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Respiratory Flashcards

1
Q

Sarcoidosis areas of effect

A

Multi system disorder, commonly lungs, lymph nodes, joints liver, skin and eyes

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2
Q

Sarcoidosis Overview

A

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

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3
Q

Who gets sarcoidosis

A

Usually adults aged 20-40, non-smokers, more common in Afro-Caribbeans and women

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4
Q

Presentation of Sarcoidosis

A

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

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5
Q

Sarcoidosis investigations

A

Spirometry: normal restrictive pattern
CXR: bilateral hilar lymphadenopathy, fibrosis
Urine: increased calcium
DCLO: normal or reduced
Bloods: raised ESR, WCC, serum ACE, calcium

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6
Q

Sarcoidosis management

A

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

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7
Q

Bronchiectasis overview

A

Chronic dilation of the airways, with increased mucus and decreased compliance due to scarring

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8
Q

Causes of bronchiectasis

A

Idiopathic, malignancy, chronic infection, immunodeficiency, genetic (cystic fibrosis), autoimmune (rheumatoid, ulcerative colitis), COPD/asthma, allergic lung inflammation, recurrent pulmonary aspiration, ciliary dyskinesia,

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9
Q

Presentation of Sarcoidosis

A

Increased mucus production, shortness of breath, fatigue, wheezing, chest pain, finger clubbing, haemoptysis, fever

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10
Q

Bronchiectasis investigations

A

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

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11
Q

Bronchiectasis management

A 
Postural drainage 
Salbutamol inhaler 
Long term antibiotics 
Nebuliser saline
(Carbocysteine)
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12
Q

Influenza overview

A

Viral infection caused by influenza A/B viruses

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13
Q

Presentation of influenza

A

Fever, malaise, exhaustion, myalgia, fever, cough, runny nose, vomiting and diarrhoea

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14
Q

Influenza management

A

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

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15
Q

Upper respiratory tract infection overview

A

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

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16
Q

Upper respiratory tract infection presentation

A

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

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17
Q

Upper respiratory tract infection management

A

Rest and Hydration

Be careful as can progress to lower respiratory illness

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18
Q

Bronchiolitis overview

A

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

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19
Q

Bronchiolitis presentation

A

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)

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20
Q

Bronchiolitis risk factors

A

Time of year, age, not breastfed, born prematurely, neuromuscular disorders

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21
Q

Bronchiolitis management

A

Rest and hydration
Supplementary Oxygen if required
Those at particular risk (premature or have significant pulmonary disease) can receive monthly antibody injections (Palivizumab)

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22
Q

Epiglottitis overview

A

Inflammation of the epiglottis, usually bacterial! (Haemophilus influenzae, group A streptococcus). Can be deadly due to blockage of airflow

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23
Q

Epiglottitis presentation

A

Fevers, difficulty breathing, stridor, retractions (ribs emphasised on inhalation), trpodding, hot potato voice

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24
Q

Epiglottis investigations

A

X-ray: swollen epiglottis & aryepiglottic folds
CT: Narrowed airway (NOT RECOMMENDED)
Endoscope: epiglottis red and swollen

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25
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
26
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
27
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)
28
Croup investigations
X-ray: 'steeple' sign (airways marrow to a point towards epiglottis)
29
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
30
Acute bronchitis overview
UTRI has progressed down into chest to cause a lower respiratory tract infection. Characterised by inflammation of the bronchi.
31
Acute bronchitis presentation
Recent URTI/current URTI Productive cough, aches and pains, tiredness Sore chest and stomach muscles, shortness of breath
32
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
33
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
34
Cystic fibrosis areas of effect
Sinuses, lungs, pancreas, intestines, gall bladder, heart, liver,
35
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
36
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
37
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
38
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
39
Acute respiratory distress syndrome overview
Non cardio genie pulmonary oedema caused by widespread inflammation of the lungs. Juice in alveoli
40
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)
41
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
42
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
43
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
44
Idiopathic pulmonary fibrosis
Pulmonary fibrosis of unknown cause Chronic process causing progressing loss of lung tissue Over production of collagen by myofibroblasts
45
Who gets idiopathic pulmonary fibrosis
Old people Men Smokers
46
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
47
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
48
Treatment of idiopathic pulmonary fibrosis
50% 5 year mortality rate Smoking cessation and anti fibrotic (perfenidone) Supplemental oxygen Lung transplant
49
Tuberculosis overview
An infection caused by mycobacterium tuberculosis Can effect all organs but primarily affects the lungs Usually contracted by inhalation of contaminated droplets
50
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)
51
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
52
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
53
Who gets tuberculosis
Deprived people | People originating from or have traveled to: Indian subcontinent, SE Asia, and Africa
54
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
55
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
56
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
57
Pleural effusion overview
Excess fluid present in the pleural space | Comes in 3 flavours transudative, exudative, and lymphatic
58
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
59
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)
60
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
61
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
62
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
63
Pneumothorax overview
Presence of air within the pleural space
64
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
65
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
66
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)
67
Presentation of pneumothorax
History of shortness of breath and pleuritic chest pain | Reduced expansion, hyper resonance and reduced breath sounds over effected area, hypoxia
68
Investigations for pneumothorax
CXR: peripheral loss of lung markings
69
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
70
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
71
Tension pneumothorax management
If suspected, do not delay for results of CXR | Proceed with immediate aspiration, followed by a chest drain
72
Pulmonary embolism overview
Blockage in within the pulmonary arteries | Usually caused by a thrombus originating within the deep veins of the leg
73
Pulmonary embolism risk factors
Wirchow's triad 1. Slowed blood flow (stasis) - turbulent blood flow, bed rest, prolonged travel, pregnancy 2. Hypercoagulation - genetics, surgery/trauma, medications (birth control) 3. Damage to endothelium - infections, chronic inflammation, toxins (tobacco smoke
74
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
75
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
76
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
77
Investigations for cause of ?PE
Thrombophillia screening Cancer screening Autoantibodies (SLE)
78
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)
79
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
80
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
81
Extra management of pulmonary embolism
IVC filter to prevent further embolisation of recurrent clots Intra-catheter directed thrombolysis Thrombo-embolectomy (v. rare)
82
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
83
Extrinsic allergic alveolitis overview
Type 3 hypersensitivity (IgG driven) caused by the inhalation of an allergen Can present both acutely and chronically
84
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
85
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
86
Acute presentation of extrinsic allergic aalveolitis investigations
Bloods: neutrophilia, increased erythrocyte sedimentation rate CXR: upper zone consolidation Spirometry: reversible restrictive pattern
87
Chronic presentation of extrinsic allergic aalveolitis investigations
Blood: positive serum precipitins CXR: upper lobe fibrosis (honeycomb lung) Spirometry: restrictive pattern DCLO: reduced
88
Management of extrinsic allergic alveolitis
Acute: remove allergen, supplementary oxygen, tapered dose of oral steroids Chronic: allergen avoidance, long term steroids
89
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
90
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
91
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

Disease Profiles (3 decks)

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