Respiratory 10/8 Flashcards

1
Q

asthma management in children

A

hard to confidently diagnose in those under 5 yrs, clinical judgement dependent

1) . SABA
2) . SABA + paediatric dose ICS (LTRA rather than ICS if <5yrs)
3) . SABA + paediatric dose ICS + LTRA or LABA
4) . SABA + paediatric dose ICS + LTRA + LABA
5) . refer to paeds asthma specialist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

asthma management in adults

A

1) . SABA
2) . SABA + low dose ICS
3) . SABA + low dose ICS + LABA/MART (MART includes low dose ICS)
4) . SABA + medium dose ICS
5) . SABA + low dose ICS + LTRA referral to asthma specialist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

classification of acute asthma: moderate

A

moderate

  • peak flow (PEFR) 50-75% of predicted
  • speech normal
  • RR < 25 / min
  • pulse < 110 bpm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

classification of acute asthma: severe

A

severe

  • peak flow (PEFR) 33-50% of predicted
  • cannot complete sentences
  • RR > 25 / min
  • pulse > 110 bpm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

classification of acute asthma: life-threatening

A

life-threatening

  • peak flow (PEFR) < 33% of predicted
  • sats < 92%
  • ‘normal’ pC02 (4.6-6.0 kPa)
  • silent chest, cyanosis or weak respiratory effort
  • bradycardia, dysrhythmia or hypotension
  • exhaustion, confusion or coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

management of acute asthma

A
  • admission (life-threatening or some severe episodes)
  • oxygen
  • high dose SABA (nebulised if life threatening)
  • nebulised ipratropium bromide (SAMA) in all with sev/life-threatening or unresponsive to SABA + ICS alone
  • corticosteroid (start stat pred even if asthma attack resolved by salbutamol alone)
  • continue usual regimen
  • IV MgSO4
  • IV aminophylline may be of use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

features of pulmonary fibrosis

A
  • SOB/progressive exertional dyspnoea
  • fine end-inspiratory crepitations
  • dry cough
  • clubbing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pulmonary causes of RESTRICTIVE lung disease

A

pulmonary causes:

  • pulmonary fibrosis
  • pneumoconiosis
  • pulmonary oedema
  • lobectomy/pneumonectomy
  • parenchymal lung tumours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

non-pulmonary causes of RESTRICTIVE lung disease

A

Non-pulmonary causes:

  • skeletal abnormalities (e.g. kyphoscoliosis)
  • neuromuscular diseases (e.g. motor neuron disease, myasthenia gravis, Guillan-Barre syndrome)
  • connective tissue diseases
  • obesity or pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

causes of OBSTRUCTIVE lung disease

A
  • COPD
  • asthma
  • bronchiectasis
  • cystic fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

causes of lower lobe lung fibrosis

A
  • idiopathic pulmonary fibrosis
  • most connective tissue disorders (EXCEPT ankylosing spondylitis) e.g. SLE
  • drug-induced: amiodarone, bleomycin, methotrexate - asbestosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

causes of upper lobe lung fibrosis

A

CHARTS:

C = coal worker’s pneumoconiosis

H = hypersensitivity pneumonitis (extrinsic allergic alveolitis) / histiocytosis

A = ankylosing spondylitis (rare)

R = radiation

T = tuberculosis

S = sarcoidosis/silicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

example causes of hypersensitivity pneumonitis/extrinsic allergic alveolitis

A
  • bird-fancier’s lung
  • farmer’s lung
  • malt worker’s lung
  • mushroom worker’s lung
  • chemical industry
  • working with paints, powders
  • smelters and hard metal workers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

features of hypersensitivity pneumonitis/extrinsic allergic alveolitis

A

ACUTE

  • fever
  • SOB
  • dry cough
  • lymphocytosis on bronchoalveolar lavage
  • ground glass nodules on CT

CHRONIC

  • pulmonary fibrosis
  • weight loss
  • honeycombing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

management of hypersensitivity pneumonitis/EAA

A
  • identify and avoid causative agent
  • corticosteroid trial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

complications of asbestos exposure

A
  • pleural plaques
  • pleural thickening
  • lung fibrosis
  • mesothelioma
  • lung cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

sites of extra-pulmonary secondary tuberculosis

A
  • central nervous system (tuberculous meningitis - the most serious complication)
  • vertebral bodies (Pott’s disease)
  • cervical lymph nodes (scrofuloderma)
  • renal
  • gastrointestinal tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

screening/diagnosis of TB

A
  • Mantoux test
  • CXR
  • ghon complex (ghon focus cavitation in upper lobe with bilateral hilar enlargement)
  • sputum culture = gold standard (takes 1-3 weeks)
  • NAAT (nucleic acid amplification test) less sensitive than sputum culture but faster results
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

drug therapy for ACTIVE TB

A

first 2 months = RIPE

  • rifampicin
  • isoniazid (with pyridoxine to prevent peripheral neuropathy)
  • pyrazinamide
  • ethambutol

continuation 4 months = RI

  • rifampicin
  • isoniazid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

drug therapy for LATENT TB

A

Either:

  • 3 months isoniazid (with pyridoxine to prevent peripheral neuropathy) and rifampicin

Or:

  • 6 months isoniazid (with pyridoxine to prevent peripheral neuropathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

drug therapy for tuberculous meningitis

A

As active TB (RIPE), with 10 months of continuation phase with rifampicin and isoniazid (with pyridoxine)

  • corticosteroid given
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is bronchiectasis?

A

permanent dilation of the airways secondary to chronic infection or inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

causes of bronchiectasis

A
  • idiopathic
  • post-infective: tuberculosis, measles, pertussis, pneumonia
  • immune deficiency
  • COPD
  • cystic fibrosis
  • bronchial obstruction e.g. lung cancer/foreign body
  • connective tissue disease
  • ciliary dyskinetic syndromes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

features of bronchiectasis

A
  • persistent productive cough
  • dyspnoea
  • haemoptysis
  • rhinosinusitis symptoms
  • recurrent chest infections
  • tramlines sign (CXR) and signet ring sign (CT)
  • can get manifestations in joints, GORD, IBD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

management of bronchiectasis

A
  • identifying and treating underlying cause
  • airway clearance techniques +/- pulmonary rehabilitation
  • annual influenza vaccine
  • antibiotics for exacerbations
  • surgical options include local lung resection and lung transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

most common organisms isolated in bronchiectasis

A
  • Haemophilus influenzae (most common)
  • Pseudomonas aeruginosa
  • Streptococcus Pneumoniae
  • Staphylococcus aureus
27
Q

features of COPD

A
  • cough: often productive
  • dyspnoea
  • wheeze
  • in severe cases, right-sided heart failure may develop resulting in peripheral oedema
28
Q

staging of COPD

A

FEV1 % of predicted Staging

Mild > 80% Stage 1

Moderate 50-79% Stage 2

Severe 30-49% Stage 3

Very severe < 30% Stage 4

29
Q

management of COPD

A
  • smoking cessation support
  • offer vaccinations (influenza and pneumococcal)
  • pulmonary rehab if indicated
30
Q

indications that a COPD sufferer may have asthma features

A
  • 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%)
31
Q

causes of ARDS (acute resp distress syndrome)

A

non-cardiogenic pulmonary oedema and diffuse lung inflammation

  • pulmonary

> chest sepsis

> aspiration

> TRALI

  • non-pulmonary

> systemic sepsis

> acute pancreatitis

> DIC

> drug overdose (eg. salicylates/heroin/methadone)

32
Q

management of ARDS

A
  • ABCDE
  • treat underlying cause
  • ventilatory/haemodynamic support
  • DVT prophylaxis
33
Q

Wells score for PE

A

3 points:

  • clinical signs and symptoms of a deep vein thrombosis (DVT)
  • no alternative diagnosis is more likely than a PE
    1. 5 points:
  • tachycardia (heart rate >100 beats/minute)
  • immobile for more than 3 days or has had major surgery within the last month
  • previous PE or DVT

1 point:

  • haemoptysis
  • active malignancy
34
Q

management of PE

A

ABCDE

  • oxygen, fluids, analgesia may be required
  • anticoagulation with DOAC when suspected or confirmed
  • LMWH then warfarin if DOAC not suitable eg. renal failure, triple + antiphospholipid
  • anticoagulation should last at least 3 months (provoked = 3mo, unprovoked = 6mo)
  • thombolysis eg. alteplase is indicated in massive PE
  • IVC filter an option in recurrent
35
Q

features of pleural effusion

A
  • dyspnoea
  • reduced exercise tolerance
  • chest pain
  • asymmetric chest expansion
  • stony dullness on percussion
  • reduced tac vocal frem/vocal res
36
Q

causes of pleural effusion

A

EXUDATIVE

  • infection
  • malignancy
  • inflammatory conditions eg. RA, SLE
  • pulmonary infarct/trauma

TRANSUDATIVE

  • increased hydrostatic pressure eg. heart failure
  • decreased oncotic pressure eg. cirrhosis, nephrotic syndrome/CKD, malabsorption (eg. coeliac)
37
Q

management of pleural effusion

A
  • treat underlying cause
  • intercostal drain
  • pleurodesis (recurrent/persistent)
38
Q

causes of bilateral hilar lymphadenopathy

A
  • inflammatory: sarcoidosis
  • infective: tuberculosis and mycoplasma
  • neoplastic: bronchial carcinoma and lymphoma
  • interstitial lung disease: inorganic (such as silicosis) or organic (such as extrinsic allergic alveolitis)
39
Q

features of acute sarcoidosis

A
  • fever
  • polyarthralgia
  • erythema nodosum
  • bilateral hilar lymphadenopathy
40
Q

extra-pulmonary features of chronic sarcoidosis

A
  • general = weight loss, fever, lymphadenopathy
  • neuro = meningitis, periph neuropathy, bilateral Bell’s palsy
  • ocular = uveitis, keratoconjunctivitis sicca
  • cardiac = arrhythmias, restrictive cardiomyopathy
  • abdo = hepatosplenomegaly, renal stones
  • derm = erythema nodosum
41
Q

blood markers for sarcoidosis

A
  • ↑ ESR
  • ↑ serum calcium
  • ↑ ACE
  • ↓ lymphocytes
42
Q

causative organisms of community-acquired pneumonia

A
  • streptococcus pneumoniae (accounts for around 80% of cases)
  • haemophilus influenzae
  • staphylococcus aureus: commonly after influenza infection
  • atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)
  • viruses
  • klebsiella pneumoniae typically in alcoholics
43
Q

causative organisms of hospital-acquired pneumonia

A
  • pseudomonas aeruginosa
  • staphylococcal aureus
  • enterobacteria
44
Q

CURB65

A

Confusion (abbreviated mental test score <= 8/10)

Urea > 7 mmol/L

Respiration rate >= 30/min

Blood pressure: systolic <= 90 mmHg, diastolic <= 60mmHg

65 years +

home based care 0-1

hospital 2+

ITU 3+

45
Q

pathophysiology of CF

A

CF is an autosomal recessive condition caused by a mutation in chromosome 7 at the CF transmembrane conductance regulator (CFTR) gene.

The result of this mutation is increased sodium absorption and abnormal chloride secretion in the epithelial cells lining the airways. This leads to thicker mucus impairing the function of cilia.

46
Q

neonatal features of CF

A
  • failure to thrive
  • meconium Ileus
  • rectal prolapse
47
Q

pulmonary features of CF

A
  • chronic sinusitis
  • cough, wheeze, haemoptysis
  • recurrent LRTIs
  • bronchiectasis
  • pneumothorax
  • cor pulmonale (right HF)
48
Q

extra-pulmonary features of CF

A
  • GI: pancreatic insufficiency (DM1), steatorrhoea, cirrhosis, portal hypertension, gallstones
  • MSK: clubbing, osteoporosis, arthritis
  • infertility
49
Q

management of CF

A
  • education
  • chest physio
  • dietitian (high calorie, high fat diet/vitamin supplementation (ADEK)/pancreatic enzymes with meals)
  • treat exacerbations with Abx, dornase alfa nebs (mucolytic), bronchodilators
  • lung transplant
50
Q

causes of spontaneous pneumothorax

A

PRIMARY

  • no underlying lung pathology, eg. tall, thin young men

SECONDARY

  • obstructive lung disease
  • infective lung disease
  • fibrotic lung disease (inc. CF, idiopathic pulmonary fibrosis)
  • connective tissue disease
  • neoplasm
51
Q

causes of traumatic pneumothorax

A

IATROGENIC

  • central line insertion
  • positive pressure ventilation

NON-IATROGENIC

  • penetrating trauma
  • blunt trauma with rib fracture
52
Q

features of pneumothorax

A
  • sudden-onset shortness of breath
  • pleuritic chest pain
  • reduced chest expansion
  • hyper-resonant on affected side
  • reduced/absent breath sounds on affected side
53
Q

features of tension pneumothorax

A

as regular pneumothorax, with:

  • haemodynamic compromise signs eg. tachycardia, hypotension
  • tracheal deviation
54
Q

management of pneumothorax

A

TENSION

  • ABCDE
  • high flow O2 via non-rebreath
  • needle decompression

PRIMARY

  • if no SOB/<2cm then conservative, with follow up appt
  • SOB/>2cm then needle decompression SECONDARY
  • if no SOB/<1cm then monitor for 24hrs
  • if no SOB but 1-2cm then needle decompression
  • if SOB/>2cm then chest drain and admission required
55
Q

causes of T1RF

A

VQ mismatch

  • volume of air passing in and out of the lungs is comparatively smaller than the volume of blood perfusing the lungs
  • asthma
  • heart failure
  • pulmonary embolism
  • pneumonia
  • pneumothorax
56
Q

causes of T2RF

A

alveolar hypoventilation

  • lungs fail to effectively oxygenate and blow off carbon dioxide
  • obstructive lung disease (COPD)
  • restrictive lung diseases (idiopathic pulmonary fibrosis)
  • respiratory depression (opiates)
  • neuromuscular disease (Guillan-Barre syndrome, motor neuron disease)
  • thoracic wall disease (rib fracture)
57
Q

causes of pulmonary fibrosis

A
  • lung damage:

> infarction, pneumonia, tuberculosis

  • irritants:

> coal dust, silica

  • diffuse parenchymal lung disease:

> idiopathic pulmonary fibrosis and extrinsic allergic alveolitis/hypersensitivity pneumonitis

58
Q

management of pulmonary fibrosis

A
  • treat underlying cause
  • conservative: smoking cessation, pulmonary rehabilitation
  • medical:

> long-term oxygen therapy

> antifibrotic drugs eg. pirfenidine

  • surgical: lung transplant
59
Q

atelectasis

A

postoperative complication in which basal alveolar collapse can lead to respiratory difficulty - treated with chest physio and sat upright

60
Q

types of NSC lung cancer

A
  • adenocarcinoma

> this is now the most common type of lung cancer

> often seen in non-smokers

  • squamous

> parathyroid hormone-related protein (PTHrP) secretion causes hypercalcaemia

  • large cell

> may secrete β-hCG

  • alveolar cell carcinoma

> not related to smoking, ++sputum

  • bronchial adenoma
61
Q

SC lung cancer

A
  • associated with ectopic ADH, ACTH secretion

> ADH → hyponatraemia

> ACTH → Cushing’s syndrome

> ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis

> Lambert-Eaton syndrome: antibodies to calcium channels causing myasthenic-like syndrome

62
Q

prescribed methods of smoking cessation

A

NRT

varenicline

bupropion

63
Q

pneumothorax management

A
64
Q
A