Respiratory Flashcards

1
Q

Moderate Asthma features

A

PEFR 50 – 75% predicted
Increasing symptoms
No features of severe asthma

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2
Q

Severe Asthma features

A

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

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3
Q

Life-threatening asthma features

A

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

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4
Q

Investigations for asthma

A

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

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5
Q

BTS asthma guidlines

A
  1. low dose ICS + SABA
  2. Regular preventer
  3. Add inhaled LABA to low dose ICS (fixed dose or MART)
  4. Consider increasing ICS to medium dose OR adding LTRA
    If no response to LABA consider stopping LABA
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6
Q

BTS paediatric guidlines

A
  1. Very lose dose ICS + SABA
  2. Children >5 - ICS
    Children <5 add LTRA
  3. Children >5add inhaled LABA or LTRA
  4. Increase ICS to low dose OR children >5 add LTRA or LABA. if no reponse to LABA consider stopping
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7
Q

Acute asthma attack treatment

A

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

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8
Q

CURB-65

A

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

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9
Q

Treatment of COPD

A

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

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10
Q

COPD home o2 considered if

A

ABG on 2 occasions 3 weeks apart show
<7.3 or
7.3-8 + peripheral oedema, polycythaemia, pulm. HTN

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11
Q

Wells score

A

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

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12
Q

Tx PE

A

DOAC/LWH/Warfarin
Thrombolysis if hypotensive
If recurrent, ivc filter

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13
Q

HAS BLED Score

A

H – Hypertension
A – Abnormal renal and liver function
S – Stroke
B – Bleeding
L – Labile INRs (whilst on warfarin)
E – Elderly
D – Drugs or alcohol

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14
Q

ORBIT tool for assessing a patient’s risk of major bleeding whilst on anticoagulation.

A

Low haemoglobin or haematocrit
Age (75 or above)
Previous bleeding (gastrointestinal or intracranial)
Renal function (GFR less than 60)
Antiplatelet medications

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15
Q

Causes of exudative pleural effusion

A

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

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16
Q

Causes of transudative pleural effusion

A

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

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17
Q

Lights criteria

A

. 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.

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18
Q

Indicators of empyema

A

Pleural aspiration shows pus
acidic pH (pH < 7.2)
low glucose <2.2 mmol/L
high LDH

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19
Q

Antiphospholipid syndrome
features

A

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

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20
Q

Diagnosis antiphospholipid syndrome time frame

A

One or more of the positive blood tests are needed on 2 occasions, 12-weeks apart

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21
Q

antiphospholipid antibodies

A

Lupus anticoagulant (frequently causes the aPTT to be prolonged)
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

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22
Q

tension pneumothorax treatment

A

Insert a large bore 16 G cannula into the second intercostal space in the midclavicular line on the affected side.

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23
Q

pneumothorax management : observation

A

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

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24
Q

pneumothorax management: aspiration

A

Secondary : 1-2cm even if no SOB
Primary: If SOB and/or there is a > 2cm rim of air on the chest xray

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25
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.
26
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
27
Addiotional pneumothorax education
Life long ban on sea diving, air travel restrictions until confirmed pneumothorax resolution, smoking cessation
28
Management ILD
Supportive care, home O2, patient support groups, specialist nurse, breathlessness management Antifibroitc drugs: Pirfenidones, nintedanib Lung transplant for younger patients
29
Drugs causing pulmonary fibrosis
Cyclophosphamide Amiodarone Bleomycin Nitrofurantoin Methotrexate
30
Other secondary fibrosis causes
RA Alpha 1 antitrypsin deficiency Lupus SLE Systemic sclerosis (scleroderma) Sarcoidosis
31
Type 1 Respiratory failure
PaO2 less than 8 and a PaCO2 which is low or normal (PaCO2 <6.0 kPa).
32
Type 2 respiratory failure
PaO2 of less than 8 and a raised PaCO2 (PaCO2 >6.0 kPa).
33
Alpha- antitrypsin deficiency associated with
young onset COPD, bronchiectasis, secondary pulmonary fibrosis, liver disease, skin problems (panniculitis), and inflammation of the blood vessels (vasculitis)
34
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.
35
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
36
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
37
Obstructive sleep apnoea investigations
Epworth sleepiness questionnaire Sleep diary full/respiratory polysomnography
38
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.
39
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)
40
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
41
Pathophysiology of Pulmonary hypertension
may result from PE, chronic lung disease or chronic left heart disease
42
Sarcoidosis lung features
Mediastinal lymphadenopathy parenchymal lung disease. Pulmonary fibrosis (may improve with oral steroids for 6m) dyspnoea, non-productive cough Pulmonary nodules
43
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
44
Sarcoidosis ophthalmologic features
Anterior uveitis papilloedema. Conjunctivitis Optic neuritis
45
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.
46
Lofgren’s Syndrome
specific presentation of sarcoidosis. Erythema nodosum Bilateral hilar lymphadenopathy Polyarthralgia (joint pain in multiple joints)
47
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
48
Sarcoidosis histology
histology from a biopsy shows characteristic non-caseating granulomas with epithelioid cells.
49
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
50
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
51
Sarcoidosis prognosis
Sarcoidosis spontaneously resolves within 6 months in around 60% of patients
52
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
53
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
54
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
55
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)
56
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.
57
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
58
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
59
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
60
Tests to carry out on TB sample
Sputum Mycobacterium blood cultures Nucleic acid amplification
61
pharmacological Tx TB
R – Rifampicin for 6 months I – Isoniazid for 6 months P – Pyrazinamide for 2 months E – Ethambutol for 2 months
62
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”
63
MDR-TB
being resistant to Isoniazid and Rifampicin
64
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.
65
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%)
66
Bronchiectasis clinical presentation
regularly cough up large volumes of sputum, or in individuals who present with recurrent chest infections,intermittent haemoptysis,Rhinosinusitis
67
Bronchiectasis o/e
Finger clubbing; coarse inspiratory crepitations; crackles, High-pitched inspiratory squeaks and pops are commonly heard, dyspnoea , wheeze
68
Bronchiectasis Ix
HRCT chest is the gold standard to diagnose, assess extent and distribution of disease •Mosaic perfusion/air trapping on expiratory CT
69
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
70
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
71
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
72
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.
73
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.
74
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