Respiratory Flashcards
Moderate Asthma features
PEFR 50 – 75% predicted
Increasing symptoms
No features of severe asthma
Severe Asthma features
PEFR 33-50% predicted
Resp rate >25 (>12 year olds) ,30 if between 5 and 12, 40 if between 2-5)
Heart rate >110(>12 year olds)
Unable to complete sentences in one breath
Spo2 equal or <92
Use of accessory muscles
Life-threatening asthma features
33,92,CHEST
<33%PEFR
<92%Sats
Cyanosis
Hypotension (Haemodynamic instability (i.e. shock))
Exhaustion, altered consciousness/confusion/coma
Silent chest- No wheeze. This occurs when the airways are so tight that there is no air entry at all.
Tachyarrhythmias
paOQ <8
Normal CO2
Investigations for asthma
Spirometry for obstructive evidence FEV1/FVC <0.7
Evidence of reversibility by spirometry and giving inhaled bronchodilator- level of reversibility that is supportive of asthma is 200 mls and 12% improvement of FEV1
Exhaled breath nitric oxide FeNO ( goes up if you have airway eosinophilic inflammation, >40ppb in adults or >35 ppb in children)
Blood eosinophilia ( 4% or more in FBC is suggestive)
Look for evidence of atopy by skin prick test or blood test,
Can look for variability over time by either peak flow diary (variability >20%)
Direct bronchial challenge test with histamine or methacholine
BTS asthma guidlines
- low dose ICS + SABA
- Regular preventer
- Add inhaled LABA to low dose ICS (fixed dose or MART)
- Consider increasing ICS to medium dose OR adding LTRA
If no response to LABA consider stopping LABA
BTS paediatric guidlines
- Very lose dose ICS + SABA
- Children >5 - ICS
Children <5 add LTRA - Children >5add inhaled LABA or LTRA
- Increase ICS to low dose OR children >5 add LTRA or LABA. if no reponse to LABA consider stopping
Acute asthma attack treatment
sit patient up
high flow o2
Salbutamol neb 5mg
Ipatropium bromide 0.5mg
Prednisolone 40mg po or hydrocortisone iV 100mg
Magnesium sulphate 2g IV
Aminophylline
CURB-65
Confusion (abbreviated mental test score <= 8/10)
Urea >7
Respiratory rate >= 30/min
Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
Aged >= 65 years
Treatment of COPD
Symptoms/ airflow obstruction → bronchodilators SABA/SAMA , LAMA + LABA,for people with asthma/eosinophilic features also add ICS..
Exercise capacity/physical activity
Comorbidities optimisation
BMI → Underweight with COPD increases risk of dying, so need to maintain healthy weight, or even a bit above
Smoking→ cessation is priority, only thing proven to reduce mortality from COPD
Exacerbations→ Prevention by inhaled bronchodilators and also inhaled steroids for the right patients
pneumococcal and influenza vaccinations
COPD home o2 considered if
ABG on 2 occasions 3 weeks apart show
<7.3 or
7.3-8 + peripheral oedema, polycythaemia, pulm. HTN
Wells score
Clinical features DVT — +3
HR> 100 — +1.5
Immobilization for >3d or surgery in the prev 4w— +1.5
Prev DVT/PE — +1.5
Haemoptysis — +1
Cancer (receiving tx, treated in the last 6m, or palliative) — +1
An alternative diagnosis is less likely than PE — +3
Tx PE
DOAC/LWH/Warfarin
Thrombolysis if hypotensive
If recurrent, ivc filter
HAS BLED Score
H – Hypertension
A – Abnormal renal and liver function
S – Stroke
B – Bleeding
L – Labile INRs (whilst on warfarin)
E – Elderly
D – Drugs or alcohol
ORBIT tool for assessing a patient’s risk of major bleeding whilst on anticoagulation.
Low haemoglobin or haematocrit
Age (75 or above)
Previous bleeding (gastrointestinal or intracranial)
Renal function (GFR less than 60)
Antiplatelet medications
Causes of exudative pleural effusion
high protein count (>3g/dL or 30g/L)
inflammation results in protein leaking out of the tissues into the pleural space
eg lung cancer, PE, pneumonia, pancreatitis, RA
Causes of transudative pleural effusion
relatively lower protein count (<3g/dL or 30g/L)
relate to fluid moving across into the pleural space
eg Congestive cardiac failure , Constrictive, pericarditis , Hypoalbuminaemia, Hypothroidism, Meig’s syndrome, cirrhosis,Nephrotic syndrome
Lights criteria
. If the protein level is between 25-35g/L you use Light’s criteria to establish the type of effusion.
Exudative if >=1 of the following criteria are met:
Pleural fluid protein/ serum protein >0.5
Pleural fluid/serum LDH >0.6
Pleural fluid LDH >2/3 upper limit of normal serum LDH
Transudative if none of the above levels are met.
Indicators of empyema
Pleural aspiration shows pus
acidic pH (pH < 7.2)
low glucose <2.2 mmol/L
high LDH
Antiphospholipid syndrome
features
Clots - Usually VTE(dvt/pe), but arterial embolism (eg. MI or stroke) can also occur.
Livedo reticularis - A mottled, purple lace-like appearance of the skin on the lower limbs.
Obstetric loss - Recurrent miscarriages, pre-eclampsia and premature births can occur
Thrombocytopenia
ophthalmic vaso-occlusive pathologies
Diagnosis antiphospholipid syndrome time frame
One or more of the positive blood tests are needed on 2 occasions, 12-weeks apart
antiphospholipid antibodies
Lupus anticoagulant (frequently causes the aPTT to be prolonged)
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies
tension pneumothorax treatment
Insert a large bore 16 G cannula into the second intercostal space in the midclavicular line on the affected side.
pneumothorax management : observation
primary pneumothorax no SOB and there is a < 2cm rim of air on the chest xray
If secondary, can observe if no SOB and <1cm
pneumothorax management: aspiration
Secondary : 1-2cm even if no SOB
Primary: If SOB and/or there is a > 2cm rim of air on the chest xray
Pneumothorax management: chest drain
If aspiration fails twice it will require a chest drain. Secondary pneumothorax greater than 2 goes straight to chest drain
Unstable patients or bilateral or secondary pneumothoraces generally require a chest drain.
Chest drain triangle of safety borders
5th intercostal space (inf nipple line)
Mid axillary line/lateral edge latissimus doors
Ant axillary line/lateral edge pectorals major
Addiotional pneumothorax education
Life long ban on sea diving, air travel restrictions until confirmed pneumothorax resolution, smoking cessation
Management ILD
Supportive care, home O2, patient support groups, specialist nurse, breathlessness management
Antifibroitc drugs: Pirfenidones, nintedanib
Lung transplant for younger patients
Drugs causing pulmonary fibrosis
Cyclophosphamide
Amiodarone
Bleomycin
Nitrofurantoin
Methotrexate
Other secondary fibrosis causes
RA
Alpha 1 antitrypsin deficiency
Lupus SLE
Systemic sclerosis (scleroderma)
Sarcoidosis
Type 1 Respiratory failure
PaO2 less than 8 and a PaCO2 which is low or normal (PaCO2 <6.0 kPa).
Type 2 respiratory failure
PaO2 of less than 8 and a raised PaCO2 (PaCO2 >6.0 kPa).
Alpha- antitrypsin deficiency associated with
young onset COPD, bronchiectasis, secondary pulmonary fibrosis, liver disease, skin problems (panniculitis), and inflammation of the blood vessels (vasculitis)
obstructive sleep apnoea syndrome
abnormal number of apnoeas (c essation of breathing for 10 s or more)AND symptoms.
episodes of complete to partial upper airway obstruction during sleep usually associated with oxyhemoglobin desaturations and arousal from sleep,excessive daytime sleepiness with irregular breathing at night.
Obstructive sleep apnoea symptoms
chronic snoring, insomnia, gasping/choking noises and breath holding, unrefreshing sleep on waking , excessive daytime sleepiness ,Mood swings, personality changes, or depression., nocturia
Pickwickian syndrome
condition in which severely overweight people fail to breathe enough whilst asleep, resulting in high blood carbon dioxide (CO2) levels.
Also called Obesity hypoventilation syndrome
Obstructive sleep apnoea investigations
Epworth sleepiness questionnaire
Sleep diary
full/respiratory polysomnography
Obstructive sleep apnoea management
weight loss, exercise, smoking cessation, and reducing alcohol intake, if appropriate, sleeping on side, assess CVS disease/diabetes, monitor bp, driving advice, support groups
Oral appliance therapy
Continuous Positive CPAP
Implantable hypoglossal neurostimulation
Upper airway surgery
For children, tonsillectomy is often curative.
Pulmonary hypertension management
Physical activity
Should be counselled against conception and pregnancy
Vaccination
Anticoagulation
Diuretics if associated with heart failure
Digoxin if they have tachyarrhythmias
Calcium channel blockers
Vasodilators eg Prostanoids ( prostacyclin)
Pulmonary arterial hypertension clinical presentation
late presentation
Left parasternal heave
Loud P2 heart sound
Sot pansystolic murmur with tricuspid regurgitation
Right heart failure leads to jugular venous distension,a ascites, peripheral oedema and hepatomegaly
Clinical signs of associated disease, such as systemic sclerosis or chronic liver disease should be sought
Pathophysiology of Pulmonary hypertension
may result from PE, chronic lung disease or chronic left heart disease
Sarcoidosis lung features
Mediastinal lymphadenopathy
parenchymal lung disease.
Pulmonary fibrosis (may improve with oral steroids for 6m)
dyspnoea, non-productive cough
Pulmonary nodules
Sarcoidosis skin features
erythema nodosum
Lupus pernio is characterized by red to purple or violaceous, indurated plaques and nodules that usually affect the nose, cheeks, ears, and lips, but it can appear on the dorsa of the hands, and on the fingers, toes, and forehead
Sarcoidosis ophthalmologic features
Anterior uveitis
papilloedema.
Conjunctivitis
Optic neuritis
Sarcoidosis
multisystem disorder of unknown aetiology characterised by the accumulation of T lymphocytes and macrophages and the formation of non-caseating granulomas. Granulomas are nodules of inflammation full of macrophages.
Lofgren’s Syndrome
specific presentation of sarcoidosis.
Erythema nodosum
Bilateral hilar lymphadenopathy
Polyarthralgia (joint pain in multiple joints)
Sarcoidosis Ix
Raised serum ACE. as a screening test
Hypercalcaemia (due to increased production of 1,25-dihydroxyvitamin D by macrophages)
Raised serum soluble interleukin-2 receptor
Raised CRP
Raised immunoglobulins
CXR, CT:hilar lymphadenopathy andpulmonary nodules
Histology from biopsy for dx
Sarcoidosis histology
histology from a biopsy shows characteristic non-caseating granulomas with epithelioid cells.
Sarcoidosis tests for multi system
U&Es for kidney involvement
Urine dipstick or urine albumin-creatinine ratio to look for proteinuria indicating nephritis
LFTs for liver involvement
Ophthalmology review for eye involvement
ECG and echocardiogram for heart involvement
Ultrasound abdomen for liver and kidney involvement
Sarcoidosis management
In acute symptomatic sarcoidosis bed rest and NSAIDs are initially indicated.
oral steroids are usually first line where treatment is required given at high dose orally for 4-6 weeks
Second line options are methotrexate or azathioprine
Sarcoidosis prognosis
Sarcoidosis spontaneously resolves within 6 months in around 60% of patients
Mesothelioma clinical presentation
shortness of breath and chest pain, dry cough
unilateral pleural effusion and pleural thickening
20- to 40-year latency period between exposure and development of malignancy
Mesothelioma Tx
Surgery
Chemo/ radio
Therapeutic thoracentesis
Pleurodesis, defined as the artificial obliteration of the pleural space, can be performed to prevent re-accumulation of pleuritic fluid
Mycobacterium tuberculosis
aerobe acid-fast bacilli
Zeihl-Neelsen stain turns TB bacteria bright red against a blue background
Rhodamine auramine staining helps makes bacteria more visible and more sensitive
TB symptoms
• productive, prolonged cough (duration of >= 3 weeks),
• chest pain,
• hemoptysis.
• fever, chills, night sweats,
• weight loss, appetite loss,
•easy fatigability and lethargy..
•Lymphadenopathy
•Erythema nodosum
• Lupus vulgaris- Small sharply defined reddish-brown papules merge into plaques with a gelatinous consistency
•Spinal pain in spinal TB (also known as Pott’s disease of the spine)
BCG vaccine
intradermal infection of live attenuated (weakened) TB
Prior to the vaccine patients are tested with the Mantoux test and given the vaccine only if this test is negative. also assessed for the possibility of immunosuppression and HIV due to the risks related to a live vaccine.
Mantoux test
used to look for a previous immune response to TB. This indicates possible previous vaccination, latent or active TB.
Involves injecting tuberculin into the intradermal space on the forearm. creates a bleb under the skin. After 72 hours the test is “read”. NICE suggests considering an induration of 5mm or more a positive result. After a positive result they should be assessed for active disease. Positive tests means they have been exposed at some point to TB
TB Interferon-Gamma Release Assays (IGRAs)
•involves taking a sample of blood and mixing it with antigens from the TB bacteria. In a person that has had previous contact with TB the white blood cells have become sensitised to those antigens and they will release interferon-gamma, a Th-1 cytokine,as part of an immune response - positive result
•Main role is in screening for latent disease
TB CXR features
abnormalities often seen in the apical and posterior segments of the upper lobe ( more oxygen in upper lung and the bacterium is aerobic)
fibronodular, irregular shadowing, cavities (gas filled spaces in the lungs) typically upper zones , volume loss, disseminated military tb has millet seeds dispersed throughout lung fields
Tests to carry out on TB sample
Sputum
Mycobacterium blood cultures
Nucleic acid amplification
pharmacological Tx TB
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months
TB additional management
• isolate (until 2w tx and clinically better)
• Counseling and testing for HIV infection
• CD4+ T-lymphocyte count for HIV-positive persons
• Hepatitis B and C serologic tests, if risks present
• blood tests for renal function (ethambutol increased toxicity), liver function (isoniazid, rifampicin and pyrazinamide).
• Visual acuity and color vision tests (when ethambutol used)
• Directly Observed Therapy “DOTS”
MDR-TB
being resistant to Isoniazid and Rifampicin
Bronchiectasis
permanent and abnormal dilation of the proximal and medium-sized bronchi (>2 mm in diameter) caused by weakening or destruction of the muscular and elastic components of the bronchial walls.often caused as a consequence of recurrent and/or severe infections secondary to an underlying disorder.
Causes of Bronchiectasis
Congenital: Cystic fibrosis ,Kartagener’s syndrome ,Alpha-1-antitrypsin deficiency
Post infection: H. influenzae; Strep. pneumoniae; Staph. Aureus; Measles, bronchiolitis, pneumonia; TB; HIV, Pseudomonas aeruginosa
Bronchial obstruction (tumour, foreign body)
allergic bronchopulmonary aspergillosis
COPD
Hypogammaglobulinemia
Rheumatoid arthritis (2%–5%)
Bronchiectasis clinical presentation
regularly cough up large volumes of sputum, or in individuals who present with recurrent chest infections,intermittent haemoptysis,Rhinosinusitis
Bronchiectasis o/e
Finger clubbing; coarse inspiratory crepitations; crackles, High-pitched inspiratory squeaks and pops are commonly heard, dyspnoea , wheeze
Bronchiectasis Ix
HRCT chest is the gold standard to diagnose, assess extent and distribution of disease
•Mosaic perfusion/air trapping on expiratory CT
Bronchiectasis Mx
Airway clearance techniques and mucolytics
- oral hydration , Chest physiotherapy,nebulised hyperosmolar agents promote mucus clearance by inducing coughing, mucolytics eg N-acetylcysteine, carbocysteine ,positive expiratory pressure devices,Exercise, Patient education and support groups, Smoking cessation , consider inhaled bronchodilator ,abx, long‐term use of macrolides, Corticosteroids (eg prednisolone) and itraconazole for ABPA /asthma, surgery, lung transplant
CF genetics
multisystem disorder that affects the chloride transport system in exocrine tissue, mutations in the CF transmembrane conductance regulator (CFTR) gene on chromosome 7,autosomal recessive
CF clinical features
Failure to thrive
meconium ileus
rectal prolapse.
early onset <40 yrs, history of malabsorption, male infertility and childhood steatorrhoea. Sinus disease/nala polyp and Family history ,Cough ( wet sounding), recurrent infections,Bronchiectasis
CF Dx
New born immunoreactive trypsinogen test
Sweat test - gold standard,A negative test has <30 mmol/L chloride, a borderline test 30–60 mmol/L and a positive test >60 mmol/L
Genetics: Screening for known common CF mutations should be considered.
CF Ix
Blood: FBC, U&E, LFT; clotting; vitamin A, D, E levels; annual glucose tolerance test
Bacteriology: Cough swab, sputum culture.
Radiology: CXR; hyperinflation; upper lobe bronchiectasis predominates
Abdominal ultrasound: Fatty liver; cirrhosis; chronic pancreatitis;
Spirometry: Obstructive defect. Aspergillus serology/skin test (20% develop ABPA).
Biochemistry: Faecal fat analysis.
CF Mx
Chest physiotherapy
Exercise
High calorie diet
Abx
Mucolytics may be useful
Bronchodilators.
Gastro: psupplements
Treatment of CF-related diabetes (screen annually with OGTT from 12yrs); screening/treatment of osteoporosis (DEXA bone scanning); arthritis, sinusitis, and vasculitis; fertility and genetic counselling.
Vaccinations including pneumococcal, influenza and varicella
