Respiratory Flashcards
Sarcoidosis areas of effect
Multi system disorder, commonly lungs, lymph nodes, joints liver, skin and eyes
Sarcoidosis Overview
chronic granulatomous (type IV hypersensitivity) disorder of unknown origin.
Charecterised by granulomas associated with the accumulation of T cells and macrophages.
Chronic inflammation in lungs leads to fibrosis
Who gets sarcoidosis
Usually adults aged 20-40, non-smokers, more common in Afro-Caribbeans and women
Presentation of Sarcoidosis
Resp: dry cough, progressive shortness of breath, chest pain, reduced exercise tolerance
General: lymphadenopathy, poly arthritis, erythema nodosum
GI: Hepato-splenomegaly
Ophthalmological: conjunctivitis, dry eyes, glaucoma
Neurological: Bell’s palsy, neuropathy
Metabolic: hypercalcemia
Sarcoidosis investigations
Spirometry: normal restrictive pattern
CXR: bilateral hilar lymphadenopathy, fibrosis
Urine: increased calcium
DCLO: normal or reduced
Bloods: raised ESR, WCC, serum ACE, calcium
Sarcoidosis management
Most patients don’t need treatment, as the majority of cases will resolve after 2 years
Treatment indicated if symptoms include: interstitial lung disease, hypercalcemia, cardiac/neurological involvement, uveitis
Treatment plan: oral or inhaled steroids +/- immunosuppressants
Bronchiectasis overview
Chronic dilation of the airways, with increased mucus and decreased compliance due to scarring
Causes of bronchiectasis
Idiopathic, malignancy, chronic infection, immunodeficiency, genetic (cystic fibrosis), autoimmune (rheumatoid, ulcerative colitis), COPD/asthma, allergic lung inflammation, recurrent pulmonary aspiration, ciliary dyskinesia,
Presentation of Sarcoidosis
Increased mucus production, shortness of breath, fatigue, wheezing, chest pain, finger clubbing, haemoptysis, fever
Bronchiectasis investigations
Blood test for underlying cause (associated conditions, infection)
CXR or CT scan to show location and extent of respiratory damage/scarring (signet ring sign)
Spirometry should show restrictive curve
Sputum culture
Bronchiectasis management
Postural drainage Salbutamol inhaler Long term antibiotics Nebuliser saline (Carbocysteine)
Influenza overview
Viral infection caused by influenza A/B viruses
Presentation of influenza
Fever, malaise, exhaustion, myalgia, fever, cough, runny nose, vomiting and diarrhoea
Influenza management
Hydration and rest
Prescribe anti viral if in the midst of a recognised flu outbreak and the person part of an at risk group. Antivirals (oral oseltamivir and inhaled zanamivir) should only be started before 48 hours have passed since onset of symptoms
At risk groups and health care workers should get the annual flu vaccine
Upper respiratory tract infection overview
Usually a viral infection (rhinovirus, RSV, Coronavirus) or sometimes bacterial (Streptococcus pneumoniae, Staphylococcus aureus) or fungal (Aspergillus) in immunocompromised people), affecting the paranasal sinuses, nasal cavity, pharynx, and/or the larynx
Upper respiratory tract infection presentation
Rhinitis -> Runny nose/nasal congestion, sneezing
Rhinosinusitis -> Pain/pressure on face, change in voice (bunged up)
Pharyngitis -> Sore throat
Tonsillitis -> Pain/swelling, difficulty swallowing
Laryngitis-> Hoarse voice, dry cough
Epiglottitis -> Trouble breathing (EMERGENCY)
NO SYSTEMIC UPSET & CLEAR CHEST
Upper respiratory tract infection management
Rest and Hydration
Be careful as can progress to lower respiratory illness
Bronchiolitis overview
Inflammation of the small airways of the lungs (bronchioles), usually a result of an infection from the respiratory syncytial virus (RSV), mostly affecting young children, most children will be infected at least once.
RSV causes the the lining cells of the airway to merge into large multinucleated cells called syncytia
Bronchiolitis presentation
Initially congestion, sore throat, cough
Progressing into difficulty breathing, wheezing, fever
Hypoxia can cause increased heart and resp rate, leading to exhaustion and hospitalisation
Infants can exhibit central apnea (periods of no breathing)
Bronchiolitis risk factors
Time of year, age, not breastfed, born prematurely, neuromuscular disorders
Bronchiolitis management
Rest and hydration
Supplementary Oxygen if required
Those at particular risk (premature or have significant pulmonary disease) can receive monthly antibody injections (Palivizumab)
Epiglottitis overview
Inflammation of the epiglottis, usually bacterial! (Haemophilus influenzae, group A streptococcus). Can be deadly due to blockage of airflow
Epiglottitis presentation
Fevers, difficulty breathing, stridor, retractions (ribs emphasised on inhalation), trpodding, hot potato voice
Epiglottis investigations
X-ray: swollen epiglottis & aryepiglottic folds
CT: Narrowed airway (NOT RECOMMENDED)
Endoscope: epiglottis red and swollen
Epiglottitis management
Supplemental oxygen or even intubation or cricothyroidotomy if very severe
Relevant antibiotics
IV steroids to reduce immune response
H. Influenzae vaccine to prevent epiglottitis
Croup overview
Acute respiratory condition characterised by laryngotracheitis, also known as laryngotracheobronchitis. Usually caused by viral vectors (RSV, parainfluenza, adenoviruses, could be bacterial (C. diphtheriae) if unvaccinated. Most common in children under 6 y/o
Croup presentation
Sore throat, hoarse voice, ‘barking’ cough, tachypnea, grunting, inspiratory stridor
Severe: HYPOXIA, RESP. FAILURE, PULSUS PARADOXUS (decrease of systolic arterial pressure > 10mmHg on inspiration)
Croup investigations
X-ray: ‘steeple’ sign (airways marrow to a point towards epiglottis)
Croup management
Rest and Hydration
Single dose of dexamethasone or prednisilone to reduce swelling in throat
Nebuliser epinephrine and humidified supplemental oxygen if patient is struggling to breath
Acute bronchitis overview
UTRI has progressed down into chest to cause a lower respiratory tract infection. Characterised by inflammation of the bronchi.
Acute bronchitis presentation
Recent URTI/current URTI
Productive cough, aches and pains, tiredness
Sore chest and stomach muscles, shortness of breath
Acute bronchitis management
Usually clears by itself in 3 weeks
Rest and hydration
Antibiotics (amoxicillin or doxycycline) can be discovered if >65 or has other co-morbidities like COPD
Cystic fibrosis overview
Autosomal Recessive deltaF508 mutation in the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) Gene
Prevents the pumping of chlorine ions into secretions, leading to the secretions being dry
Cystic fibrosis areas of effect
Sinuses, lungs, pancreas, intestines, gall bladder, heart, liver,
Who gets diagnosed with cystic fibrosis?
Children and young adults, usually of Northern European descent
1/25 people in the UK carry the gene
Both parents carry mutation/family members already have condition
Presentation of cystic fibrosis
History of delayed meconium or meconium ileus
Poor weight gain and failure to thrive, due to pancreatic insufficiency, steatorrhea - fat containing stools, pancreatitis, diabetes
Defective cilia lead to bacterial recurrent infection, CF exacerbation (cough, fever, pneumonia), bronchiectasis, haemoptysis, pulmonary fibrosis
Infertility in men (no vas deferens), digital clubbing, nasal polyps
Cystic fibrosis investigations
New born screening for immunoreactive trypsinogen (IRT), found in the blood in the case of pancreatic damage
Sweat test shows high levels of chloride (>60mmol)
Genetic testing
Cystic fibrosis management
Chest physiotherapy (postural drainage), mucolytics
Pulmonary lung function tests to track deterioration (obstructive)
Prophylactic antibiotics
Fat soluble vitamins, extra calories, replacement pancreatic enzymes
Ivecaftor used in G551D mutation, CFTR in membrane but not activated
Lung transplant
Acute respiratory distress syndrome overview
Non cardio genie pulmonary oedema caused by widespread inflammation of the lungs.
Juice in alveoli
Causes of acute respiratory distress syndrome
Cytokines (TNF-alpha, Interleukin 1) present in blood are taken up from blood stream. Inflammation causes blood clots, endothelium becomes leaky, pneumocytes die and form hyaline membrane.
Shock, trauma and burns, infection (sepsis,malaria), drugs (aspirin, heroin), GI (acute liver failure, pancreatitis), Obstetric (eclampsia, amniotic fluid embolus), Resp (pneumonia, inhalation injuries, vasculitis)
Presentation of acute respiratory distress syndrome
Shortness of breath + tachypnoea hours-days after initial injury
Rapidly deteriorates into resp. failure
Cyanosis, bilateral crepitations, tachycardia, peripheral vasodilation
Investigations for acute respiratory distress syndrome
CXR: opacity/white out across both lungs
PF ratio: PaO2/FiO2 < 300mmHg
Pulmonary artery catheter: capillary wedge pressure = normal
Management of acute respiratory distress syndrome
Supplemental oxygen or mechanical ventilation (positive-end expiratory pressure prevents alveolar collapse)
Treat underlying cause
Treat any persistent lung damage appropriately
Idiopathic pulmonary fibrosis
Pulmonary fibrosis of unknown cause
Chronic process causing progressing loss of lung tissue
Over production of collagen by myofibroblasts
Who gets idiopathic pulmonary fibrosis
Old people
Men
Smokers
Presentation of idiopathic pulmonary fibrosis
History of dry cough, shortness of breath, malaise, weight loss and fatigue
Digital clubbing, bibasal inspiratory crackles, and cyanosis
Respiratory failure
Investigations for idiopathic pulmonary fibrosis
CXR: lower zone fibrosis
CT: honeycombing and interstitial thickening
Spirometry: decreased totally lung capacity, decreased FVC, decreased FEV1, normal FEV1/FVC. Restrictive pattern
ABG: reduced PaO2/increased PaCO2
DCLO: reduced
Treatment of idiopathic pulmonary fibrosis
50% 5 year mortality rate
Smoking cessation and anti fibrotic (perfenidone)
Supplemental oxygen
Lung transplant
Tuberculosis overview
An infection caused by mycobacterium tuberculosis
Can effect all organs but primarily affects the lungs
Usually contracted by inhalation of contaminated droplets
Tuberculosis primary infection
Bacterium reaches alveoli (usually in upper lung)
Macrophage and T cell immune response results in the formation of a caseating granuloma called the ghon focus, lymph node involvement vghon complex, calcification = ranke complex
3 outcomes: 50% result in spontaneous resolution, primary TB induced (symptomatic), or bacteria becomes dormant in granuloma (latent infection)
Tuberculosis latent infection
Bacteria lays dormant in patient and is asymptomatic
Bacteria can be reactivated due to changes like: diabetes, homelessness or drug abuse, steroids and HIV
Miliary tuberculosis
Occurs due to dissemination due to entry into blood stream
Assman focus: secondary pulmonary lesions that have spread from the initial site, usually small and numerous
Who gets tuberculosis
Deprived people
People originating from or have traveled to: Indian subcontinent, SE Asia, and Africa
Presentation of Tuberculosis
History of malaise, fever, night sweats, productive cough, SOB, chest pain, hoarseness, haemoptysis, and bone pain
Erythema nodossum, lymphadenopathy, vertebral collapse, erythema nodossum, and meningitis
Tuberculosis investigations
CXR: pneumonia, cavitating upper lobe lesions, lymphadenopathy, fibrosis/calcified lesions
Skin: Purified protein derivative intradermal skin test/manors test, shows exposure (past or present) to TB or BCG vaccine
Blood: Interferon Gamma Release Assay (IGRA)
Sputum: PCR and Zhiel Nielsen stain shows up red
Tuberculosis management
Active TB:
Rifampicin, Isoniazid, Pyrazinamide, Ethambutol for 2 months, AND rifampicin and isoniazid for a further 4 months
Latent TB:
Rifampicin and isoniazid for 3 months OR isoniazid for 6 months
Compliance is very important as it reduces infectiousness
Pleural effusion overview
Excess fluid present in the pleural space
Comes in 3 flavours transudative, exudative, and lymphatic
Exudate effusion explanation and causes
Pleural effusion that contains >30g/l of protein
This is caused by anything that causes an inflammation of pulmonary capillaries like: trauma, malignancy, infection, autoimmune diseases
Transudate effusion explanation and causes
Effusion with a protein content of <30g/l
This is caused by an increase in hydrostatic pressure within the blood pulmonary arteries (heart failure) or a decrease in osmotic pressure within the pulmonary capillaries (cirrhosis of the liver or nephrotic syndrome)
Presentation of pleural effusion
Can be asymptomatic
History of shortness of breath and pleuritic chest pain
Stony dull to percussion and reduced breath sounds in the area effected
Investigations for pleural effusion
CXR: blunting of the costophrenic angle, dense shadows with meniscus
Thoracentesis (chest drain): yellow=parapneumonic, neutrophils=parapneumonic or PE, Lymphocytes=malignancy or TB or autoimmune, mesothelial cells=PE, abnormal mesothelial cells=mesothelioma
Management of a pleural effusion
Thoracentesis = hollow needle inserted just above a rib in order to remove the fluid
Treat underlying cause
Plurodesis (the binding of the two pleural walls) if pleural effusion is recurrent
Pneumothorax overview
Presence of air within the pleural space
Tension pneumothorax
Presence of air in the pleural space that is at high pressure due to the entry hole acting as a one way valve
High pressure can cause deviation of structures: lungs, heart, trachea
What causes a pneumothorax
Spontaneous: bullae (air pocket) forms in lung due to small leak in alveoli, this air pocket breaks
Trauma
Iatrogenic: mechanical ventilation, GVP line placement
Who gets a pneumothorax
Primary: thin, tall, adolescent, male with a history of holding their breath, no underlying cause
Secondary: underlying health cause (CF, carcinoma, asthma, emphysema, marfans)
Presentation of pneumothorax
History of shortness of breath and pleuritic chest pain
Reduced expansion, hyper resonance and reduced breath sounds over effected area, hypoxia
Investigations for pneumothorax
CXR: peripheral loss of lung markings
Primary spontaneous pneumothorax management
If <2cm and asymptomatic there is no need for treatment
If >2cm or symptomatic attempt aspiration up to two times, if not possible, insert a chest drain
Aspiration = insertion of a 16g cannula into the 2nd intercostal space, on the midclavicular line
?pleurodesis if recurrent
Secondary spontaneous pneumothorax management
0-1cm and asymptomatic: oxygen and admit for observation for 24 hours
1-2cm and asymptomatic: attempt aspiration, if this fails, insert chest drain
> 2cm or symptomatic: insert chest drain
Tension pneumothorax management
If suspected, do not delay for results of CXR
Proceed with immediate aspiration, followed by a chest drain
Pulmonary embolism overview
Blockage in within the pulmonary arteries
Usually caused by a thrombus originating within the deep veins of the leg
Pulmonary embolism risk factors
Wirchow’s triad
- Slowed blood flow (stasis) - turbulent blood flow, bed rest, prolonged travel, pregnancy
- Hypercoagulation - genetics, surgery/trauma, medications (birth control)
- Damage to endothelium - infections, chronic inflammation, toxins (tobacco smoke
Pulmonary embolism presentation
History of leg pain/swelling, shortness of breath, chest pain, haemoptysis, syncope/sudden death (-> occlusion of pulmonary saddle)
Tachycardia, tachypnoea, cyanosis, fever, low BP, crackles and dullness (effusion), rub
Pulmonary embolism investigations
ABG: decreased PaO2, decreased SaO2, normal or low PaCO2 (type 1 respiratory failure
CXR: normal before infarction, progress to basal atelectasis, consolidation, pleural effusion
D-dimmer: raised
ECG: acute right heart strain pattern (S1Q3T3, T inversion in V1-V3)
Troponin and BNP: raised
Circumstantial pulmonary embolism investigations
If unwell with suspected intermediate to high risk PE: CT pulmonary angiogram to look for artery filling defect
In the ambulatory setting with suspected low risk PE: V/Q scan or CTPA
Pregnant: ultrasound on legs -> positive findings -> presume PE and treat accordingly OR just perfusion scan. Disregard damage to baby if mother is in danger
Investigations for cause of ?PE
Thrombophillia screening
Cancer screening
Autoantibodies (SLE)
Anticoagulant management following Pulmonary evidence
Anticoagulants: therapeutic dose of s/c low molecular weight heparin (dalteparin/fragmin), rarely IV heparin.
Begin this immediate if high suspicion of PE, if low suspicion, wait for test results
Start warfarin simultaneously
Stop heparin when INR>2 (3-5 days)
Alternatively: solely use DOACs -> direct oral thrombin inhibitor (dabigatran) or factor X inhibitor (rivaroxaban/apixaban)
Target INR ranges for pulmonary embolism
First event: 2-3
Recurrent PE: 3 or more
Recurrent PE whilst on warfarin: 3.5
Warfarin interactions: alcohol, antibiotics, amiodarone, cimetidine, grapefruit… BE CAREFUL
Thrombolysis management following a Pulmonary embolism
In case of life-threatening massive/sub-massive PE (low BP (<90mmHg systolic for 15 mins), severe hypoxia, imminent or actual cardiopulmonary arrest)
IV tissue plasminogen activator (tPA) - tenecteplase
Contraindications: haemorrhagic stroke are any time, ischaemic stroke within last 6 months, recent major trauma/surgery, current haemorrhage
Relative contraindications: pregnancy/post-partum, TIA in last 6 months, peptic ulcers, refractory resuscitation/hypertension, advanced liver disease
Extra management of pulmonary embolism
IVC filter to prevent further embolisation of recurrent clots
Intra-catheter directed thrombolysis
Thrombo-embolectomy (v. rare)
Duration of anti-coagulant treatment following a pulmonary embolism
Unprovoked 1st PE -> 6 months
Provoked PE/temporary risk factor -> 3 months
Unprovoked low risk distal DVT -> 3 months
High risk proximal DVT -> 6 months
Recurrent DVT/PE -> life long
Extrinsic allergic alveolitis overview
Type 3 hypersensitivity (IgG driven) caused by the inhalation of an allergen
Can present both acutely and chronically
Extrinsic allergic alveolitis causes
Spores from hay: farmer’s lung
Protein in bird poo: pigeon fancier’s lung
Aspergillus from malt: malt worker’s lung
No cause is discovered in 30% of cases
Presentation of extrinsic allergic alveolitis
Acute (4-6 hours after exposure): flu like symptoms (fever, rigor, myalgia, dry cough, shortness of breath, crepitations)
Chronic (repeated low dose exposure): fibrosis of the lungs due to chronic inflammation, progressive shortness of breath, weight loss, type 1 respiratory failure, cor pulmonale
Acute presentation of extrinsic allergic aalveolitis investigations
Bloods: neutrophilia, increased erythrocyte sedimentation rate
CXR: upper zone consolidation
Spirometry: reversible restrictive pattern
Chronic presentation of extrinsic allergic aalveolitis investigations
Blood: positive serum precipitins
CXR: upper lobe fibrosis (honeycomb lung)
Spirometry: restrictive pattern
DCLO: reduced
Management of extrinsic allergic alveolitis
Acute: remove allergen, supplementary oxygen, tapered dose of oral steroids
Chronic: allergen avoidance, long term steroids
Coal Miner’s Pneumoconiosis
Interstitial lung disease caused by inhalation of coal dust
Initially asymptomatic, but later presents with progressive massive fibrosis in the mid lung
Callan syndrome = the association between rheumatoid, pulmonary rheumatoid nodules and coal miners pneumoconiosis
Silicosis
Interstitial lung disease caused by inhalation of silicone
Seen in glass worker’s, metal miners, and stone quarries
Presents with progressive shortness of breath
CXR = upper lobe fibrosis, egg shell calcification at the hilar nodes
Asbestosis
Interstitial lung disease associated with inhalation of asbestosis
As well as ILD, asbestos can also cause pleural disease: benign pleural plaques, pleural thickening, mesothelioma
