Resp Flashcards
O2 dissociation curve
Right = raised oxygen delivery to tissues, raised acidity/CO2/temp/DPG Left = lower oxygen delivery to tissues, lower acidity/CO2/temp/DPG
Bohr effect
Increasing acidity (or pCO2) means O2 binds less well to Hb –> better tissue oxygenation
Haldane effect
Increased pO2 means CO2 binds less well to Hb –> better CO2 elimination
Causes of raised TLCO?
Asthma Pulmonary hemorrhage (wegener's, goodpasture's) Left-to-right cardiac shunts Polycythemia Hyperkinetic states Male gender, exercise
Assessment for LTOT?
Very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be 'considered' for patients with severe airflow obstruction (FEV1 30-49% predicted) • Cyanosis • Polycythaemia • Peripheral oedema • Raised jugular venous pressure • Oxygen saturations 92% on room air
Indications for LTOT?
pO2 of < 7.3 kPa or pO2 of 7.3 - 8 kPa and one of the following: • Secondary polycythaemia • Nocturnal hypoxaemia • Peripheral oedema • Pulmonary HTN
How to assess for LTOT?
measurine arterial blood gases on 2 occasions at least 3 weeks apart in
patients with stable COPD on optimal
management
Recommended settings in NIV?
EPAP - 4-5
IPAP - 12-15
FiO2 - not >40%
CAP organisms
Streptococcus pneumoniae (accounts for around 80% of cases) • Hemophilus influenzae • Staphylococcal aureus • Atypical pneumonias (e.g. due to Mycoplasma pneumoniae) • Viruses
Step pneumonia?
commonly causes reactivation of the herpes simplex virus resulting in ‘cold
sores and associated with foreign travel
- Rapid onset
- High fever
- Pleuritic chest pain
- Herpes labialis
Klebsiella pneumonia?
classically in alcoholics. CXR features may
include abscess formation in the middle/upper lobes and empyema. The mortality approaches 30-50%
Staph Aureus pneumonia?
normally causes pneumonia only AFTER a preceding influenzal viral
infection. Characteristically causes multiple abscesses in up to 25% of patients and empyema in 10%,
septicemia develops with metastatic abscess in other organs such as brain and bones
Bacterial organisms causing IECOPD?
Hemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
Viral is most common
Mycoplasma pneumonia?
- Affects youngerpatients frequently amongst those living in boarding houses (housings, hostels)
- associated with erythema multiforme (target lesion) and cold
autoimmune hemolytic anemia (IgM) - Diagnosis with serology, PCR, ?positive coombs test after 10 days
Treat with macrolides/tetracyclines
Mycoplasma features?
- Flu-like symptoms classically PRECEDE a dry cough
- Bilateral consolidation on x-ray
COMPLICATIONS
- Cold agglutins (IgM) may cause an hemolytic anemia, thrombocytopenia
- Erythema multiforme, erythema nodosum
- Meningoencephalitis, Guillain-Barre syndrome
- Bullous myringitis: painful vesicles on the tympanic membrane
- Pericarditis/myocarditis
- Gastrointestinal: hepatitis, pancreatitis
- Renal: acute glomerulonephritis –> HAEMATURIA
PCP pneumonia extrapulmonary features?
Hepatosplenomegaly
Lymphadenopathy
Choroid lesions
PCP pneumonia investigations?
CXR: typically shows bilateral interstitial pulmonary infiltrates but can present with other x-ray findings e.g. lobar consolidation. May be normal
Exercise-induced desaturation
Sputum often fails to show PCP, bronchoalveolar lavage (BAL) often needed to demonstrate
PCP (silver stain)
What kind of organism is legionella?
Gram -ve bacilli
Legionella pneumonia features?
Flu-like symptoms
50% of cases have GI symptoms such as nausea, vomiting, diahrrhea and abdominal pain.
Dry cough
Lymphopenia
Hyponatremia
Deranged LFTs
Hematuria occurs and occasionally renal failure
Examples of EAA?
Bird fanciers’ lung (avian proteins)
Farmers lung (spores of micropolyspora faeni)
Malt workers’ lung (aspergillus clavatus)
Mushroom workers’ lung (thermophilic actinomycetes)
What type of hypersesnsitivity is EAA?
largely caused by immunecomplex
mediated tissue damage (type III hypersensitivity = acute phase) although delayed
hypersensitivity (type IV = chronic phase) is also thought to play a role in EAA, especially in the
chronic phase
Features/Ix EAA?
Acute: occur 4-8 hrs after exposure, SOB, dry cough, fever
Chronic: similar
CXR: upper lobe fibrosis
BAL (bronchoalveolar lavage): lymphocytosis
Blood: NO eosinophilia
Circulating IgG precipitant - no IgE therefore not allergy
Pathologies causing upper lung fibrosis?
Extrinsic allergic alveolitis Coal worker's pneumoconiosis/progressive massive fibrosis Silicosis Sarcoidosis Ankylosing spondylitis (rare) Histiocytosis Tuberculosis
Pathologies causing lower lung fibrosis?
Cryptogenic fibrosing alveolitis
Most connective tissue disorders (except ankylosing spondylitis)
Drug-induced: amiodarone, bleomycin, methotrexate
Asbestosis
Features of asbestosis?
Progressive SOB
Chest pain
Pleural effusion
Pleural thickening Pleural plaques (not premalignant) - occur after latent period of 20-40 years
Types of lung cancer and %?
Squamous: 35% Adenocarcinoma: 30% Small (oat) cell: 15% Large cell: 10% Other: 5%
Paraneoplastic features of lung ca?
Squamous cell: PTHrp (hypercalcaemia), clubbing, HPOA
Small cell: ADH (hyponatraemia), ACTH (cushings, HTN, hyperglycaemia, low K, alkalosis) , Lambert-Eaton syndrome (myasthenia)
Adeno - gynaecomastia
Contraindications to lung ca surgery?
SVC obstruction, FEV < 1.5, MALIGNANT
pleural effusion, and vocal cord paralysis
Locations of lung ca?
Small cell - central
Squamous - central
Adeno - peripheral
Causes of cavitations on CXR?
Tuberculosis
Lung cancer (especially squamous cell)
Abscess (staph aureus, klebsiella and Pseudomonas)
Wegener’s granulomatosis
Pulmonary embolism
Rheumatoid arthritis
Aspergillosis, histoplasmosis, coccidioidomycosis
Sarcoid?
Multisystem disorder of unknown aetiology characterized by non-caseating
granulomas.
It is more common in young adults and in people of African descent.
Sarcoidosis remits without treatment in approximately two-thirds of people.
Investigations in sarcoidosis?
Diagnosis - no reliable test, largely clinical. ACE levels = sensitivity 60% specificity 70% - may have a role in monitoring disease activity.
Bloods - hypercalcaemia (10%) and raised ESR
Spirometry: may show a restrictive defect
Tissue biopsy: non-caseating granulomas
Gallium-67 scan - not used routinely
Features of sarcoid with POOR prognosis?
Insidious onset, symptoms > 6 months
Absence of erythema nodosum
Extrapulmonary manifestations: e.g. Lupus pernio, splenomegaly
CXR: stage III-IV features
Black people
CXR features in sarcoidosis?
0 = normal
1 = BHL
2 = BHL + infiltrates
3 = infiltrates
4 = fibrosis
Indications for steroids in sarcoidosis?
Hypercalcemia
Worsening lung function
Eye (bilateral posterior uveitis is common eye manifestation)
Heart or neuro involvement
Mikulicz syndrome?
chronic condition characterized by the abnormal enlargement of parotids,
lacrimal and salivary glands. The tonsils and other glands in the soft tissue of the face and neck may
also be involved. It is associated with sarcoidosis
Causes of BHL?
Sarcoidosis
Tuberculosis
Lymphoma/other malignancy
Pneumoconiosis e.g. Berylliosis
Fungi e.g. Histoplasmosis, coccidioidomycosis (VHL + Cavitation in CXR)
What is Lofgren’s syndrome?
Acute form sarcoidosis characterized by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia.
typically occurs in young females
excellent prognosis
Blood eosinophilia
Caues of pulmonary eosinophiilia?
Churg-Strauss syndrome (eosinophilia + asthma + hemorrhage) Allergic bronchopulmonary aspergillosis (ABPA) Loffler's syndrome Eosinophilic pneumonia Hypereosinophilic syndrome Tropical pulmonary eosinophilia Drugs: nitrofurantoin, sulphonamides
Less common:
Wegener’s granulomatosis
Tropical pulmonary eosinophilia
Associated with Wuchereria bancrofti infection
Organisms in bronchiectasis?
Hemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
Causes of bronchiectasis?
Post-infective: tuberculosis, measles, pertussis, pneumonia
Cystic fibrosis
Bronchial obstruction e.g. Lung cancer/foreign body
Immune deficiency: selective IgA, hypogammaglobulinemia
Allergic bronchopulmonary aspergillosis (ABPA)
Ciliary dyskinetic syndromes: kartagener’s syndrome, young’s syndrome
Yellow nail syndrome (associated with pleural effusion - exudates)
Management of bronchiectasis?
Physical training (e.g. Inspiratory muscle training) - has a good evidence base for patients withnon-cystic fibrosis bronchiectasis
Postural drainage
IV antibiotics for exacerbations + long-term rotating antibiotics (nebulized ABX) in severe
cases
Bronchodilators in selected cases
Immunisations
Surgery in selected cases (e.g. Localised disease)
Criteria for ARDS?
Acute onset
Bilateral infiltrates on CXR
Non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
pO2/FiO2 < 200 mmHg
What is ABPA? Common question stem for this?
Results from an allergy to Aspergillus spores
Often give a history of bronchiectasis and eosinophilia
Features of ABPA?
Bronchoconstriction: wheeze, cough, dyspnea
Bronchiectasis (proximal)
Eosinophilia
Flitting CXR changes
Positive radioallergosorbent (RAST) test to aspergillus
Positive IgG precipitins (not as positive as in aspergilloma)
Raised IgE
Management ABPA?
Steroids
Itraconazole
What is an aspergilloma?
a fungus ball which often colonises an existing lung cavity (e.g. secondary to TB,
lung cancer or cystic fibrosis)
Features of aspergilloma?
Asymptomatic normally (cough, haemoptysis)
CXR shows round opacity
High titres aspergillus precipitins
Mutation in CF?
Deletion at delta F508 on the long arm of
chromosome 7.
Organisms in CF?
Staph aureus
Pseudomonas aeruginosa (Rx: Inhaled Tobramycin)
Burkholderia cepacia (can cause rapid fever, pneumonia, sepsis, wt loss - poor outcomes)
Aspergillus
Sweat test for CF?
2 reliable positive results on 2 separate days is diagnostic for CF. it is positive when chloride is > 60
Bronchiolitis obliterans?
Fibrous scarring of the small airways
It is seen following: toxic-fume inhalation; mineral-dust exposure; viral infection; mycoplasma and legionella infection; bone marrow, heart–lung and lung transplantation; rheumatoid arthritis; SLE; and as a side-effect of penicillamine
Causes of exudates?
Infection: pneumonia, TB, subphrenic abscess
Connective tissue disease: RA ( glucose < 1.6, LDH > 700, pH < 7.2, R.F > 1:320, cholesterol), SLE
Neoplasia: lung cancer, mesothelioma, metastases
Pancreatitis
Pulmonary embolism
Dressler’s syndrome
Yellow nail syndrome
Causes of transudates?
Heart failure
Hypoalbuminemia (liver disease, nephrotic syndrome, malabsorption)
Hypothyroidism
Meigs’ syndrome: triad of ascites, pleural effusion (right side) and benign ovarian tumor
(fibroma).
Features of different types of lung mets?
Cavitation - squamous cell carcinoma.
Calcification - osteosarcomas and chondrosarcomas as well as metastases from papillary thyroid carcinoma.
Adenocarcinoma metastases spread along the walls of alveoli, instead of destroying the lung parenchyma, resulting in consolidation like that seen with pneumonia.
Haemorrhagic pulmonary metastases - choriocarcinoma and angiosarcoma.
Miliary pattern- renal cell carcinoma and malignant melanoma
Causes of occupational asthma?
Isocyanates - the most common cause. Example occupations include spray painting and foam moulding using adhesives
Platinum salts
Soldering flux resin
Glutaraldehyde
Flour
Epoxy resins
Proteolytic enzymes
NICE COPD management?
SABA or SAMA
If breathless then need to consider whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’
No asthmatic/steroidy features –> LABA + LAMA (if on SAMA switch to SABA)
Asthmatic/steroidy features - LABA + ICS —> triple therapy if remains breathless (LAMA + LABA + ICS - discontinue SAMA start SABA)
Asthmatic/steroid responsive features for COPD management?
any previous, secure diagnosis of asthma or of atopy
a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)
Genotypes in A1AT?
PiZZ = 10% of normal enzyme
PiMZ = no lung dysfunction
What can LRTAs unmask/precipitate?
Churg Strauss (eosinophilic granulomatosis with polyangiitis)
Cherry red lesion?
Lung carcinoid
Kartegener’s syndrome?
dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
pH of pleural fluid for chest drain insertion?
7.2
