Respiratory p1 Flashcards
1
Q
What does spirometry measure?
A
Volume and speed flow of air during exhalation and inhalation
2
Q
What is FEV1?
A
Forced expiratory volume: volume that has been exhaled at the end of the first second of forced expiration
3
Q
What is FVC?
A
Volume that has been exhaled after a maximal expiration following a full inspiration
4
Q
What is Kco?
A
Diffusion capacity of the lung per unit area for CO
5
Q
What is TLco?
A
Diffusion capacity of the total lung capacity for CO
6
Q
What is an obstructive patten on spirometry?
A
Normal (or increased FVC), reduced FEV1:FVC
7
Q
What is a restrictive pattern on spirometry?
A
Reduced FVC, normal (or increased) FEV1:FVC
8
Q
What does decreased TLco/Kco indicate?
A
issue with gas change, which can be due to either alveolar disease or vascular disease
Rules out chest wall / diaphragm pathology
9
Q
What is asthma?
A
Chronic inflammatory condition of the airways, characterised by airway hypersensitivity
10
Q
What are the symptoms of asthma?
A
wheezing and SOB Worse @ night or with exercise Diurnal variation Peak flow worst in morning chest tightness Bilateral widespread “polyphonic” wheeze
11
Q
What will you find on examination for asthma?
A
Widespread expiratory wheeze
Pulmonary function = Decreased FEV1 relieved by B2 agonist
12
Q
What are the common precipitants of asthma?
A
Environmental: pets, grass pollen, dust mites Viral infections Cold air Emotion Drugs: NSAIDS, aspirin, B-blockers Atmospheric pollution Occupational pollutants
13
Q
What are the important history points for asthma?
A
Known precipitants, diurnal variation in symptoms, acid reflux
atopy hx, occupation and days off work/school
Exacerbations and whether they needed hospitalisation/ITU
14
Q
How is asthma diagnosed?
A
CLINICAL: can do structured clinical assessment to see if:
episodes are recurrent, symptoms are variable, PH/FH or atopy
Recorded observation of wheeze
Variable PEF/FEV1
Absence of symptoms - look for alternate diagnosis
High probability: initiate treatment and if symptoms improve, diagnosis confirmed
Can do spirometry or FeNO if spirometry is normal
15
Q
What will be the findings of asthma from spirometry?
A
FEV1 / FVC will be less than 70%
bronchodilators will reverse this
16
Q
What is extrinsic asthma caused by?
A
Type 1 hypersensitivity reaction
17
Q
Who does extrinsic asthma occur in?
A
Atopic individuals who show positive skin prick tests to common allergens, implying a definite extrinsic cause
18
Q
What is intrinsic asthma caused by?
A
Non-immune mechanisms
19
Q
Who does intrinsic asthma occur in?
A
Middle aged individuals, with no causative agent
20
Q
What is late onset asthma more likely to be?
A
intrinsic
21
Q
Describe the disease process of ACUTE asthma
A
- SM contraction narrows airway: bronchospasm due to production of histamine, prostaglandin D2 and leukotrienes (SM contraction NARROWS airway)
- Narrowing of airway due to chemotaxins (late phase)
- Airway hyperactivity
22
Q
Describe the disease process of chronic asthma
A
Bronchoconstriction due to increased responsiveness of SM
Hypersecretion of mucus plugging the airway
Mucosal oedema = narrow airways
Can lead to pulmonary HTN in long standing disease
23
Q
What might be observed in the sputum sample of a patient with chronic asthma?
A
Charcot-Leyden crystal (from eosinophil granules)
Curschman spirals (mucus plugs from small airways)
24
Q
What are the features of acute severe asthma?
A
RR >25 HR >110 PEF 33-50% of best Can't complete sentences in one breath Accessory mm of respiration
25
What are the features of life-threatening asthma?
```
PEF <33% best
SpO2 <92%
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, hypotension or dysrhythmia
exhaustion or confusion
```
26
What is the investigation of choice for life threatening asthma?
ABG
27
What are the blood gas features of a life threatening attack?
NORMAL PaCO2 - should be low due to hyperventilation
severe hypoxia <8
Low ph
A raised PaCO2 = near fatal asthma
28
What is the management of acute asthma attack?
A-E
Oxygen 15L via non-rebreathe
Salbutamol 5mg via oxygen driven nebuliser
Ipratropium bromide 0.5mg via oxygen-driven nebuliser
Oral pred 50mg or IV hydrocortisone 100mg
29
What is the additional management of life threatening asthma?
Discuss with ICU
Add Magnesium sulphate 2g IVI over 20 minutes
nebuliser salbutamol 5mg every 15-30 minutes
?IV aminophylline (senior)
Intubation if VERY severe
30
What is the management for acute severe asthma once stable?
Continue prednisolone for 5 days and nebuliser salbutamol / ipratropium 4 hourly until discharge
Chart PEF before and after salbutamol nebulisers 4/day
Prior to discharge, check inhaler technique, agree on asthma plan and ensure GP follow up within 2 working days.
31
What is the treatment algorithm for asthma
1. SABA
2. ADD ICS - 200-400mg
3. ADD LTRA
4. ADD LABA (and consider whether to keep LTRA)
5. Change (ICS+LABA) to MART (which includes both
6. Increase the dose of ICS
7. LAMA or theophylline and seek specialist opinion
32
What drugs might be added for asthma after specialist opinion?
Oral B2 agonists, oral corticosteroids or anti IgE drugs (omalizumab)
33
How do B2 agonists work?
Relax bronchial smooth muscle, leading to bronchodilator
Side effects are due to accent on other B adrenoceptors:
B1 in heart - tachycardia
B2 in skeletal mm: tremor, cramps, hypokalaemia
34
How long do SABAs work for?
4-6 hours
| LABAs >12 hours
35
how do inhaled corticosteroids work?
Reduce exacerbations due to anti-inflammatory effects
Side effects = oral candidiasis + pneumonia, plus systemic effects of corticosteroid
36
What LTRAs are there?
Montelukast
37
How do LTRAs work?
Block the effect of leukotrienes in the airways, benefitting the actions of inhaled ICS
38
What are the side effects of LTRAs?
thirst, GI disturbances and very rarely, Churg-Strauss (systemic vasculitis)
39
How do theophylline/aminophylline work?
Relax SM, so dilate airways but also reduce exacerbations
Side effects = dose related (similar to caffeine) so in high doses: headache, insomnia, nausea, tachycardia and arrhythmias
40
What is COPD?
Progressive airflow limitation that is not fully reversible
Associated with an abnormal inflammatory response of the lungs to noxious particles or gases, predominantly inhaled cigarette smoke
41
What is the cause of COPD?
Emphysema + chronic bronchitis
Decreased outflow pressure + increased airway resistance
42
What is emphysema?
dilation of any part of the respiratory acinus (air spaces distal to the terminal bronchioles) with destructive changes in the alveolar walls
Absence of scarring
43
How does tissue destruction occur in emphysema?
Increased secretion and activation of extracellular proteases by inflammatory cells (after exposure to noxious particles)
44
What is centrilobar emphysema?
Changes are limited to the central part of the lobule directly around the terminal bronchiole with normal alveoli elsewhere
45
What is panacinar emphysema?
Destruction and distension of the whole lobule, which can happen in smokers but is more common in alpha-1-antitrypsin deficiency
46
What is the effect of A-1-antitrypsin deficiency?
A-1-antitrypsin Normally inactivates neutrophil elastase
| without it, overactivity of neutrophil elastase and destruction of alveoli
47
what are bullae?
dilated air spaces >1cm
48
How does emphysema affect gas exchange?
Loss of connective tissue in the alveolar walls leads to a loss of elastic recoil of the lungs, leading to air entrapment in the lungs and inadequate ventilation
Reduction in area available for gas exchange means there is reduced oxygen uptake
49
What is chronic bronchitis?
Daily cough with sputum for at least 3 months per year for 2 years
50
What is the pathophysiology of chronic bronchitis?
Abnormal amounts mucus - plugging of the airway lumen
Hypersecretion = hypertrophy and hyperplasia of bronchial mucus secreting glands
Can be shown by Reid index
51
What is bronchiolitis?
Inflammation of the airways <2mm in diameter
Macrophage and lymphoid cell infiltration leading to scarring and narrowing of the airways
52
What are the risk factors for COPD?
```
Cigarette smoking
Occupational exposure to dusts
A-1-antitrypsin deficiency
recurrent chest infections in chuldhood
Low s/e status
Asthma/atopy
```
53
How does cigarette exposure affect COPD?
stimulates neutrophils to produce elastase
Can inactivate A-1-antitrypsin
Directly causes mucous gland hypertrophy
54
What is the clinical presentation of COPD?
Productive morning cough, followed by many years of smoker's cough
increased frequency of LRTIs
Slowly progressive dyspnoea with wheezing
Symptoms exacerbated in the acute infective episodes
Respiratory failure
Chronic right heart failure (cor pulmonate) - occurs late
55
What are the signs of COPD?
Mild disease - widespread wheeze
Severe disease:
Observation: tachypnoea, cyanosis and flapping tremor of outstretched hands
Inspection: hyperinflation, intercostal recession on inspiration, lip pursing on expiration, signs of respiratory distress
Palpation: poor chest expansion
Percussion: Hyper-resonant throughout, loss of cardiac dullness
Auscultation: deceased breath sounds, prolonged expiratory phase, polyphonic wheeze
56
What are the complications of COPD?
```
Acute exacerbations
Polycythaemia
Respiratory failure
Cor pulmonale
Pneumothorax (due to ruptured bullae)
Lung carcinoma
```
57
What is a 'blue bloater'
Patients with severe chronic bronchitis/COPD = insensitive to CO2 and rely on hypoxic drive to stimulate respiratory effort
Not breathless BUT cyanosed and oedematous
58
What type of respiratory failure will be shown in ABG of a blue bloater?
T2RF: low oxygen, retaining CO2
| Oxygen given with care
59
What is a 'pink puffer'?
These patients remain sensitive to CO2, thus keep a low CO2 and a near normal O2
Tachypnoeic and tachycardic and use accessory muscles to increase ventilation and are breathless but not cyanosed
Very thin - large amounts of calories used to breath
60
How is COPD diagnosed?
Clinical
Post-bronchodilator spirometry
CXR to rule out other pathology
FBC: identify anaemia or secondary polycythaemia
61
What are the stages of COPD?
Stage 1: mild: FEV1 80% of predicted value or higher. Diagnosis of COPD made clinically
Stage 2: moderate: FEV1 50-79%
Stage 3: severe: FEV1 30-59%
Stage 4: very severe: FEV1 <30% predicted
62
What are the CXR features of COPD?
Hyperinflation
>6 anterior, >10 posterior ribs
flattened hemidiaphragms, large central pulmonary arteries
reduced peripheral vascular markings and bullae
63
What are the Further tests for COPD?
Sputum culture - abnormal organisms (?bronchiectasis)
ECG: signs of RA/RV hypertrophy if cor pulmonate
ABG: normal in mild disease, developing to type 1/2 respiratory failure, chronic compensated respiratory acidosis
DLCO: diffusion capacity of the lung for CO; reduced emphysema
64
How should a patient with COPD be counselled?
Lifestyle advice: SMOKING CESSATION
pneumococcal and yearly flu vaccine
How to recognise exacerbation
Medication
65
Treatment algorithm for COPD?
1. SABA or SAMA
2a. If NO asthmatic features (FEV1>50%), LABA or LAMA
2b. If asthmatic features (FEV1 <50%): LABA+ICS or LAMA
3. 2a: LABA + ICS
2b: LAMA + LABA + ICS
66
What specialist treatments might be needed for COPD?
Pulmonary rehab
Oral aminophylline/theophylline: if still symptomatic following triple therapy
Mucolytics: stable COPD + chronic productive cough
Nutritional supplementation
Long term oxygen therapy
67
When might you assess 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 less than or equal to 92% on room air
LTOT introduced by specialists and can be ambulatory -patients MUST NOT SMOKE
68
What surgeries might be considered in COPD?
Pleurectomy for recurrent pneumothoraces
Bullectomy for isolated bullous disease
Lung volume reduction surgery
Removal of diseased tissue allows functioning lung to expand
69
What is the cause of exacerbation of COPD?
bacterial/viral infections, or exposure to pollutants
dyspnoea and wheeze become worse, with production of purulent sputum
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
70
When should hospital admission be considered for exacerbation of COPD?
severe breathlessness, rapid symptom onset, acute confusion, cyanosis, low oxygen saturations or worsening peripheral oedema
71
what is the outpatient management of COPD exacerbation?
Increase dose/frequency of SABA using a spacer if they do not already use one
30mg prednisolone for 7-14 days for breathlessness and osteoporosis prophylaxis
Oral abs for people with purulent sputum or clinical signs of pneumonia depending on local abx prescribing guidelines
Safety net
azithromycin prophylaxis is recommended in select patients
72
What is inpatient management of exacerbation of COPD?
Oxygen titrated to alert
nebulised bronchodilators
88-92% venturi
30mg pred / 200mg hydrocortisone
abx according to local guidelines
NIV:
BiPAP if patient still deteriorating
73
How can people be helped to stop smoking?
National campaigns, advertising bans and high taxes
stop smoking clinic
NRT: patch, lozenge, gum
varencycline - a nicotinic receptor partial agonist
bupropion - a norepinephrine and dopamine reuptake inhibitor
n.b. But / varencycline CI in pregnancy
74
What is bronchiectasis?
Chronic dilation of the airways - leading to chronic infection/inflammation
75
What are the symptoms of bronchiectasis?
Recurrent cough, producing copious quantities of infected sputum
Intermittent haemoptysis (can be the only symptom)
Persistent halitosis
Dyspnoea
Recurrent febrile episodes and episodes of pneumonia
76
What are the sings of bronchiectasis?
Clubbing
coarse inspiratory crackles over infected area, typically bibasal
wheeze
often low body habitus due to high energy demands
77
What are the causes of bronchiectasis?
Idiopathic
Post-infective
CF
Bronchial-obstruction (tumour, foreign body)
Allergic broncho-pulmonary aspergillosis
ciliary dyskinetic syndrome
Immune deficiency - specific IgA hypogammagloblinaemia
Connective tissue disease (e.g. RA)
78
Where is bronchiectasis most common?
Lung bases
79
Describe the pathology of bronchiectasis?
Airways = dilated, with purulent secretions and chronic inflammation in the wall with inflammatory granulation tissue
granulation tissue can bleed leading to haemoptysis
with repeated exacerbations there can be fibrous scarring, leading to respiratory failure
80
What investigations should you do for bronchiectasis?
Sputum culture
CXR
CT: assess distribution of disease, can see dilated airways with signet ring sign
Spirometry: obstructive pattern - reversibility should be assessed
81
What is the management of bronchiectasis?
```
Stop smoking
Physiotherapy
Postural drainage
Abx for exacerbations
Immunisations
Bronchodilators can be useful in some cases
```
Surgery = rarely indicated as disease is rarely confined to one lobe
82
What is the most common organism isolated from patients with bronchiectasis?
Haemophilus MOST COMMON
pseudomonas
klebsiella
strep pneumoniae
83
What are the complications of bronchiectasis?
```
pneumonia
Pneumothorax
Empyema
Lung abscess
Haematogenous spread of infection
severe life threatening haemoptysis: more common in CF
```
84
What is CF?
autosomal recessive condition
mutation in CFTR gene on chromosome 7, position 508
Most common abnormality = point deletion
85
How is CF caused?
CFTR point deletion
gene coding for cAMP regulated chloride channel present on multiple epithelial surfaces predominantly in the pancreas and respiratory tract ]
Malfunctioning CFTR genes lead to abnormally thick secretions, thus leading to pancreatic insufficiency and recurrent chest infections
86
What are the clinical features of CF?
Recurrent chest infections + breathlessness + haemoptysis
spontaneous pneumothorax
chronic sinusitis
nasap polyps
resp failure and cor pulmonate can eventually develop
87
What are the GI effects of CF?
Meconium ileus is common at birth
Steatorrhea due to pancreatic dysfunction, malabsorption
increased frequency of gallstones and peptic ulceration
cirrhosis
88
What are the other effects of CF?
Clubbing
infertility - congenital absence of the vas
DM
Rickets/osteomalacia due to vitamin D deficiency
89
What organisms cause pulmonary infections in CF?
S.aureus
Haemophilus influenza
gram -ve bacilli
later pseudomonas predominates and this is associated with a poor prognosis
90
What are the main investigations for CF?
```
Bloods: FBC, U+E, LFT, clotting
Sodium sweat tests: >70mmoll
annual diabetes screening
sputum culture
CXR: hyperinflation, evidence of bronchiectasis
```
Abdo USS: fatty liver/cirrhosis, chronic pancreatitis
Spirometry: obstructive defects
91
What is the management of CF?
Chest: physio + antibiotics + bronchodilators
2 parenteral antibiotics for exacerbations
Mucolytics: DNAse daily nebulisers
airway clearance devises
lung transplant: if respiratory failure develops
GI: pancreatic enzyme replacement, ADEK supplementation
Liver transplantation for advanced cirrhosis
Tx of diabetes, fertility treatment and genetic counselling
92
What is pneumonia?
Signs of infection of the pulmonary parenchyma PLUS new shadowing on Xray (must be radiologically confirmed)
93
Who is pneumonia more common in?
```
Males
elderly
smokers
alcoholics
those with chronic diseas
secondary to bronchial obstruction (cancer)
```
94
What are the clinical features of pneumonia?
acute systemic illness: fever, rigors and vomiting
cough - initially short, dry and painful progressing to productive with mucopurulent sputum
dyspnoea
pleuritic chest pain, may be referred to shoulder or anterior abdominal wall
acute confusion
May be very few symptoms in the elderly
95
What are the examination findings with pneumonia?
tachypnoea
decreased Chest expansion on the affected side
dullness to percussion over the affected area
coarse crackles and a pleural rub over the affected area with bronchial breathing
Increased vocal resonance: 'blue balloons' can be heard better (can't hear as well in effusions, pneumothorax or collapse)
Upper abdominal tenderness: in lower lobe pneumonia
96
What are the three types of pneumonia?
CAP
HAP
Pneumonia occurring in immunocompromised hosts, or patients with underlying lung damage
97
What % of CAP is conventional and atypical bacteria?
conventional 60-80%, mostly streptococcus also haemophilia
atypical 10-20% (mycoplasma, chlamydia or legionella)
98
Name the organisms that cause pneumonia
Smoking helps make losers cough
```
S.pneumoniae
H.inflenzae
M.pneumoniae
L.pneumoniae
C.pneumoniae
```
Klebsiella in alcoholics/diabetics - commonly due to aspiration
99
What is the most common cause of pneumonia?
S.pneumoniae (in those who do not have COPD)
| Vaccine - given to immunosuppressed
100
what kind of pneumonia does S.pneumoniae cause?
classical lobar pneumoniae + rust coloured sputum
101
Who did H.influenzae tend to affect?
Children before HiB vaccine
Important in COPD
102
Who does M.pneumoniae affect?
Young patients
| Can occur in epidemics
103
How does M.pneumoniae present?
Long history of illness with prominent extra-pulmonary features: rash, hepatitis, D&V, pericarditis, meningoencephalitis
Classical patchy consolidation on CXR across multiple lobes. Treatment = with erythromycin for at least 2 week
104
Who does L.pneumoniae tend to affect?
Classically - smokers who have returned from holiday
severe disease - hyponatraemia and neuro involvement
proteinuria /haematuria and classically affects both lung bases on CXR
Treatment = with erythromycin
105
Who does C.pneumoniae tend to affect?
URTI in infancy, CAP in elderly
106
What investigations would you do for pneumonia?
```
Obs and sats probe
Bloods: FBC, CRP, U+E, LFT
Blood cultures
CXR
Sputum sample for culture
Plus mycoplasma PCR if suspected
Urine for legionella / pneumococcal antigen if moderate/severe. Empirical treatment will not cover legionella (Serum mycoplasma IGM if u suspect)
```
Throat swab - severe or viral
107
How is the severity of pneumonia determined?
```
CURB 65
Confusion: mini-mental test score <8
Urea >7mmol/l
Resp rate >30/min
Blood pressure SPB <90 or DPB <60
65 years or older
```
one point for each
108
How is CURB 0/1 managed?
Non-severe
Oral amoxicillin, managed as OP
oral doxycycline if penicillin allergic
109
How is CURB65 2 managed
Oral amoxicillin and clarithromycin, usually admitting
| Oral doxycycline if penicillin allergic
110
How is CURB65 >2 managed?
ADMIT TO HDU
IV clarithromycin plus co-amoxiclav
if penicillin allergy / suspect MRSA, treat with levofloxacin and vancomycin
Treatment for at least 10 days
111
How is aspiration managed?
Metronidazole
| May have chest physiotherapy to encourage effective coughing
112
How is HAP managed?
Assess MRSA risk factors
Mild HAP - oral doxycycline
Severe HAP: oral co-trimoxazole
113
How is pneumonia followed up?
Follow up CXR at 6 weeks to ensure resolution of consolidation and assess for persistent abnormalities of the lung parenchyma
Non resolution should raise the possibility of end-bronchial obstruction as a cause of the pneumonia e.g. lung cancer
(cough can persist)
week 1: fever should resolve
week 4: chest pain and sputum should have significantly reduced
week 6: cough and shortness of breath should have significantly reduced
month 3: most symptoms should have resolved, except for tiredness
month 6: should be returned to normal
114
What are the complications of pneumonia?
parapneumonic effusion / empyema
Post infective bronchiectasis
lung abscess: clubbing
Sepsis
115
What are the two classifications of pneumonia (SITE) ?
Lobar pneumonia and bronchopneumonia
based on the main site of the inflammatory response within the lung parenchyma
Inflammatory exudate within the alveolar air spaces is what renders the infected area of the lung macroscopically solid in 'consolidation'
116
Describe the location of bronchopneumonia
primary infection centres around the bronchi, spreading to involve adjacent alveoli which become consolidated
Initial consolidation is patchy (involves lobules), but if untreated can become confluent
117
Who is bronchopneumonia most common in?
Infancy and old age due to immobility and retention of secretions, thus bronchopneumonia most commonly affects the lower lobes (gravity)
118
Describe the location of lobar pneumonia?
Organisms gain entry to distal air spaces rather than colonising bronchi, thus there is rapid spread of infection through alveolar air spaces
Macroscopically, the whole of the lobe becomes consolidated and airless
These patients are normally adults, and become severely ill with associated bacteraemia
