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respiratory unit 2 Flashcards

1
Q

which drugs should be avoided in asthmatic patients?

A

Beta-blockers, NSAIDs, aspirin

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2
Q

why is aspirin contraindicated in asthma?

A

aspirin inhibit cylclo-oxygenase which contributes to the conversion of arachidonic acid to bronchodilatory PGs

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3
Q

when does intrinsic asthma develop and what are symptoms triggered by?

A

adulthood and triggered by non-allergic factors such as viral infection, irritants and exercise

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4
Q

what causes mucosal oedema?

A

Platelet activating factor released by macrophages sustains bronchial hyperactivity causing respiratory capillaries to leak plasma leading to oedema

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5
Q

what contributes to airway remodelling?

A

PAF causing accumulation of eosinophils which release inflammatory mediators causing epithelial damage and hypertrophy and hyperplasia of bronchial smooth muscle

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6
Q

what does the hx of an asthma pt include?

A

presence of atopy and allergic rhinitis in the close family

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7
Q

what is the pulse rate in acute severe asthma?

A

> 110 beats/min in adults

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8
Q

what is breathing like in acute severe asthma?

A

shallow and rapid breathing = >30 breaths/min and low O2 saturation (<92%)

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9
Q

what is the most useful test for abnormalities in airway function?

A

FEV - inhale deeply as possible and exhale completely into a mouth piece

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10
Q

how much can normal individuals usually exhale?

A

70% of their total capacity in 1 second

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11
Q

what does a peak flow meter measure?

A

peak expiratory flow rate (PEF) - maximum flow rate that can be forced during expiration

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12
Q

what diurnal availability is suggestive of asthma?

A

more than 60L/min (or more than 20%)

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13
Q

when can adrenal suppression occur with inhaled corticosteroids?

A

belcometasone >1500ncg or budesonide >400ncg in children

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14
Q

how many weeks trial is recommended for LT antagonists?

A

4-6 week trial then STOP if no improvement

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15
Q

what therapeutic range should theophylline be maintained in?

A

10-20mg/L

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16
Q

what range can theophylline cause nausea and vomiting in?

A

common in over 20mg/L but can be seen in as low as 13mg/L

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17
Q

when should an acute asthma attack result in hospital admission?

A

PEF <50% OR pts has trouble completing sentences in one breath, life threatening features present, pt is too breathless to talk

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18
Q

how would you manage acute asthma?

A

short course of oral steroid at high dose e.g. prednisolone 40-50mg OD for 7 days, increase B2 agonist dose if deteriorates further then oxygen administration to reach >92%, IV HC if pt cannot take oral medication

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19
Q

what is the main disadvantage of MDIs?

A

they require good technique

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20
Q

what should pregnant women receiving steroid dose exceeding 7.5mg/day for >2 weeks recieve prior to delivery?

A

parental HC 100mg 6-8/hr during labour

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21
Q

what is step 3 of the asthma management ladder?

A

addition of LABA AND assess control of asthma

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22
Q

when would you add 400ncg of an ICs in the asthma managment ladder?

A

step 2 when SABA is inadaquate

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23
Q

what is the minimum volume that should be nebulised in a nebuliser?

A

3-4ml

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24
Q

side effects of corticosteroids

A

oral candidiasis, sore throat, croaky voice

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25
how would you minimise oro-pharyngeal side effects?
brush teeth after inhalation, using a large volume spacer, rinsing mouth with water
26
what suggests asthma is partly controlled?
day time symptoms more than twice a week, need for reliever more than twice a week, PEF <80%
27
what does symbicort contain?
formaterol and budesonide
28
what does seretide contain?
salmeterol and fluticasone
29
fostair?
formetarol and beclametasone
30
relvar?
fluticasone and vilanterol
31
what is pneumonia?
inflammation of small airway sacs (alveoli) at the end of the branched airways which become solid and filled with puss hindering oxygenation
32
what is the CURB65 score?
1 point for each; confusion, raised respiratory rate (>30 breaths/min) , low BP (diastolic 60mmhg or less OR systolic less than 90), over 65 years
33
what should you not routinely offer patients with low severity CAP?
dual A/B therapy OR a fluoroquinolone
34
treatment for LS-CAP?
5 days amoxicillin OR macrolide/tetracycline
35
treatment for severe CAP
5-7 days dual therapy with beta lactamase and a macrolide
36
how long should the hospital acquired antibiotic course of pneumonia be?
5-10 days
37
for CAP when would chest pain and cough resolve by?
4 weeks for chest pain and 6 weeks for cough and 6 months to feel back to normal
38
what is the classification of haemophyllis influenza?
Anaerobic coccobacillary, pathogenic bacterium, Gram-negative, belongs to the Pasteurellaceae family
39
what is the name of the bacteria which is Gram-negative bacterium of the genus Legionella, a thin, aerobic, pleomorphic, flagellated, nonspore-forming.
Legionella pneumophilia
40
what is the classification for Streptococcus pneumoniae accounting for 36% of CAP incidence?
Alpha haemolytic, gram positive, encapsulated, aerobic dipplococcus
41
if FEV1 is >80% can diagnosis of COPD be made?
only in the presence in the cough
42
what are the 4 major pathological changes in COPD?
central airway hypertrophy, peripheral airways, pulmonary vasculature, lung parenchyma
43
what factors within smoking are predictive of COPD mortality?
number of cigarettes smoked, total pack years and number of years smoking
44
how do genetic influence risk of COPD?
a1-antitrypsin deficient individuals are at increased risk of emphysema
45
what cytokines do inflammatory mediators cause the release of?
TNF-a, LT-B4, IL-8
46
what is a main proteinase and what is it released by?
neutrophil elastin released by macrophages OR neutrophils
47
what is the main anti-proteinase and how does smoking effect it?
a1-antitrypsin and smoking is known to inactivate this protein
48
why is the responsiveness to corticosteroids reduced in COPD?
corticosteroids recruit histone deacetylase to switch off inflammatory genes but in COPD histone deacetylase is IMPAIRED
49
name 3 common bacterial pathogens
haemophillis influenzae, streptococcus pneumonaie and moraxella catarrhalis
50
what is bronchiectasis?
bronchi become permenantly dilated and mucus can accumulate
51
when does pulmonary hypertension develop in COPD?
late in COPD after gas exchange abnormalities have developed
52
how do chest radiographs differ in emphysema and chronic bronchitis?
emphysema = flattened diaphragm with loss of peripheral markings and appearance of bullae chronic bronchitis = bronchovascular markings and cardiomegaly due to RV dysfunction and failure
53
what is mepolizumab?
MAB, used in severe refractory eosinophilic asthma. It is anti-IL-5 reducing the production and survival of eosinophils.
54
what is a benefit of mepolizumab?
The benefit of mepolizumab is that it is a standard dosing regime of 100mg every 4 weeks.
55
when can mepolizumab only be used?
Can only be used as addition to standard therapy and when a patient’s blood eosinophil count is 300 cells/microlitre or more in the previous 12 months.
56
what is the major drawbacks of monoclonal antibodies?
proteins so have to be given subcutaneously
57
what is type 2 respiratory failure?
Hypoxaemia (low levels of oxygen) with a high Pa CO2. Most commonly seen in COPD patients.
58
what is type 2 respiratory failure?
Hypoxaemia with a high Pa CO2. Most commonly seen in COPD patients.
59
what is referred to as blue bloater?
chronic bronchitis patients - in which hypercapnia and hypoxia are common
60
what are symptoms of emphysema?
referred to as pink puffer which is hyperventilating to compensate for hypoxia, dyspnoea even at rest, thin pursed lips, sputum is mucoid

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