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CP3 Medicine > Respiratory p1 > Flashcards

Respiratory p1 Flashcards

1
Q

What does spirometry measure?

A

Volume and speed flow of air during exhalation and inhalation

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2
Q

What is FEV1?

A

Forced expiratory volume: volume that has been exhaled at the end of the first second of forced expiration

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3
Q

What is FVC?

A

Volume that has been exhaled after a maximal expiration following a full inspiration

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4
Q

What is Kco?

A

Diffusion capacity of the lung per unit area for CO

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5
Q

What is TLco?

A

Diffusion capacity of the total lung capacity for CO

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6
Q

What is an obstructive patten on spirometry?

A

Normal (or increased FVC), reduced FEV1:FVC

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7
Q

What is a restrictive pattern on spirometry?

A

Reduced FVC, normal (or increased) FEV1:FVC

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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

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9
Q

What is asthma?

A

Chronic inflammatory condition of the airways, characterised by airway hypersensitivity

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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
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11
Q

What will you find on examination for asthma?

A

Widespread expiratory wheeze

Pulmonary function = Decreased FEV1 relieved by B2 agonist

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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
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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

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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

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15
Q

What will be the findings of asthma from spirometry?

A

FEV1 / FVC will be less than 70%

bronchodilators will reverse this

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16
Q

What is extrinsic asthma caused by?

A

Type 1 hypersensitivity reaction

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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

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18
Q

What is intrinsic asthma caused by?

A

Non-immune mechanisms

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19
Q

Who does intrinsic asthma occur in?

A

Middle aged individuals, with no causative agent

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20
Q

What is late onset asthma more likely to be?

A

intrinsic

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21
Q

Describe the disease process of ACUTE asthma

A
  1. SM contraction narrows airway: bronchospasm due to production of histamine, prostaglandin D2 and leukotrienes (SM contraction NARROWS airway)
  2. Narrowing of airway due to chemotaxins (late phase)
  3. Airway hyperactivity
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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

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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)

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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
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25
Q

What are the features of life-threatening asthma?

A 
PEF <33% best 
SpO2 <92% 
Silent chest, cyanosis or feeble respiratory effort 
Bradycardia, hypotension or dysrhythmia 
exhaustion or confusion
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26
Q

What is the investigation of choice for life threatening asthma?

A

ABG

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27
Q

What are the blood gas features of a life threatening attack?

A

NORMAL PaCO2 - should be low due to hyperventilation
severe hypoxia <8
Low ph

A raised PaCO2 = near fatal asthma

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28
Q

What is the management of acute asthma attack?

A

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

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29
Q

What is the additional management of life threatening asthma?

A

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

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30
Q

What is the management for acute severe asthma once stable?

A

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.

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31
Q

What is the treatment algorithm for asthma

A
  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
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32
Q

What drugs might be added for asthma after specialist opinion?

A

Oral B2 agonists, oral corticosteroids or anti IgE drugs (omalizumab)

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33
Q

How do B2 agonists work?

A

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

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34
Q

How long do SABAs work for?

A

4-6 hours

LABAs >12 hours

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35
Q

how do inhaled corticosteroids work?

A

Reduce exacerbations due to anti-inflammatory effects

Side effects = oral candidiasis + pneumonia, plus systemic effects of corticosteroid

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36
Q

What LTRAs are there?

A

Montelukast

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37
Q

How do LTRAs work?

A

Block the effect of leukotrienes in the airways, benefitting the actions of inhaled ICS

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38
Q

What are the side effects of LTRAs?

A

thirst, GI disturbances and very rarely, Churg-Strauss (systemic vasculitis)

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39
Q

How do theophylline/aminophylline work?

A

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

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40
Q

What is COPD?

A

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

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41
Q

What is the cause of COPD?

A

Emphysema + chronic bronchitis

Decreased outflow pressure + increased airway resistance

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42
Q

What is emphysema?

A

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

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43
Q

How does tissue destruction occur in emphysema?

A

Increased secretion and activation of extracellular proteases by inflammatory cells (after exposure to noxious particles)

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44
Q

What is centrilobar emphysema?

A

Changes are limited to the central part of the lobule directly around the terminal bronchiole with normal alveoli elsewhere

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45
Q

What is panacinar emphysema?

A

Destruction and distension of the whole lobule, which can happen in smokers but is more common in alpha-1-antitrypsin deficiency

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46
Q

What is the effect of A-1-antitrypsin deficiency?

A

A-1-antitrypsin Normally inactivates neutrophil elastase

without it, overactivity of neutrophil elastase and destruction of alveoli

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47
Q

what are bullae?

A

dilated air spaces >1cm

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48
Q

How does emphysema affect gas exchange?

A

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
Q

What is chronic bronchitis?

A

Daily cough with sputum for at least 3 months per year for 2 years

50
Q

What is the pathophysiology of chronic bronchitis?

A

Abnormal amounts mucus - plugging of the airway lumen

Hypersecretion = hypertrophy and hyperplasia of bronchial mucus secreting glands

Can be shown by Reid index

51
Q

What is bronchiolitis?

A

Inflammation of the airways <2mm in diameter

Macrophage and lymphoid cell infiltration leading to scarring and narrowing of the airways

52
Q

What are the risk factors for COPD?

A 
Cigarette smoking
Occupational exposure to dusts
A-1-antitrypsin deficiency 
recurrent chest infections in chuldhood
Low s/e status 
Asthma/atopy
53
Q

How does cigarette exposure affect COPD?

A

stimulates neutrophils to produce elastase
Can inactivate A-1-antitrypsin
Directly causes mucous gland hypertrophy

54
Q

What is the clinical presentation of COPD?

A

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
Q

What are the signs of COPD?

A

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
Q

What are the complications of COPD?

A 
Acute exacerbations 
Polycythaemia
Respiratory failure 
Cor pulmonale
Pneumothorax (due to ruptured bullae)
Lung carcinoma
57
Q

What is a ‘blue bloater’

A

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
Q

What type of respiratory failure will be shown in ABG of a blue bloater?

A

T2RF: low oxygen, retaining CO2

Oxygen given with care

59
Q

What is a ‘pink puffer’?

A

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
Q

How is COPD diagnosed?

A

Clinical
Post-bronchodilator spirometry

CXR to rule out other pathology

FBC: identify anaemia or secondary polycythaemia

61
Q

What are the stages of COPD?

A

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
Q

What are the CXR features of COPD?

A

Hyperinflation
>6 anterior, >10 posterior ribs
flattened hemidiaphragms, large central pulmonary arteries
reduced peripheral vascular markings and bullae

63
Q

What are the Further tests for COPD?

A

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
Q

How should a patient with COPD be counselled?

A

Lifestyle advice: SMOKING CESSATION
pneumococcal and yearly flu vaccine
How to recognise exacerbation
Medication

65
Q

Treatment algorithm for COPD?

A
  1. SABA or SAMA

2a. If NO asthmatic features (FEV1>50%), LABA or LAMA
2b. If asthmatic features (FEV1 <50%): LABA+ICS or LAMA

  1. 2a: LABA + ICS
    2b: LAMA + LABA + ICS
66
Q

What specialist treatments might be needed for COPD?

A

Pulmonary rehab

Oral aminophylline/theophylline: if still symptomatic following triple therapy

Mucolytics: stable COPD + chronic productive cough

Nutritional supplementation

Long term oxygen therapy

67
Q

When might you assess for LTOT?

A

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
Q

What surgeries might be considered in COPD?

A

Pleurectomy for recurrent pneumothoraces
Bullectomy for isolated bullous disease
Lung volume reduction surgery

Removal of diseased tissue allows functioning lung to expand

69
Q

What is the cause of exacerbation of COPD?

A

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
Q

When should hospital admission be considered for exacerbation of COPD?

A

severe breathlessness, rapid symptom onset, acute confusion, cyanosis, low oxygen saturations or worsening peripheral oedema

71
Q

what is the outpatient management of COPD exacerbation?

A

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
Q

What is inpatient management of exacerbation of COPD?

A

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
Q

How can people be helped to stop smoking?

A

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
Q

What is bronchiectasis?

A

Chronic dilation of the airways - leading to chronic infection/inflammation

75
Q

What are the symptoms of bronchiectasis?

A

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
Q

What are the sings of bronchiectasis?

A

Clubbing
coarse inspiratory crackles over infected area, typically bibasal
wheeze
often low body habitus due to high energy demands

77
Q

What are the causes of bronchiectasis?

A

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
Q

Where is bronchiectasis most common?

A

Lung bases

79
Q

Describe the pathology of bronchiectasis?

A

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
Q

What investigations should you do for bronchiectasis?

A

Sputum culture
CXR
CT: assess distribution of disease, can see dilated airways with signet ring sign
Spirometry: obstructive pattern - reversibility should be assessed

81
Q

What is the management of bronchiectasis?

A 
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
Q

What is the most common organism isolated from patients with bronchiectasis?

A

Haemophilus MOST COMMON
pseudomonas
klebsiella
strep pneumoniae

83
Q

What are the complications of bronchiectasis?

A 
pneumonia 
Pneumothorax
Empyema
Lung abscess
Haematogenous spread of infection 
severe life threatening haemoptysis: more common in CF
84
Q

What is CF?

A

autosomal recessive condition
mutation in CFTR gene on chromosome 7, position 508
Most common abnormality = point deletion

85
Q

How is CF caused?

A

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
Q

What are the clinical features of CF?

A

Recurrent chest infections + breathlessness + haemoptysis

spontaneous pneumothorax
chronic sinusitis
nasap polyps
resp failure and cor pulmonate can eventually develop

87
Q

What are the GI effects of CF?

A

Meconium ileus is common at birth
Steatorrhea due to pancreatic dysfunction, malabsorption
increased frequency of gallstones and peptic ulceration
cirrhosis

88
Q

What are the other effects of CF?

A

Clubbing
infertility - congenital absence of the vas
DM
Rickets/osteomalacia due to vitamin D deficiency

89
Q

What organisms cause pulmonary infections in CF?

A

S.aureus
Haemophilus influenza
gram -ve bacilli

later pseudomonas predominates and this is associated with a poor prognosis

90
Q

What are the main investigations for CF?

A 
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
Q

What is the management of CF?

A

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
Q

What is pneumonia?

A

Signs of infection of the pulmonary parenchyma PLUS new shadowing on Xray (must be radiologically confirmed)

93
Q

Who is pneumonia more common in?

A 
Males
elderly
smokers
alcoholics 
those with chronic diseas
secondary to bronchial obstruction (cancer)
94
Q

What are the clinical features of pneumonia?

A

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
Q

What are the examination findings with pneumonia?

A

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
Q

What are the three types of pneumonia?

A

CAP
HAP
Pneumonia occurring in immunocompromised hosts, or patients with underlying lung damage

97
Q

What % of CAP is conventional and atypical bacteria?

A

conventional 60-80%, mostly streptococcus also haemophilia

atypical 10-20% (mycoplasma, chlamydia or legionella)

98
Q

Name the organisms that cause pneumonia

A

Smoking helps make losers cough

S.pneumoniae
H.inflenzae
M.pneumoniae 
L.pneumoniae 
C.pneumoniae

Klebsiella in alcoholics/diabetics - commonly due to aspiration

99
Q

What is the most common cause of pneumonia?

A

S.pneumoniae (in those who do not have COPD)

Vaccine - given to immunosuppressed

100
Q

what kind of pneumonia does S.pneumoniae cause?

A

classical lobar pneumoniae + rust coloured sputum

101
Q

Who did H.influenzae tend to affect?

A

Children before HiB vaccine

Important in COPD

102
Q

Who does M.pneumoniae affect?

A

Young patients

Can occur in epidemics

103
Q

How does M.pneumoniae present?

A

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
Q

Who does L.pneumoniae tend to affect?

A

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
Q

Who does C.pneumoniae tend to affect?

A

URTI in infancy, CAP in elderly

106
Q

What investigations would you do for pneumonia?

A 
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
Q

How is the severity of pneumonia determined?

A 
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
Q

How is CURB 0/1 managed?

A

Non-severe
Oral amoxicillin, managed as OP
oral doxycycline if penicillin allergic

109
Q

How is CURB65 2 managed

A

Oral amoxicillin and clarithromycin, usually admitting

Oral doxycycline if penicillin allergic

110
Q

How is CURB65 >2 managed?

A

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
Q

How is aspiration managed?

A

Metronidazole

May have chest physiotherapy to encourage effective coughing

112
Q

How is HAP managed?

A

Assess MRSA risk factors
Mild HAP - oral doxycycline
Severe HAP: oral co-trimoxazole

113
Q

How is pneumonia followed up?

A

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
Q

What are the complications of pneumonia?

A

parapneumonic effusion / empyema
Post infective bronchiectasis
lung abscess: clubbing
Sepsis

115
Q

What are the two classifications of pneumonia (SITE) ?

A

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
Q

Describe the location of bronchopneumonia

A

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
Q

Who is bronchopneumonia most common in?

A

Infancy and old age due to immobility and retention of secretions, thus bronchopneumonia most commonly affects the lower lobes (gravity)

118
Q

Describe the location of lobar pneumonia?

A

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

CP3 Medicine (19 decks)

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