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Phase 3b > Respiratory > Flashcards

Respiratory Flashcards

1
Q

what is COPD?

A

long term condition of the lungs where the flow of air to lungs is restricted (obstructed)

chronic bronchitis and emphysema

chronic inflammation that affects central airways, peripheral airways, lung parenchyma and alveoli and pulmonary vasculature

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2
Q

what happens in COPD?

A

chronic inflammation that affects central airways, peripheral airways, lung parenchyma and alveoli and pulmonary vasculature

narrowing and remodelling of the airways, increased number of goblet cells, enlargement of mucus secreting glands of the central airways and subsequent vascular bed changes leadings to pulmonary hypertension

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3
Q

what can cause COPD?

A

smoking
chronic exposure to pollutants at work (mining, building and chemical industries)
outdoor pollution
cadmium - used in smelting
alpha-1 anti trypsin deficiency - can cause early onset COPD

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4
Q

what is chronic bronchitis?

A

narrowing of the airways
airflow limitation as a result of hypertrophy and hyperplasia of mucus secreting glands of bronchial tree, bronchial wall inflammation and mucosal oedema

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5
Q

what is emphysema?

A

dilatation and destruction of the lung tissues distal to the terminal bronchioles - changes leaf to loss of elastic recoil, which normally keep the airways open during expiration

therefore associated with expiratory airflow limitation and air trapping

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6
Q

what are the symptoms of COPD?

A

cough - usually the first symptom
breathlessness and wheeze - initially with exercise but may progress to SOB at even rest

dyspnoea

they may also have a barrel chest

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7
Q

in COPD what is the cough like?

A

it is productive
tends to come and go at first
gradually becomes more persistent

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8
Q

on examination what may you find with COPD?

A 
hyper-resonance on percussion 
distant breath sounds on auscultation 
poor air movement on auscultation 
wheezing on auscultation 
coarse crackles
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9
Q

what investigations would you order for COPD?

A 
spirometry (FEV1/FVC ratio <0.70
pulse oximetry 
ABG
CXR
FBC
ECG
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10
Q

what do you see on a chest Xray for COPD?

A

hyperinflation
bullae
flat hemidiaphragm
increased intercostal spaces

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11
Q

how would you treat COPD?

A

stop smoking
give influenza and pneumococcal vaccine

if lifestyle alone is not enough

Add SAMA or LAMA to use as needed

If this is not sufficient and still getting symptoms
offer LAMA or LABA

If this doesnt work try triple therapy:
LABA plus LAMA plus ICS

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12
Q

what are the complications of COPD?

A 
cor pulmonate 
recurrent pneumonia
depression 
pneumothorax 
respiratory failure 
anaemia
polycythaemia
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13
Q

what is the staging for COPD?

A

stage 1: FEV1 (of predicted) - >80%
stage 2 - 50-79%
stage 3 - 30-49%
stage 4 - <30%

all have post bronchodilator FEV1/FVC

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14
Q

what is asthma?

A

chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity
reversible bronchospasm resulting in airway obstruction

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15
Q

what are some risk factors for asthma?

A
  • personal or family history of atopy
  • antenatal factors - maternal smoking, viral infection during pregnancy (especially RSV)
  • low birth weight
  • not being breastfed
  • maternal smoking around child
  • exposure to high concentrations of allergens (e.g. house dust mite)
  • air pollution
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16
Q

what are the symptoms of asthma?

A
  • dyspnoea - precipitated by allergen exposure, exposure to cold air, tobacco smoke
  • cough - often worse at night
  • expiratory wheeze
  • nasal polyps

usually episodic symptoms, diurnal variability (worse at night).

polyphonic wheeze

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17
Q

what are some typical triggers for asthma?

A 
Infection
Night time or early morning
Exercise
Animals
Cold/damp
Dust
Strong emotions
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18
Q

what type of wheeze is typically heard in asthma?

A

polyphonic wheeze

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19
Q

what investigations would you perform for asthma?

A

fractional exhaled nitric oxide (smoking staus can lower this leading to a false negative)
spirometry - FEV1/FVC ratio (<80% of predicted)
FEV1 (<80% of predicted)
bronchodilator reversibility
peak expiratory flow variability
direct bronchial challenge test with histamine or methacholine

in asthma, the FEV1 is significantly reduced and FVS is normal

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20
Q

what is the treatment for asthma?

A

BTS guidelines stepwise ladder

  1. add a short-acting beta 2 agonist inhaler (e.g. salbutamol) as required for infrequent wheezy episodes
  2. add a regular low dose corticosteroid inhaler - budesonide inhaler
  3. add LABA inhaler (salmeterol) - continue the LABA only if the patient has a good response
  4. consider a trial f an oral leukotriene receptor antagonist (i.e. montelukast), oral beta 2 agonists (ie. oral salbutamol), oral theophylline or an inhaled LAMA (tiotropium)
  5. titrate inhaled corticosteroid up to a high dose, combine additional treatments from step 4 and refer to a specialist.
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21
Q

how is an acute asthma attack managed?

A

o - oxygen

S - salbutamol - try inhaled first (nebulised), use IV if inhaled can not be used reliably
H - hydrocortisone
I - ipratropium
T - theophylline

M - magnesium sulphate
E - escalate

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22
Q

what is hypersensitiivity pneumonitis also known as?

A

Extrinsic allergic alveolitis

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23
Q

what is extrinsic allergic alveolitis?

A

it is a condition caused by hypersensitivity induced lung damage due to a variety of inhaled organic particles

It is thought to be largely caused by immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) is also thought to play a role in EAA, especially in the chronic phase.

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24
Q

what are some examples of extrinsic allergic alveolitis?

A
  • bird fanciers’ lung: avian proteins
  • farmers lung: spores of Saccharopolyspora rectivirgula (formerly Micropolyspora faeni)
  • malt workers’ lung (turning germinating barley): Aspergillus clavatus
  • mushroom workers’ lung: thermophilic actinomycetes*
  • farmers lung (from mouldy hay or other veg material)- micropolyspora faeni
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25
Q

what are the clinical features of hypersensitity pneumonitis?

A

fever
malaise
dry cough
SOB several hours after exposure to allergen

acute will happed 4-8 hours after exposure

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26
Q

what investigations would you perform for hypersensitivity pneumonitis?

A
  • immunological response to causative antigen
  • fbc - leukocytosis; normocytic, normochromic anaemia
  • ESR
  • albumin - low
  • CXR - infiltrates, nodular or patchy, fibrosis
  • CT chest
  • pulmonary function tests
  • diffusing lung capacity of carbon monoxide

consider bronchiolar lavage and lung biopsy

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27
Q

how do you manage hypersensitivity pneumonitis?

A
  • avoidance of antigen

acute and sub-acute symptoms - corticosteroid taper

with chronic symptoms - long term low-dose corticosteroid therapy

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28
Q

what is bronchiectasis?

A

Bronchiectasis is a permanent dilatation and thickening of the airways secondary to chronic infection or inflammation, characterised by chronic cough, excessive sputum production, bacterial colonisation, and recurrent acute .

It can be widespread throughout the lungs (diffuse) or more localised (focal)

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29
Q

what are some causes of bronchiectasis?

A
  • post-infective: tuberculosis, measles, pertussis, pneumonia
  • cystic fibrosis
  • bronchial obstruction e.g. lung cancer/foreign body
  • immune deficiency: selective IgA, hypogammaglobulinaemia
  • allergic bronchopulmonary aspergillosis (ABPA)
  • ciliary dyskinetic syndromes: Kartagener’s syndrome, Young’s syndrome
  • yellow nail syndrome
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30
Q

what are the symptoms of bronchiectasis?

A
  • cough (may be associated with large amounts of purulent sputum and, less commonly haemoptysis - can be worsened by lying flat or on one side)
  • sputum production
  • crackles, high pitches inspiratory squeaks and rhonchi
  • dyspnoea
  • fever
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31
Q

what investigations would you perform for bronchiectasis?

A

CXR - may be normal or show obscured hemidiaphragm, thin-walled ring shadows with or without fluid levels, tram lines, tubular or ovoid opacities

chest CT
FBC
sputum culture and sensitivity
serum alpha-1 antitrypsin phenotype and level 
serum immunoglobulins 
sweat chloride test 
rheumatoid factor 
pulmonary function tests
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32
Q

what are the most common organisms isolated from patients with bronchiectasis ?

A

Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae

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33
Q

how are bronchiectasis managed?

A
  • assess for treatable causes
  • exercise and improve nutrition
  • airway clearance therapy /postural drainage
  • inhaled bronchodilator and mucoactive agents can be added can be added

in an acute exacerbation - short term oral antibiotic (amoxicillin or clarithromycin), and increase airway clearance

in severe cases (3 or more exacerbations per year) they may need long term antibiotics

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34
Q

what is cystic fibrosis?

A

it is a autosomal recessive condition affecting mucus glands, It is caused by a genetic mutation of the cystic fibrosis transmembrane inductance regulatory (CFTR) gene on chromosome 7 which codes for a cAMP-regulated chloride channel.

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35
Q

what is the inheritance of cystic fibrosis?

A

AR

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36
Q

how many people are carriers of cystic fibrosis ?

A

1 in 25 people are carriers

37
Q

what are the key consequences of the cystic fibrosis mutation?

A
  • Thick pancreatic and biliary secretions that cause blockage of the ducts, resulting in a lack of digestive enzymes such as pancreatic lipase in the digestive tract
  • Low volume thick airway secretions that reduce airway clearance, resulting in bacterial colonisation and susceptibility to airway infections
  • Congenital bilateral absence of the vas deferens in males. Patients generally have healthy sperm, but the sperm have no way of getting from the testes to the ejaculate, resulting in male infertility
38
Q

what are the presenting features of cystic fibrosis ?

A
  • neonatal period (around 20%): meconium ileus, less commonly prolonged jaundice
  • recurrent chest infections (40%)
  • malabsorption (30%): steatorrhoea, failure to thrive
  • other features (10%): liver disease
39
Q

what are some other features of cystic fibrosis?

A 
short stature
diabetes mellitus 
delayed puberty 
rectal prolapse 
nasal polyps 
male infertility 
finger clubbing 
failure to thrive 
abode distension 
chronic cough 
thick sputum production
40
Q

how is cystic fibrosis diagnosed?

A

It is usually picked up shortly after birth in the newborn blood spot testing

the sweat test is the gold standard for diagnosis

Genetic testing for CFTR gene can be performed during pregnancy by amniocentesis or CVS or after birth.

41
Q

what can cause a false positive sweat test?

A 
malnutrition
adrenal insufficiency
glycogen storage diseases
nephrogenic diabetes insipidus
hypothyroidism, hypoparathyroidism
G6PD
ectodermal dysplasia
42
Q

what can cause a false negative sweat test?

A

The most common reason for false negative tests is skin oedema, often due to hypoalbuminaemia/ hypoproteinaemia secondary to pancreatic exocrine insufficiency.

43
Q

how is cystic fibrosis managed?

A
  • regular (at least twice a day) chest physio and postural drainage
  • high calorie diet - including high fat intake
  • vitamin supplementation
  • pancreatic enzyme supplements taken with meals - (pancreatin contains lipase, protease and amylase) (CREON tablets - these replies the missing lipase)
  • heart and lung transplant
  • prophylactic flucloxacillin - for staph aureus infection
  • treat chest infections
  • bronchodilators can be used
  • inhaled mucolytic - dornase alfa and hypertonic saline inhaled
  • vaccinations
  • ursodeoxycholic acid for hepatobillary disease
44
Q

what can be used in patients with chronic infection with pseudomonas aeruginosa?

A

inhaled tobramycin

45
Q

what organisms colonise CF patients frequently?

A

Staphylococcus aureus
Pseudomonas aeruginosa
Burkholderia cepacia*
Aspergillus

46
Q

what are some causes of pulmonary hypertension?

A

it occurs due to an increase in pulmonary vascular resistance or an increase in pulmonary blood flow.

  • primary pulmonary hypertension
  • connective tissue disease such as SLE
  • left sided heart failure due to MI or systemic hypertension
  • chronic lung disease e.g. COPD
  • pulmonary vascular disease such as PE
  • miscellaneous such as sarcoidosis, glycogen storage disease and haematological disorders
47
Q

what are symptoms of pulmonary hypertension?

A

SOB is the main presenting symptom

other symptoms include syncope, tachycardia, raised JVP, hepatomegaly, peripheral oedema

48
Q

what investigations would you perform for pulmonary hypertension?

A
  • ECG - shows right ventricular hypertrophy (seen as larger R waves on the right sided chest leads (v1-3) and s waves on the left sided chest leads (V4-6), right axis deviation, right bundle branch block
  • CXR - dilated pulmonary arteries, right ventricular hypertrophy
    others: A raised NT-proBNF blood test result indicates right ventricular failure, Echo can be used to estimate pulmonary artery pressure
49
Q

how do you manage pulmonary hypertension?

A

Primary pulmonary hypertension can be treated with

  • IV prostanoids (epoprostenol)
  • endothelin receptor antagonists (macitentan)
  • phosphodiesterase-5 inhibitors 9 sildenafil)

for general management

  • oxygen therapy or symptomatic relief
  • diuretic treatment for heart failure
  • vasodilation with calcium channel blockers
  • anticoagulation
50
Q

what is cor pulmonale?

A

right heart failure resulting from chronic pulmonary hypertension

51
Q

what is a pleural effusion?

A

a collection of fluid in the pleural cavity

52
Q

what are the two types of pleural effusion?

A

exudative - a high protein count - Results from inflammation - protein leaks out of tissues into pleural space (lung cancer, pneumonia, RA, TB)
transudative - lower protein count - fluid moving across into the pleural space (CCF, hypoalbuminaemia, hypothyroidism, meigs syndrome

53
Q

what is the presentation of pleural effusion?

A 
shortness of breath 
dull to percuss over the effusion 
reduced breath sounds 
tracheal deviation AWAY from the effusion if it is massive 
non-productive cough or chest pain
54
Q

what are the investigations for pleural effusion? what would they show?

A

CXR -PA and lateral CXR - blunting of the costophrenic angle, fluid in the lung fissures, larger effusions will have a meniscus, tracheal and mediastinal deviation if it i a massive effusion.

contrast CT is often performed to investigate underlying cause

pleural USS

Pleural aspiration - USS recommended to reduce complication rate - fluid should be sent for pH, protein, LDH, cytology and microbiology

55
Q

how do you manage a pleural effusion?

A

Conservative management may be appropriate as small effusions will resolve with treatment of the underlying cause. Larger effusions often need aspiration or drainage.

Pleural aspiration involves sticking a needle in and aspirating the fluid. This can temporarily relieve the pressure but the effusion may recur and repeated aspiration may be required.

Chest drain can be used to drain the effusion and prevent it recurring.

if infective - IV abx (amoxicillin and metronidazole)

56
Q

what characteristics in the pleural aspirate in a pleural effusion sure suggestive of certain findings?

A

low glucose: rheumatoid arthritis, tuberculosis

raised amylase: pancreatitis, oesophageal perforation

heavy blood staining: mesothelioma, pulmonary embolism, tuberculosis

57
Q

what is an empyema?

A

Empyema is where there is an infected pleural effusion. Suspect an empyema in a patient who has an improving pneumonia but new or ongoing fever. Pleural aspiration shows pus, acidic pH (pH < 7.2), low glucose and high LDH. Empyema is treated by chest drain to remove the pus and antibiotics.

58
Q

what is a pneumothorax?

A

occurs when air gets into the pleural space separating the lung from the chest wall.

59
Q

what is the typical patient to preset with a pneumothorax?

A

young, tall, think man presenting with sudden breathlessness and pleuritic chest pain, probably whilst playing sport

60
Q

what are the causes of pneumothorax?

A

spontaneous
trauma
Iatrogenic such as due to lung biopsy, mechanical ventilation or central line insertion
lung pathology such as infection, asthma or COPD

61
Q

what are some risk factors for pneumothorax?

A

pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia
connective tissue disease: Marfan’s syndrome, rheumatoid arthritis
ventilation, including non-invasive ventilation
catamenial pneumothorax is the cause of 3-6% of spontaneous pneumothoraces occurring in menstruating women. It is thought to be caused by endometriosis within the thorax

62
Q

what are the symptoms of a pneumothorax?

A 
symptoms tend to come on suddenly 
features include:
dyspnoea
chest pain: often pleuritic
sweating
tachypnoea
tachycardia
63
Q

what investigations should you order for a pneumothorax?

A

1st line - CXR

you may also consider CT chest, Chest USS and bronchoscopy

64
Q

what is the management if a primary pneumothorax?

A

Recommendations include:
if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
otherwise aspiration should be attempted
if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
patients should be advised to avoid smoking to reduce the risk of further episodes - the lifetime risk of developing a pneumothorax in healthy smoking men is around 10% compared with around 0.1% in non-smoking men

65
Q

what is the management of secondary pneumothorax?

A

if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
regarding scuba diving, the BTS guidelines state: ‘Diving should be permanently avoided unless the patient has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postoperatively.’

66
Q

what is the managemet of an iatrogenic pneumothorax?

A

Reccomentdations :
less likelihood of recurrence than spontaneous pneumothorax
majority will resolve with observation, if treatment is required then aspiration should be used
ventilated patients need chest drains, as may some patients with COPD

67
Q

what is a tension pneumothorax?

A

tension pneumothorax is caused by trauma to the chest wall that creates a one way valve that lets air in but not out of the pleural space.
so more and more air gets trapped and creates pressure inside the thorax that will push the mediastinum across, kink the big vessels

68
Q

what are the signs of tension pneumothorax?

A

Tracheal deviation away from side of pneumothorax
Reduced air entry to affected side.
Increased resonant to percussion on affected side.
Tachycardia.
Hypotension.

69
Q

how do you manage a tension pneumothorax?

A

Insert a large bore cannula into the second intercostal space in the midclavicular line

if a tension pneumothorax is suspected do not wait for any investigaitions, once the pressure is relieved with a cannula then a chest drain is required for definitive managemet.

70
Q

chest drains are insterted into the tirangle of saftey - what is this triangle formed by?

A

The 5th intercostal space (or the inferior nipple line)
The mid axillary line (or the lateral edge of the latissimus dorsi)
The anterior axillary line (or the lateral edge of the pectoris major)

the needle is inserted just above the rib to avoid the neurovascular bundle that runs just below the rib. - once chest drain is inserted obtain a chest xray to check the positioning

71
Q

what is goodpastures syndrome?

A

Goodpasture’s syndrome is rare condition associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis. It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen.

72
Q

what are the two age peaks in Goodpasture’s syndrome?

A

20-30 and 60-70

more common in men

73
Q

what are the features of Goodpasture’s syndrome?

A

the three common symptoms are:
reduced urine output
haemoptysis
oedema

there may also be SOB, cough, fever, nausea, crackles on lung examination

74
Q

what investigations would you perform for Goodpasture’s?

A

renal biopsy
renal function testing
anti-GBM antibody titre will be positive

75
Q

what would a renal biopsy show is there was Goodpasture’s syndrome?

A

linear IgG deposits along the basement membrane

76
Q

how do you manage Goodpasture’s syndrome?

A

oral corticosteroid - prednisolone

Plasmapheresis

cyclophosphamide

77
Q

what is Wegener’s granulomatosis?

A

AKA granulomatosis with polyangiitis

it is an autoimmune condition associated with necrotising granulomatous vasculitis affecting both the upper and lower respiratory tract as well as the kidneys.

78
Q

what are the features of wegener’s granulomatosis?

A
  • upper respiratory tract: epistaxis, sinusitis, nasal crusting
  • lower respiratory tract: dyspnoea, haemoptysis
  • rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
  • saddle-shape nose deformity
  • also: vasculitic -rash, eye involvement (e.g. proptosis), cranial nerve lesions

patients typically have non-specific symptoms for 2-3 months before presentation - common ones include fatigue, malaise, fever, night sweats, anorexia and weight loss

79
Q

what investigations would you perform for wegener’s granulomatosis?

A
  • cANCA positive in > 90%, pANCA positive in 25%
  • chest x-ray: wide variety of presentations, including cavitating lesions
  • CT chest - lung nodules which may cavitate
  • renal biopsy: epithelial crescents in Bowman’s capsule
  • urinalysis and microscopy -may show haematuria, proteinuria
80
Q

how do you manage wegener’s granulomatosis?

A

steroids
cyclophosphamide (90% response)
plasma exchange

81
Q

what are some risk factors for pulmonary embolism?

A
  • immobility
  • recent surgery
  • long haul flights
  • pregnancy
  • hormone therapy with oestrogen
  • malignancy
  • SLE
  • thrombophilia
82
Q

how would a PE present?

A 
SOB
cough with or without blood
pleuritic chest pain 
hypoxia 
tachycardia 
tachypnoea 
low grade fever 
Haemodynamic instability causing hypotension

they may also present with signs of DVT

83
Q

how would you investigate pulmonary embolism?

A

first of all perform a wells score

computed tomographic pulmonary angiography (CTPA)

ventilation perfusion (VQ) scan can be used when CTPA is contraindicated

if the diagnosis is unlikely use a d-dimer to rule out diagnosis

ABG -hypoxaemia and hypocapnia may be suggestive of a PE

NICE guidelines recommends that all patients with symptoms/signs suggestive of a PE should have history, exam an a CXR to exclude other pathology.
CXR may be normal or may show wedge shaped opacification

84
Q

what is included in the wells score?

A

clinical signs of DVT
alternative diagnosis less likely than PE
previous PE or DVT
heart rate >100bpm
surgery or immobilisation within 44 weeks
haemoptysis
active cancer

PE likely - more than points
PE unlikely - 4 points or less

*** if a PE is likely then arrange an immediate CPTA and if there is a delay in getting one then give LMWH until scan is performed

*** If PE is unlikely then arrange a D-dimer test - if +ve arrange a CTPA- if there is a delay in getting it then give LMWH until scan is performed

85
Q

what would you see on an ECG in a PE ?

A

the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen

86
Q

how do you manage a PE?

A

Supportive management: oxygen and analgesia

LMWH should give initially after a PE is diagnosed, (an exception to this is for patients with a massive PE where thrombolysis is being considered - in such situation unfractionated heparin should be used)

> vitamin K antagonist (i.e. warfarin) should be given within 24 hours of the diagnosis
LMWH should be continued for at least 5 days or until the INR is 2 or above for at least 24 hours
warfarin should be continued for at least 3 months (assess risks and benefits of extending treatment) if there is no obvious provoking factor nice advise that it should be extended past the 3 months
for patients with active cancer NICE recommend using LMWH for six months

87
Q

when should thrombolysis be given in PE?

A

Where there is a massive PE with haemodynamic compromise there is a treatment option called thrombolysis. Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. It is only used in patients with a massive PE where the benefits outweigh the risks. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.

88
Q

in adults what is considered moderate, severe and life-threatening asthma attack?

A

Moderate
PEFR 50 – 75% predicted

Severe
PEFR 33-50% predicted
Resp rate >25
Heart rate >110
Unable to complete sentences
Life-threatening
PEFR <33%
Sats <92%
Becoming tired
No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
Haemodynamic instability (i.e. shock)

Phase 3b (34 decks)

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