs of interstitial lung disease
Crackles
Finger clubbing
Chronic interstitial lung diseases
Idiopathic Pulmonary Fibrosis,
Hypersensitivity Pneumonitis,
Sarcoidosis
ACUTE: DADS
Management of Idiopathic Pulmonary Fibrosis
OAF (oral anti-fibrotic) Pirfenidone, Nintendinab (inhibits fibrotic process kinases), Palliative care, Transplant
Hypersensitivity Pneumonitis definition
Granulomatous inflammation of alveoli caused by type III and IV hypersensitivity reactions
Causes of Hypersensitivity Pneumonitis
Animal proteins, Fungi, Organisms in mouldy hay, Chemicals, Etc....
*Occupational causes
Hypersensitivity Pneumonitis investigations
CXR: Poorly defined small opacities. Honeycombing in later stages
Pulmonary function tests: Forced vital capacity <80% of predicted normal
Bloods: ↑IgG
Bronchoscopy + Biopsy: Centriacinar granulomas
Hypersensitivity Pneumonitis management
Allergen avoidance,
Corticosteroids (e.g. prednisolone)
Causes of restrictive lung disease
Most common: Interstitial lung disese (pulmonary fibrosis)
NON-LUNG CAUSES: Pleural effusion, Pneumothorax, Pleural thickening, Kyphoscoliosis, Rib fractures, Amyotrophic lateral sclerosis (muscular), Obesity, Pregnancy
Lung Interstitium definition
The (potential) space between the alveolar epithelium and the capillary endothelium
End-stage lung fibrosis/ Honeycomb lung
A shrunken, fibrotic, barely functioning lung caused by progressive fibrosis of lung tissue in interstitial lung diseases
Symptoms of Honeycomb Lung
- Dyspnoea,
- Dry cough,
Haemoptysis,
Wheeze,
Chest pain
People most likely to smoke
Permanently sick/ disabled,
Unemployed and seeking work,
Looking after home/ family
Strategies to reduce smoking
Standardised packaging, Ban in public places and workplaces, Smoking advisory service Taxation Laws forbidding vending machines, proxy purchases etc.
*5000 people in UK employed in tobacco industry
Obstructive Sleep Apnoea Syndrome (OSAS)
Recurrent episodes of upper airway obstruction leading to apnoea (cessation of breathing) during sleep
Presentations of sleep apnoea
Heavy snoring, Unrefreshing sleep, Daytime somnolence/ sleepiness, Poor daytime concentration, Oxygen desaturation (sometimes)
Paediatric presentations of sleep apnoea
Failure to thrive,
Neurocognitive defects/ ADHD,
Systemic hypertension,
Cor pulmonale
Conditions associated with sleep apnoea
Hypertension,
Increased risk of stroke,
Increased risk of heat disease (maybe)
Consequences of untreated sleep apnoea
Impaired quality of life,
Marital disharmony,
Increased risk of road traffic accident (RTA)
Management of sleep apnoea
Identify exacerbating factors
(weight reduction, alcohol avoidance, treatment of endocrine disorders - e.g. hypothyroidism)
Continuous Positive Airway pressure (CPAP),
Mandibular repositioning splint
*Advise not to drive and inform DVLA until treated
Paediatric management of sleep apnoea
Adenotonsillectomy,
CPAP,
Weight loss,
Avoid environmental tobacco smoke
Other conditions causing excessive daytime sleepiness (not OSAS)
Narcolepsy,
Neuromuscular respiratory failure
Neurological conditions associated with respiratory muscle weakness
Motor neurone disease (ALS)
Muscular dystrophy
Symptoms of respiratory muscle weakness
Dyspnoea Recurrent chest infections Orthopnoea Morning headache Disturbed sleep
Worse during/ after sleep as accessory muscles paralysed and diaphragm weak
Signs of respiratory muscle weakness
Ankle oedema Paradoxical breathing ↑ pCO2 ↓ pO2 ↑ bicarbonate (Retained from kidneys to maintain pH)
Investigations of respiratory muscle weakness
Lung function: ↓FEV1, ↓FVC , ↑FEV1/FVC
↓inspiratory and expiratory mouth pressures
Assessment of hypoventilation:
Overnight oximetry: desaturation
Early morning arterial blood gases: ↑ pCO2, ↓ pO2
Management of respiratory muscle weakness
Non-invasive ventilation (NIV),
Oxygen therapy
Orthopnoea
Shortness of breath lying flat
Epworth score
a subjective measure of sleepiness.
8 situations are rated 0-3 according to how likely the patient is to doze
Pressurised Metered Dose Inhalers (pMDI)
Normal inhaler
Aerosol so low inspiratory flow needed
Needs coordination
Children must use spacers
Dry Powder Inhalers (DPI)
Patient generates aerosol so high inspiratory flow needed
Less coordination required
Inhaled therapy for COPD
- SABA
- LAMA or LABA
- LAMA and LABA
- ICS
Signs of asthma
Polyphonic wheezes
Hyperexpanded chest
Signs of COPD
CO2 flap Hyperexpanded (barrel) chest Paradoxical movement of ribs and abdomen Reduced chest expansion Laryngeal descent ↓ dullness to percussion ↓ breath sounds
Signs of respiratory failure:
Tachypnoea, Cyanosis, Use of accessory muscles, Pursed lip breathing, Peripheral oedema
Causes of wheeze
Asthma COPD Acute bronchitis Cystic fibrosis Congestive heart failure Pulmonary neoplasia Bronchiectasis Tracheobronchomalacia
Pulmonary Infarction Investigations
FBC: ↑WBC, ↑ESR Blood gasses: ↓PO2, ↑PCO2 D-dimer: ↑ if PE CXR/CT: wedge shaped opacity CT PA: Shows occlusion V/Q scan: Low perfusion
Symptoms of pulmonary infarction
Haemoptysis
Dyspnoea
Pleuritic chest pain
Supportive therapy in the treatment of LRTIs
Oxygen
IV fluids
CPAP
Intubation + ventilation
“Tracking” of pulmonary function
Reduced pulmonary development in early life leads to early decline of pulmonary function in adulthood
PET/CT
PET and CT images are superimposed to give one, more accurate image
Whole body PET/CT used to find metastases
Factors influencing lung cancer management
Stage
Type (from tissue diagnosis)
ECOG Performance status
Pulmonary neoplasia pathogenesis
Uncontrolled cell growth caused by mutations in the epithelial cells in the airways
Carcinogens have a synergistic effect
Performance status measurement for lung cancer
0 = asymptomatic 1 = symptomatic, able to do light work 2 = has to rest but for <50% of the day 3 = has to rest > 50% of the day 4 = bedbound
Used to decide therapeutic options
Chemotherapy side effects
Nausea + Vomiting Hair loss Bleeding/ clotting problems Loss of appetite Diarrhoea Constipation Fatigue
Non-small cell lung cancer management
Surgery (usually inoperable)
Radiotherapy
Chemotherapy
Chemoradiotherapy
Stage III NSCLC Management
Radical Radiotherapy
Chemoradiotherapy
Stage IV NSCLC Management
Incurable
Palliative RT = symptomatic benefit (esp bone pain from metastases)
Palliative chemo = symptomatic benefit + survival advantage
Palliative management of lung cancer
Symptom control, may include:
- Chemotherapy
- Radiotherapy
- Opiates
- Treatment of hypercalcaemia, hyponatraemia, dehydration etc.
Decisions and planning
Sarcoidosis symptoms
Dyspnoea
Cough
Skin lesions
Arthalgia
Idiopathic pulmonary fibrosis symptoms
Dyspnoea
Cough
Fatigue
Weight loss
Hypersensitivity pneumonitis symptoms
Chronic:
Dyspnoea
Cough
Malaise
Acute Cough Fever Chills Myalgia *Can lead to respiratory failure
Functional effects of restrictive lung disease
Diseases resulting in:
- decreased lung volume
- increased inspiratory effort
- inadequate ventilation/ oxygenation
Interstitial lung diseases
Diseases causing thickening of the interstitium resulting in progressive fibrosis of lung tissue.
Normal lung tissue is gradually replaced by scar tissue
Signs of TB
May be none
ADVANCED DISEASE:
Crackles
Bronchial breathing
Finger clubbing (rare unless very chronic)
Side effects of rifampicin
Orange urine + tears
OCP ineffective
Hepatitis
Side effects of isoniazid
Hepatitis
Peripheral neuropathy
Side effects of pyrazinamide
gout
Side effects of ethambutol
Optic neuropathy
