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Medicine 1 (Year 1) > Airway disease > Flashcards

Airway disease Flashcards

1
Q

Obstructive airway diseases

A

a disease that causes obstruction affects all of the airways in both lungs - global airway obstruction.

not including lung cancer, tumour, inhaled foreign bodies and chronic scarring diseases like bronchiectasis and secondary fibrocaseous or tuberculosis as these are not primarily obstructive diseases.

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2
Q

In relation to obstructive diseases how can we measure function?

A

testing with FEV1 and FVC

take a deep breath in and try blowing out as much air as possible and as fast as possible.

fev1 - forced expiratory volume of air in first second

fev1 is usually about 70%-80% of fvc

normal fev 1 is about 2.5-4L

normal fvc is about 5L

normal ratio fev1:fvc is 0.7 -0.8

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3
Q

what % is normal fev1 of fvc

A

fev1 is usually about 70%-80% of fvc

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4
Q

what is normal fev1 volume

A

normal fev 1 is about 2.5-4L

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5
Q

what is normal fvc volume

A

normal fvc is about 5L

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6
Q

what is normal ratio fev1:fvc

A

normal ratio fev1:fvc is 0.7 -0.8

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7
Q

what is another way to measure airflow limitation other than fev1/fvc

A

peak flow

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8
Q

what is normal peak expiratory flow rate?

A

400-600litres per min

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9
Q

what is a normal peak expiratory flow rate range %

A

80-100%

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10
Q

what is the % of a moderate fail of a peak expiratory flow rate?

A

50-80%

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11
Q

what is a maked fail of a peak expiratory flor rate %?

A

<50%

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12
Q

explain asthma what is it?

A

type 1 hypersensitivity in the airways because of bronchial constriction

reduction in the luminal cross-sectional area. granulation of mast cells in airways releasing chemical factors from mast cells reduce diameter.

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13
Q

In asthma what do the chemical factors do in the airway

A

chemical factors induce inflammation by attracting inflammatory cells = swelling and oedema within the bronchial mucosa.

chemicals have a direct effect on bronchial smooth muscle leading to constriction of airways.

= airflow narrowing and limitation

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14
Q

is bronchial asthma reversible?

A

yes generally reversible obstruction spontaneously or with medical intervention

the bronchial smooth muscle contraction and inflammation can be modified with drugs.

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15
Q

aetiology of chronic bronchitis and emphysema

A

SMOKING

  • atmospheric pollution
    occupation: dust

alpha1 antiprotease (antitrypsin) deficiency extremely rare cause of emphysema

  • age and susceptibility

prevalence - men more than women

increasing in developing countries

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16
Q

Chronic bronchitis is defined clinically as:

A

cough productive of sputum most days in at least 3 consecutive months for 2 or more consecutive years

(excludes tb, bronchiectasis)

clinically may be confused with chronic bronchial asthma

complicated chronic bronchitis when sputum turns mucopurulent (acute infective exacerbation) or FEV1 falls

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17
Q

What are the morphological changes in chronic bronchitis

A

large airways: mucus gland hyperplasia, goblet cell hyperplasia, inflammation and fibrosis is a minor component

small airways: goblet cells appear, inflammation and fibrosis in long-standing disease.

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18
Q

explain globlet cells

A

Modified epithelial cells that secrete mucus on the surface of mucous membranes of intestines and airways

Their role is to protect the surface of the epithelium, lubricate it, and catch harmful particles. Although protective, goblet cells may be involved in the pathophysiology of certain respiratory diseases, such as chronic bronchitis.

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19
Q

define emphysema

A

pathological definition: increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilation or from the destruction of their walls and without obvious fibrosis

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20
Q

what is the acinus?

A

the gas exchange tissue part of the lunch and is defined by everything distal to the terminal bronchiole

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21
Q

histology emphysema

A

the air spaces become bigger - loss of alveolar walls

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22
Q

most common form of emphysema

A

centri-acinar emphysema

middle of acinus - middle disappears - holes surrounded by lung tissue

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23
Q

what is pari-acinar emphysema

A

holes all alveolar and acinous gas exchange lost. scarring is irregular and has “bullous” emphysema. bullae are spaces under the pleura full of air. This is significant because if they pop, this can cause pneumothorax

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24
Q

mechanisms airway in COPD.

A

small airways smooth muscle tone and inflammation - will respond to same drugs as asthma - inflammation component will respond. the fibrotic element will not, however.

Why i t isn’t reversible what cannot be treated is emphysema - the loos of alveolar attachment is most important

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25
Q

explain what happens with emphysema and collapsing of airway

A

when we exhale, the small airways would close/collapse, but there is a radial pull from alveoli elastic fibres which keep them open. in centri-acinal emphysema the alveolar walls are lost

airways likely to collapse when trying to breathe out

the airway will collapse trapping air inside the lung

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26
Q

What are the clinical effects of COPD?

A

hypoxaemia

airway obstruction

reduces respiratory drive

loss of alveolar surface area

shunting - during acute infective exacerbation

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27
Q

what are the pulmonary vascular changes in hypoxia

A
  • physiological pulmonary arteriolar vasoconstriction - (alveolar tension fails can be a localised effect. or all vessels constrict if there is hypoxaemia - hypertension occurs in the pulmonary vascular system. right ventricle working harder = pathological hypertrophy of right ventricle chronic cor pulmonale then result in congenital heart disease. right heart failure.

a protective mechanism (do not send blood to alveoli short of oxygen)

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28
Q

explain cor pulmonale - pulmonary hypertension

A

pulmonary vasoconstriction anatomical changes in vessels become hypertrophic and end of vessels become fibrotic = reduction in luminal cross-sectional area of the vessel Makes harder to pump blood through.

emphysema leads to a loss of blood vessel (capillary bed) = fewer blood vessels for the heart to pump blood through = pulmonary vascular resistance increased.

if continuous in hypoxic state bone marrow tries to produce more RBC - blood becomes more viscous = harder to pump through compromised vascularity.

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29
Q

explain the basics of asthma with diagnosing

some chellenges

A
  • no definition
  • no tests
  • two national guidelines
  • symptom-based
  • identical to lower respiratory tract symptoms in acuse phases
  • relapse and remission
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30
Q

Some key things regarding asthma when diagnosing for children

A
  • no wheeze = no asthma
  • tests may help decision although often don’t

if the symptoms affect the quality of life - confirm the diagnosis with a trial of inhaled corticosteroids

if the quality of life is not affected do not rush to treat, watch and see

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31
Q

what is asthma?

A

chronic condition- with wheeze, cough and shortness of breath

has multiple triggers

variable/reversible

responds to asthma treatment

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32
Q

(child asthma) what causes asthma?

A

host response to environment

infection important

physiology abnormal response before symptoms

is a syndrome.

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33
Q

different asthma syndromes

A

infant onset

childhood-onset

adult-onset

exertional asthma

occupational asthma

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34
Q

what can cause asthma

A
  • genes 30-80% causes
  • interact with the environment
  • epigenetics

allergen stimulated immune system and then an allergy response

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35
Q

what is the best assessment in children for asthma

A

history

examination not always helpful - if healthy unlilely wheezing, stethoscope wont be important and unhelpful if not wheezing

no diagnostic asthma test for children - peak flow no good,

allergy test irrelevant for asthma only environment allergy, spirometry lacks specificity,

nitric oxide can display affiliation eosinophils are allergic to blood cells - tells inflammation in the lung.

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36
Q

spirometry for asthma (child asthma)

A

useful don’t with a bronchodilator response to measure lung function - give asthma medicine and see if flow changes

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37
Q

What is nice guideline for asthma diagnosis? (child asthma)

A

1. spirometry

2. bronchodilator response (BDR)

3.FeNO nitrous oxide test

4 peak flow

yes-no mark of diagnose or test further

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38
Q

what does the BTS/Sign guideline have in classing diagnosis (child asthma)

A

1. spirometry

2. bronchodilator response (BDR)

3.FeNO nitrous oxide test

4 peak flow

score as high probability, intermediate probability or low probability

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39
Q

where is the main diagnosis problem? (child asthma)

A

uncertainty in <5 years old

tests are not reliable in < 5-year-olds

the tests cal already be difficult already

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40
Q

(child asthma) cough variant asthma__

A

not common in children, this is common in adults

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41
Q

(child asthma) when having symptoms described to you about a child, what is important?

A

to establish if it is actually a wheeze. often it’s a rattle, not a wheeze. Ask “what you mean by wheeze, is it like a whistle or rattling?”

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42
Q

common symptoms of asthma (child asthma)

A

Wheeze (needed)

shortness of breath at rest - significant difficulties <30% lung function

airway obstruction

“sooking” in of ribs with wheeze ribs sucked in tummy sticks out

coughing - dry, common night, after exercise

other circumstance - parent history asthma, eczema, hayfever, food allergy

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43
Q

responding to asthma treatment how long does it take for steroids to have maximum effect? (child asthma)

A

two months. must keep using 2 months if it doesn’t work after 2 months then it isn’t working.

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44
Q

(child asthma) when on an inhaler - what is false positive?

A

a child with transient respiratory symptoms not asthma - symptoms go away. inhaler might not have actually worked. Stop inhaler in spring see if symptoms return if not = false positive.

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45
Q

(child asthma) key to diagnosing asthma

A
  • wheeze without and without upper respiratory tract infection

shortness of breath at rest

parental asthma (helps)

responds to treatment

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46
Q

(child asthma) trialling asthma treatment for children benefit/harm

A

harm: cost, hassle, loss of height 0.5-1cm, oral thrush

benefit: helps diagnosis, if symptoms respond, improve quality of life, reduces risks of attacks

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47
Q

for children, when is it not asthma usually?

A

under 18 months, likely infection

over 5 years - likely asthma

but if it sounds like asthma and responds to asthma treatment it is asthma regardless of age

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48
Q

(child asthma) what is differential diagnosis for asthma for under 5 years of age

A
  • congenital ( a disease or physical abnormality) present from birth.
  • Cystic fibrosis (CF)
  • Primary ciliary dyskinesia (PCD) is a rare genetic condition that can lead to chronic lung,
  • bronchitis
  • foreign body
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49
Q

(child asthma) what is differential diagnosis for asthma for over 5 years of age

A
  • dysfunctional breathing
  • vocal cord dysfunction
  • habitual cough
  • pertussis (also known as whooping cough)
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50
Q

asthma vs Viral-Induced Wheezing child (child asthma)

A

treated the same bronchodilators

not separate conditions

in preschool children 99%

should be treated

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51
Q

what are the goals in treatment for asthma (childhood)

A

- have minimal symptoms during day and night

minimal need for reliever medication

- no attacks (exacerbations)

no limit of physical activity

normal lung function (in practical terms FEV1and or PEF >80% predicted or best

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52
Q

the right questions to ask when reviewing asthma (children)

to see if poorly controlled asthma

A

SANE - pneumonic

  • Short-acting beta-agonist/week (are you using more than 2x week) (if Yes poorly controlled)
  • Absence - from school/nursery

Nocturnal symptoms a week if waking >1 night a week = poorly controlled

Exertional symptoms a week

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53
Q

(child asthma) treatment decisions for well-controlled asthma patient

A
  • no change of treatment
  • consider reducing dose
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54
Q

(child asthma) treatment decisions for poorly controleld asthma

A
  • are they taking treatment? are they taking it correctly? - no change to asthma treatment
  • is this not asthma? stop asthma treatment

none of the above? - increase treatment to….

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55
Q

(child asthma) asthma step up and step down

A

start on low dose inhaled corticosteroids (as diagnostic process)

review after 2 months

  • no routine test to monitor progress, no change is easier to step down

YOU NEED to give them an easter inhaler holiday to check working anyway

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56
Q

classes of asthma medications (child asthma)

A
  • short-acting beta-agonists
  • inhaled corticosteroids
  • long-acting beta-agonists

leukotriene receptor antagonists

theophyllines

oral steroids

“add ons”

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57
Q

add treatment to short beta-agonists (child asthma)

A

add preventer - long-acting beta-agonist

leukotriene - montelukast only 1/3 significant improvement 1/3 some improvement 1/3 no improvement, better adherence, granules used for reluctant toddlers

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58
Q

severe asthma approach(child asthma)

A

when long-acting and short-acting beta-agonist doesn’t work

experimental medicine 50% psychological issues

>50% compliance issues.

question the diagnosis

a minority have a genuine disease

new medication biologics although unproven for children

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59
Q

metered-dose inhaler with spacer why do you need a spacer (children)

A

you get less than 5% of the drug in your lung

you get around 20% deposition with a spacer

4x as much drug

and SHAKE the inhaler between puffs

also, wash spacer do not rinse

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60
Q

for a parent of a child with asthma how can they improve child’s asthma without medication

A

stop tobacco smoke exposure

remove environmental triggers: cats, dogs

dust mite levels

no evidence of diet for asthma

alter humidity ionisers increase cough but dehumidifiers or humidifiers don’t improve asthma control

weight reduction good but not evidence for asthma

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61
Q

acute asthma treatment mild (child asthma)

A

short-acting beta agonists

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62
Q

acute asthma treatment moderate (child asthma)

A

short-acting beta-agonist via neb + preventer (when a child is a well neb)

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63
Q

acute asthma treatment severe asthma (child asthma)

A

iv salbutamol

iv aminophylline

iv magnesium (nebuliser)

iv hydrocortisone

intubate and ventilate

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64
Q

how to choose what treatment? (child asthma)

A

look at the patient - can talk?

respiratory rate

work of breathing

heart rate

o2 saturation

ability to complete sentences

confusion

air entry

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65
Q

for child asthma treating acutely - what is the treatment path?

A

start treatment chosen, assess in 1 hour

step-up or down as appropriate

for chronic/maintenance treatment = inhaled steroids (_not o_ral)

acute treatment = oral steroids (not inhaled)

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66
Q

(adult asthma) definition

A

complex disease no universally accepted definition

characterised by increased responsiveness of the trachea and bronchi to various stimuli and manifested by widespread narrowing of airways that changes in severity either spontaneously of as a result of therapy

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67
Q

(adult asthma) - what is it?

A

history of respiratory symptoms (most marked at beginning or end of the day) such as:

wheezing

shortness of breath

coughing

chest tightness

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68
Q

(adult asthma) why is it important

A

common 5-10% population 5,4 million at least effected

dangerous 3 asthma-related deaths a day

expensive 70,000 admissions yearly avg stay 4 days

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69
Q

pathophysiology asthma

A

1 disease of lung airway - airway inflammation mediated by immune system

2 widespread narrowing of airway

3 increased airway reactivity ► airway narrowing can be done spontaneously or to stimuli

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70
Q

risk factors for (adult asthma)

A

hereditary - recognised genetic basis - disease clusters in families + twin, family and population-based studies

atopy - body predisposition to develop antibody called immunoglobin E (IgE) in response to exposure to the environmental allergen and is an inheritable trait

associated with allergic rhinitis, asthma, hayfever eczema

increased first-degree family member of asthma or atopic disease maternal atopy

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71
Q

proven risk of asthma

A

smoking - maternal smoking

also grandmother smoking - tobacco on genes.

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72
Q

(adult asthma) occupational asthma

A

underestimated but 10-15% adult onset asthma)

interaction with smoking and atopy

isocyanates - twin pack paint

colophony - welding solder flux

laboratory animals - rodent urinary proteins

grains - wheat protein grain mites

enzymes - subtilisin, amylase

drugs - antibiotics, salbutamol

crustaceans - prawns and crabs

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73
Q

(adult asthma) links to asthma - prevalence

A

obesity - increased BMI with asthma - obesity proinflammatory

diet - vitamin e,c and d. selenium. polyunsaturated fatty acids. oily fish, Mediterranean diet, margarine

hygiene hypothesis - reduced exposure to microbes/microbial product

children born on farms less likely to develop asthma

microbial diversity appears to be important in reducing the risk of asthma

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74
Q

(adult asthma) clinical aspects

A

history important

investigation can be supportive but no single test diagnoses asthma

important to think what else it could be

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75
Q

symptom history of asthma

(adult asthma)

A

wheeze

short of breath (dyspnoea), and how severe

chest tightness

cough, proximal and usually dry

sputum (occasional)

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76
Q

symptom variation?

(adult asthma)

A

variable symptoms - daily variation (nocturnal/early morning)

weekly variation (occupation, better at weekends and holidays)

annual variation (environmental allergens)

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77
Q

what can trigger (adult asthma) symptoms

A

differs for each individual

exercise, cold air, cigarette smoke, perfumes/strong scents, Upper respiratory tract infections, pets, tree or grass pollen, food, drugs (aspirin/NSAID)

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78
Q

another aspect of asthma history

A

PMH - childhood asthma, bronchitis or wheeze in infancy; eczema; hayfever

drugs - current inhalers (check their technique) other asthma therapy, compliance; beta-blockers, aspirin NSAIDs

Family history - asthma and other atopic diseases

Social history - tobacco, recreational drugs, vaping; pets; occupation (past and present); pathological aspect.

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79
Q

(adult asthma) clinical examination

A

usually unhelpful in the clinic -; breathless on exertion; hyperinflated chest; wheeze

probably not asthma if; finger clubbing, cervical lymphadenopathy; stridor; asymmetrical expansion, dull percussion note (collapse/effusion); crepitations (bronchiactasis, cyctic fibrosis, Interstitial Lung Disease (ILD) or left ventricular function (LVF)

80
Q

differential diagnosis (adult asthma)

A

really trying to differentiate other causes of wheeze, cough, dyspnoea

Generalised airflow obstruction - COPD (irreversible airflow obstruction), bronchiectasis, cystic fibrosis

Localised airway obstruction (inspiratory stridor = large airways) Tumour, Foreign body

cardiac-related

81
Q

(adult asthma) intermediate suspicion of asthma tests

A

fev1/fvc <70% lindicates airflow obstruction

normal spirometry may still be asthmatic.

Spirometry > normal > peak flow monitoring > bronchial provocation or nitric oxide

Spirometry > obstructed (fev1/fvc) <70% fev1 <80% predicted > full pulmonary function > reversibility using beta 2 agonist (or oral steroid)

82
Q

(adult asthma) if obstructed what next test (pulmonary function)

A

full pulmonary function test - exclude COPD /emphysema

carbon monoxide gas transfer (transfer of co to hb across alveoli)

asthma gas transfer is preserved or even can be increased. in COPD reduced due to alveolar reduction and destruction of lungs by smoking.

83
Q

(adult asthma) what is a further test (reversibility)

A

response to bronchodilator

baseline 15 mins post 400 ug inhaled salbutamol

baseline 15 minutes post neb 2.5-5mg salbutamol

interpretation significant reversibility - fev1>200ml + fev1 12% baseline

84
Q

(adult asthma) reversibility to corticosteroids (anti-inflammatory)

A

separates COPD from asthma. oral steroids 0.6mh/kg prednisolone 14 days

peak flow chart and meter

baseline + 2-week spirometry peak flow.

85
Q

Normal spirometry - variable obstruction (adult asthma)

A

lung function may (usually) be normal

look for variability airflow obstuction

peak flow meter and chart twice daily (best 3 measurements for 2 weeks)

analysis subjective

morning/nocturnal dips, decline over weeks/days variability >20% on > 3 days a week

86
Q

apart from lung function tests (adult asthma) what other investigations are useful?

A

Chest x-ray - hyperinflated or hyperlucent (find no effusion, collapse, opacities, interstitial changes)

skin prick testing (atopic status)

total and specified IgE (atopic status)

Full blood count (eosinophilia (atopy)

atopy are likely to have asthma

87
Q

(adult asthma) assessment of acute asthma

A

ability to speak

heart rate

respiratory rate

PEF flow

oxygen saturation/arterial blood gas

88
Q

how is acute asthma graded (adult asthma)

A

moderate

severe

life-threatening

near-fatal

89
Q

(adult asthma)

moderate

symptoms

A

able to speak and complete sentences

RR <25

Ref 50-70% predicted or best

Sao2 >92% no need for ABG

pao2 >8kPa

90
Q

(adult asthma)

severe

symptoms

A

Any one of

inability to complete sentences in one breath

hr>110

RR >25

REF 33-50% predicted of best

Sao2>92%

pao2 >/8kpa

91
Q

(adult asthma)

life-threatening

symptoms

A

any one of

  • grunting; impaired consciousness; confusion: exhaustion; bradycardia/arrythmia/hypotension; PEF <33% predicted or best; cyanosis silent chest; poor respiratory effort

Sao2 <92% (definitely need blood gas!); pao2 <8kPa; Paco2 noemal (4.6-6.0kPa)

92
Q

(adult asthma)

near-fatal

Symptoms

A

Raised paCo2

need for mechanical ventilation

93
Q

for (adult asthma) treatment what is the goal

A
  • no daytime symptomes

no night time wakening

no need for rescue medication

no asthma attacks

no limitation on activity including exercise and normal function (in practical terms fev1 and or pef 80% predicted or best)

minimal side effects from medication

94
Q

what are non-pharmilogical management of (adult asthma)

A
  • patient education and self-management plans

exercise

smoking cessation

weight management

flu/pneumococcal vaccinations

95
Q

(adult asthma) inhalers

A

a small dose of the drug

delivery directly to the target organ (airway and lung)

the onset of effect is faster

minimal systemic exposure

systemic adverse effects are less severe and less frequent

96
Q

name the inhalers for symptom control

A

short-acting beta 2 agonists (SABA) relievers

salbutamol - meter dose inhaler andd DPI (side effect tremor and tachycardia)

terbutaline - DPI

97
Q

Name the oral therapies for (adult asthma)

A

Leukotreine receptor antagonist (montelucaste prob most common)

Theophylline

prednisolone

98
Q

treatment for mild/moderate (adult asthma) attack

A

Increase inhaler use

oral steroid

treat trigger

early follow up

backup plan

99
Q

how to teat a moderate/severe (adult asthma) acute asthma attack

A

hospital treatment

  • nebulisers - salbutalom ipratropium

oral/iv steroid (hydrocortisone iv short-acting + predisinolone (oral)

magnesium

aminophylline

triggers -infection/allergen

complications - chest xray

review

level 2/3 care (hdu itu)

100
Q

contract od asthma and COPD

A
  • age of onset

smoking history

response to treatment

treatment goals

trajectory

similar therapies

non-pharmacological interventions the same

101
Q

what is COPD definition

A

a lung disease characterised by chronic obstruction of airflow interfering with normal breathing and is not fully reversible

an umbrella term that also takes in to account chronic bronchitis and emphysema

102
Q

diagnosis of copd - symptoms of chronic bronchitis

A

cough and sputum for at least three months present in two consecutive years

103
Q

diagnosis of COPD - symptoms of emphysema

A

structural changes in the alveoli causing them to disintegrate - lose surface area

104
Q

what is main cause of COPD

A

smoking

105
Q

modifiable and non-modifiable causes of COPD

A

modifiable - smoking or low-income biomass of fuel cooking and heating, air pollution, geographical, temporal association, occupational

non-modifiable, female sex, increasing age.

106
Q

symptoms of COPD

A

cough

breathless

sputum

frequent chest infections

wheezing

weight loss

fatigue

swolen ankles

107
Q

copd key things to note symptom and factor

A

smoking history

age

onset/progression

108
Q

copd examination finding signs

A

cyanosis

pursed lip breathing

hyperinflated chest

raised jvp

using accessory muscles

peripheral oedema

cachexia severe weight loss

wheeze

109
Q

mmrc dyspnoea scale

A

0 - only breathless in strenuous exercise

1- short of breath when hurrying on level ground or walking up a slight hill

2 - on the level ground walk slower than people same age because of breathlessness or have to stop for breath when walking at my own pace

3 - I stop for breath after walking about 100 yards or after a few minutes on level ground

4 - I am too breathless to leave the house or I am breathless when dressing

110
Q

fev1 and ratio spirometry what indicates an abnormality

A

fev1<80% predicted normal

fvc <80% predicted normal

ratio fev1/fvc <0.7

111
Q

fev1 and ratio spirometry what indicates an obstructive disorder

A

fev1< 80%

fvc usually reduced but to a lesser extent than fev1

fev/fvc ratio <0.7

112
Q

fev1 and ratio spirometry what indicates a restrictive disorder

A

fev1 <80% predicted normal

fvc reduced (<80% predicted normal)

fev1.fvc ratio (>0.7)

113
Q

spirometry when diagnosing the severity: mild

A

stage 1, mild - FEV1 80% of predicted value or higher (diagnosis can only be made on basis of respiratory symptoms

114
Q

spirometry when diagnosing the severity: moderate

A

stage 2, moderate - fev1 50-79% predicted value

115
Q

spirometry when diagnosing the severity: severe

A

stage 3, severe - FEV1 30-49% of predicted value

116
Q

spirometry when diagnosing the severity: very severe

A

stage 4, very severe - fev1 less than 30% predicted value

117
Q

spirometry when diagnosing the severity: end-stage

A

end-stage COPD not part of the staging classification, but a term used in practice

118
Q

chest x-ray COPD

A

hyperinflation (more than 6 anterior ribs showing or 10 posterior ribs)

flat diaphragm

small heart

bulla (from emphysema)

119
Q

It is likely that allergies cause the development of childhood asthma.

Select one:

True

False

A

False – it is likely that an underlying abnormality in the epithelium leads to the development of both asthma and allergies.

120
Q

other tests for COPD

A

spirometry

then pulmonary function tests - lung vol - transfer of gas

radiology (high resolution computed tomography hrct)

121
Q

where is emphysema usually found in smokers

A

upper area of lungs due to inhalation injury to tissues

122
Q

acute COPD exacerbation what will be reported

A

worsening symptoms - unable to smoke; short of breath; systemic upset (eating drinking ADL); wheeze; tight chest; temperature (if infection); cough; fatigue; sputum purulence and volume

123
Q

signs of severe copd exacerbation

A

breathless and resp rate over 25 min

significant decrease in exercise tolerance

using accessory muscles at rest

signs of sepsis (if infection(

purse lip breathing

fluid retention, cyanosis spo2 92% on air; confusion

124
Q

differential diagnosis for COPD

A

pneumonia; pulmonary embolism, myocardial infarction, lung cancer, pleural effusion, pneumothorax

125
Q

management of COPD

A

change inhalers (technique, device, add bronchodilator, increase or add inhaled steroid)

oral steroid - prednisolone tablet

antibiotics

self-management for select patients

126
Q

acute exacerbation visual symptoms, test and treatment

A

confusion; cyanosis; severe breathlessness; flapping tremor; drowsy; pyrexial; wheeze; tripod position

tests - chest x-ray, blood gases. full blood count, u+E, sputum culture, Viral throat swab

treat - o2 therapy, nebulised bronchodilator (beta 2 agonist and antimuscarinic) oral/iv corticosteroid +/- antibiotic

(iv aminophylline, respiratory stimulant NIV)

127
Q

severe copd exacerbation tests

A

tests - chest x-ray, blood gases. full blood count, u+E, sputum culture, Viral throat swab

treat - o2 therapy, nebulised bronchodilator (beta 2 agonist and antimuscarinic) oral/iv corticosteroid +/- antibiotic

(iv aminophylline, respiratory stimulant NIV)

128
Q

severe copd exaverbation - treatment

A

treat - o2 therapy, nebulised bronchodilator (beta 2 agonist and antimuscarinic) oral/iv corticosteroid +/- antibiotic

(iv aminophylline, respiratory stimulant NIV)

treat other co-existing conditions

129
Q

Severe disease - respiratory failure cause

A

cause by reduces v/q match (ventilation/perfusion)

increased physiological dead space due to emphysema

130
Q

types of respiratory failure

A

type 1: reduces p02

type 2 reduces po2 and increased pco2 (ventilatory failure)

131
Q

how often do you have type 2 respiratory failure?

A

severe cases of COPD

132
Q

Signs of respiratory failure

A

flapping tremor - co2 retention hypercapnia

become acidotic and risk death

133
Q

explain cor pulmonale

A

right-sided heart failure due to lung disease - comes from smoking and hypoxia

symptom - tachycardia, oedematous, raised JVP, congested liver

ECG shows right axis deviation, p pulmonale, t wave inversion on v1-v4

echo: pulmonary hypertension, tricuspid regurgitation

134
Q

in severe copd why does oedema occur

A

cor pulmonale right-side heart failure, cause a backup of blood. causes reduce circulation volume of blood - activates a compensatory system of kidneys RAAS system - leads to fluid retention

135
Q

Why would COPD have raised harmoglobin?

A

secondary polycythemia - body produces increased erythropoietin in response to low 02 levels. increases haemoglobin, haematocrit and blood viscosity

136
Q

what is NOT a cause of COPD in osce

A

finger clubbing is NOT a symptom of COPD

137
Q

what is public health measure to prevent COPD

A

age to purchase tobacco raised from 16 - 18

picture warnings

sale of tobacco banned in vending machines

ban smoking in cars with children

standardised packagine

138
Q

the treatment plan for COPD goals

A

improve exercise tolerance

prevent exacerbation

nutrition/weight loss

complications (cor pulmonale, respiratory failure)

anxiety/depression

co-morbidities

dysfunctional breathing

palliative care

139
Q

non-pharmicological management COPD

A

SMOKING CESSATION

VACCINATION FLU/PNEUMOCOCCAL

pulmonary rehabilitation

nutritional assessment

psychological support

140
Q

pharmacological goal of COPD

A

relieve symptoms

prevent exacerbations

improve quality of life

141
Q

Inhaled therapy for COPD

A

Short-acting bronchodilators: SABA salbutamol SAMA ipratropium

long-acting bronchodilators: LAMA long-acting antimuscarinic agents - umeclidinium, tiotropium LABA long-acting beta2 agonist - salmeterol

high dose inhaled corticosteroids ics and laba - relvar - fluticasone/vilanterol; fostair MDI

142
Q

A child under 5 with a new diagnosis of asthma who is symptomatic more than 3 times a week should be started on a leukotriene receptor antagonist.

Select one:

True

False

A

True – the initial preventer medication for under 5s is a LRTA. For children over 5, it is a very low dose inhaled corticosteroid.

The correct answer is ‘True’.

143
Q

Pharmacological treatments (i.e. inhalers) give the best value for money in terms of improvement in quality of life for patients with COPD.

Select one:

True

False

A

False – the best value for money in QALY (quality-adjusted life-years) is from flu vaccination, smoking cessation and pulmonary rehabilitation. Non-pharmacological interventions in COPD are very effective and very important.

The correct answer is ‘False’.

144
Q

he hallmark of obstructive lung disease is reduced FVC.

Select one:

True

False

A

False – although the FVC may be reduced, for a lung disease to be considered obstructive there needs to be reduced FEV1:FVC (less than 0.7).

The correct answer is ‘False’.

145
Q

Decline in FEV1 over time can be reversed by stopping smoking.

Select one:

True

False

A

False – Decline in FEV1 is irreversible, however the rate of decline can be slowed.

The correct answer is ‘False’.

146
Q

It is important to take a history and perform a full respiratory examination before diagnosing a child with asthma.

Select one:

True

False

A

False – examination findings are likely to be normal. Diagnosis is from the history!

The correct answer is ‘False’.

147
Q

An excess of alpha-1-antitrypsin can lead to emphysema.

Select one:

True

False

A

False – alpha-1 antitrypsin is an enzyme which breaks down other enzymes that break down alveolar tissue. A deficiency of this enzyme tips the balance towards tissue destruction and can lead to emphysema

The correct answer is ‘False’.

148
Q

Respiratory failure in COPD is due to V/Q (Ventilation/Perfusion) mismatch.

Select one:

True

False

A

False – generally speaking, respiratory failure in COPD is due to matched defect in ventilation and perfusion. Remember that oxygenation will be impaired in any situation where blood is not getting to the alveoli (perfusion) or air is not getting to the alveoli (ventilation). In COPD, both are affected.

The correct answer is ‘False’.

149
Q

In spirometry, an FEV1:FVC of 0.5 would be considered obstructive.

Select one:

True

False

A

True – normal FEV1:FVC is about 0.7-0.8.

The correct answer is ‘True’.

150
Q

Peripheral eosinophilia is not diagnostic of asthma.

Select one:

True

False

A

True – while a peripheral eosinophilia may be suggestive of atopy (remember this is the cluster of conditions including asthma, eczema, hayfever, allergic rhinitis and other allergies), it’s important to remember that there is NO diagnostic test for asthma. Diagnosis is primarily from the history, and some tests are useful to help you gather additional information.

The correct answer is ‘True’.

151
Q

Spirometry is required to diagnose COPD.

Select one:

True

False

A

True – unlike asthma, the diagnosis of COPD requires both typical symptoms and history AND typical spirometry showing airflow obstruction. Spirometry is performed pre- and post-bronchodilator therapy, to demonstrate non-reversible (or partially reversible) obstruction.

The correct answer is ‘True’.

152
Q

Initial treatment of asthma in adults is with a low-dose inhaled corticosteroid.

Select one:

True

False

A

True – it is now known that inhaled steroids are the most effective initial treatment, and are given as a trial to assist in the diagnosis of asthma.

The correct answer is ‘True’.

153
Q

Carbon monoxide gas transfer in asthma can be normal or increased.

Select one:

True

False

A

True – gas transfer is calculated by measuring uptake of carbon monoxide, and can be helpful to distinguish between COPD and Asthma. It is reduced in COPD due to alveolar destruction. In asthma it should be normal or slightly increased.

The correct answer is ‘True’.

154
Q

In moderate or severe exacerbations of asthma, the pCO2 is normal.

Select one:

True

False

A

False – this is really important. In moderate or severe exacerbations of asthma, the respiratory rate goes up, so you would expect more CO2 to be blown off, therefore the pCO2 (measurement of the amount of CO2 dissolved in the blood, shown on a blood gas analysis) should be LOW. If a patient is having an acute asthma attack with a high respiratory rate and their pCO2 is “normal”, this means they are not ventilating adequately, and this is an indication that they require specialist input urgently as their asthma is life-threatening.

The correct answer is ‘False’.

155
Q

A child >5 on a very low dose inhaled corticosteroid who continues to require their reliever inhaler twice a week should have a long-acting beta-agonist added on to their treatment.

Select one:

True

False

A

True – the BTS/SIGN guidelines would recommend a long-acting beta agonist (LABA) as the next step, and this would be a reasonable next step as per other guidelines.

The correct answer is ‘True’.

156
Q

Smoking tends to cause emphysema in the bases of the lungs.

Select one:

True

False

A

False – as emphysema from smoking is caused by inhaled pathogens, it tends to occur in the region of the lung most easily reached by inhaled smoke: the apex. Contrast this to alpha-1-antitrypsin deficiency, where the resulting emphysema tends to affect the base.

The correct answer is ‘False’.

157
Q

For a diagnosis of chronic bronchitis to be given, a patient should have a cough productive of sputum most days, for 3 consecutive months, for at least 3 years.

Select one:

True

False

A

False – it only needs to be for 2 years.

The correct answer is ‘False’.

158
Q

In an acute asthma attack, steroids should be given via a nebuliser rather than through a metered-dose inhaler.

Select one:

True

False

A

False – in an acute asthma attack, steroids should be given orally, or sometimes intravenously.

The correct answer is ‘False’.

159
Q

Hypoxia increases the blood pressure in the lungs in COPD.

Select one:

True

False

A

True – hypoxia leads to a reflex constriction of blood vessels in the lungs. This increases the vascular resistance, meaning the right side of the heart has to work harder, and the blood pressure rises. This is called pulmonary hypertension.

The correct answer is ‘True’.

160
Q

Most infections causing exacerbations of COPD are viral.

Select one:

True

False

A

True – although patients will often receive antibiotics for acute infective exacerbations of COPD, in the majority of cases the pathogen is a virus.

The correct answer is ‘True’.

161
Q

Centri-acinar emphysema begins with dilatation of the alveoli.

Select one:

True

False

A

False – centri-acinar emphysema begins with dilatation of the respiratory bronchiole, and then progresses to loss of alveolar tissue.

The correct answer is ‘False’.

162
Q

Forced Vital Capacity (FVC) divided by the Forced Expired Volume in one second (FEV1) is a useful clinical measure of lung function.

Select one:

True

False

A

False. That statement is the wrong way round. A useful clinical measure of lung function is FEV1 divided by FVC (not the other way around). This tells you what proportion of the FVC a patient can exhale in one second.

The correct answer is ‘False’.

163
Q

The saturation of haemoglobin decreases as blood passes through the tissues because of an increase in pH.

Select one:

True

False

A

False. Haemoglobin saturation decreases as blood passes through the tissue because the tissues have a lower partial pressure of oxygen (40mmHg) than is found in the plasma (100mmHg). As such oxygen moves down its partial pressure gradient into the tissues until equilibrium is reached. Alkalosis (a rise in extracellular fluid pH) actually causes haemoglobin to hang onto its oxygen more – it increases the affinity of haemoglobin for oxygen so would increase saturation.

164
Q

A pneumothorax (air in the pleural cavity) disrupts the relationship between the visceral pleural membrane and the lungs

Select one:

True

False

A

False. It disrupts the relationship between the parietal pleural membrane and the visceral pleural membrane. The visceral pleural membrane would remain attached to the lung surface in a pneumothorax.

165
Q

The haemoglobin-O2 saturation curve is moved to the left by a decrease in body temperature..

Select one:

True

False

A

True. A decrease in body temperature increases the affinity of haemoglobin for oxygen and thus shifts the binding curve to the left. This is one of the reasons hypothermia is so dangerous – at a body temperature of 20oC the haemoglobin remains fully saturated meaning while the blood is jam packed full of oxygen the peripheral tissues cannot access it because the haemoglobin won’t release it.

166
Q

lveolar ventilation volume is more than pulmonary ventilation volume.

Select one:

True

False

A

False. Pulmonary (or minute) ventilation describes the total amount of air breathed in or out per minute (basically tidal volume x respiration rate). Alveolar ventilation accounts for the volume of air that gets stuck in dead space and never reaches the alveoli, so dead space volume must be subtracted from tidal volume before multiplying by respiration rate ((TV-DS) x RR), making alveolar ventilation smaller than pulmonary ventilation i.e. not all the air you breathe in reaches the level of the alveoli and participates in gas exchange!

167
Q

shift of the oxygen dissociation curve of haemoglobin to the right decreases the oxygen content of blood at a given oxygen pressure.

Select one:

True

False

A

True. A rightward shift means that for any given value of PO2, less oxygen will be bound to haemoglobin than if that shift had not happened – look at the S shaped curve if you don’t believe it!

The correct answer is ‘True’.

168
Q

Respiratory acidosis often accompanies severe lung pathology.

Select one:

True

False

A

True. Most lung pathologies lead to an impairment of gas exchange for one reason or another. This impairment increases CO2 levels in arterial blood. An increase in CO2 leads to an increase in H+ concentration (revise the chemical equation shown in the lectures if you don’t understand why this happens). As the increase in H+ are due to respiratory dysfunction this is called a respiratory acidosis.

169
Q

Lung compliance is defined as the magnitude of the change in lung volume produced by a given change in transpulmonary pressure.

Select one:

True

False

A

True. Compliance describes the change in lung volume for any given change in transpulmonary pressure (sometimes graphs show intrapleural pressure rather than TP but the effect is the same).

170
Q

A pneumothorax (air in the pleural cavity) increases the functional residual capacity.

Select one:

True

False

A

False. FRC (volume of air left in the lungs after a forced expiration) will decrease in pneumothorax as the affected lung has recoiled and thus has a smaller volume than before.

171
Q

During quiet inspiration in the upright position, most of the tidal volume is distributed to alveoli at the base of the lung

Select one:

True

False

A

True. Compliance is greatest at the base of the lung so a greater volume of inspired air ends up at the base of the lung compared to the apex.

172
Q

The sum of the resting tidal volume and the inspiratory reserve volume is the inspiratory capacity

Select one:

True

False

A

True. This is the volume of air you are capable of inspiring.

The correct answer is ‘True’.

173
Q

criteria for long term o2 COPD

A

quit smoking for at least 6 months

stay hypoxic so blood gas is <7.3

be hypoxic at rest

or pao2 7.3-8kpa if@ polycythaemia; nocturnal hypoxia; peripheral oedema; pulmonary hypertension

174
Q

what kind of infection is most common in COPD

A

viral infection

175
Q

primary care management acute exacerbation of COPD

A

Short-acting bronchodilators (SABA) salbutamol SAMA ipratropium - nebs if cannot use inhalers

steroids - prednisolone 40mg per day for 5-7 days

antibiotic - most exacerbation viral - if evidence infection (fever, increase volume/purulence sputum)

consider hospital admission if unwell (tachycardia. low spo2 <90-92%) and hypotension

176
Q

acute exacerbation COPD - investigation

A
  • full blood count - biochemistry and glucose - theophylline concentration (in patients using theophylline preparation) - arterial blood gas documenting amount of o2 given and by what device - ECG - chest x-ray - blood cultures in febrile patients - sputum microscopy, culture and sensitivity
177
Q

acuse exacerbation of COPD - ward bade management

A

02 therapy keep spo2 88-92%

nebulised bronchidilators

  • corticosteroids
  • antibiotics (oral vs Iv)

assess for evidence of respiratory failure - clinical - arterial blood gas (ABG)

178
Q

acute exacerbation COPD - when in respiratory failure what do you consider

A

non-invasive ventilation (NIV)

179
Q

COPD palliative considerations

A

teach management of breathlessness and dysfunctional breathing - pharmacological help (morphine) - psychological support - palliative care referral

anticipatory care planning - hospital admission planning - ceiling of treatment - ward-based HDU - DNACPR

180
Q

Emphysema is the dilatation of bronchioles leading to air trapping.

Select one:

True

False

A

False – emphysema is the increase in size of the airspaces that are distal to the terminal bronchioles (i.e. the respiratory bronchioles and alveoli). This can be due to dilatation or destruction of their walls, and causes obstruction through air trapping.

181
Q

In assessing severity of acute asthma in adults, subjective parameters (eg. distress) are just as important as observations and blood gases.

Select one:

True

False

A

False – patients and doctors tend to underestimate asthma severity, and a life-threatening attack may not be associated with significant distress. Objective measurements such as vital observations (pulse rate, oxygen saturations, peak flow) and blood gas analysis are most useful.

182
Q

The initial treatment for asthma in children over 5 is very low dose oral steroids.

Select one:

True

False

A

False – very low dose inhaled steroids are the initial treatment for paediatric asthma. Oral steroids are only used by specialists in treatment-resistant asthma.

183
Q

Omalizumab is a specialist treatment for asthma, and dampens all components of the inflammatory response.

Select one:

True

False

A

False – omalizumab is a specialist treatment, and is termed a “biologic” because it is an antibody. It specifically targets IgE (an antibody involved in the allergy response), compared to e.g. prednisolone which has a much more generalised anti-inflammatory action.

184
Q

Washing a spacer device before using it increases the static charge and decreases the drug delivery to the lungs.

Select one:

True

False

A

False – washing the spacer device leaves a coating of detergent, which will decrease the static charge. This means the drug is less likely to stick to the spacer, and increases drug delivery to the lungs.

185
Q

Treatment-resistant, severe asthma is relatively common in children.

Select one:

True

False

A

False – Severe airways disease that does not respond to maximal treatment is extremely uncommon in children. More commonly, there are complex psychological and illness behaviour elements to the presentation, which can include not taking the treatment as prescribed. These should be thoroughly explored as part of the patient-centred management.

186
Q

Spirometry is required to diagnose chronic bronchitis.

Select one:

True

False

A

False – it is a clinical diagnosis, meaning there are no specific tests for chronic bronchitis.

187
Q

Terbutaline is a short-acting beta agonist used as a reliever medication in asthma.

Select one:

True

False

A

True – although salbutamol is the most commonly-used reliever medication, terbutaline is also used.

188
Q

The prevalence of COPD is increasing, but the incidence is decreasing.

Select one:

True

False

A

True – remember that “prevalence” refers to the total number of people with a condition at any given moment, while “incidence” refers to the rate of new diagnoses.

189
Q

Asthma is associated with low exhaled nitric oxide (FeNO) due to airway inflammation.

Select one:

True

False

A

False – FeNO works like a breathalyser for airway inflammation. A high degree of inflammation will lead to a high FeNO, which would be suggestive of asthma.

190
Q

Female sex is a risk factor for COPD.

Select one:

True

False

A

True – although the prevalence of COPD among males has historically been higher than that among females (due to a higher prevalence of smoking), a female smoker is more likely to develop COPD than a male smoker.

191
Q

Ipratropium bromide is a long-acting beta agonist.

Select one:

True

False

A

False – ipratropium bromide is a muscarinic antagonist. It works by relaxing the smooth muscle of the airways.

192
Q

Patients are eligible for longterm oxygen therapy if they have a PaO2 of <7.3 AND additional complications of chronic hypoxia.

Select one:

True

False

A

False – patients are eligible for LTOT if they have a PaO2 (measured from an arterial blood sample) of <7.3 regardless of additional features. If they have complications of chronic hypoxia such as polycythaemia, pulmonary hypertension, peripheral oedema or nocturnal worsening of hypoxia, LTOT is offered sooner, at a PaO2 of <8.

193
Q

More than 50% of long-term smokers will develop COPD.

Select one:

True

False

A

False – surprisingly, less than half of long-term smokers will develop COPD in their lifetime. This demonstrates the interaction between genetic predisposition and environmental factors in the development of COPD

194
Q

In moderate or severe exacerbations of asthma, the pCO2 is normal.

Select one:

True

False

A

False – this is really important. In moderate or severe exacerbations of asthma, the respiratory rate goes up, so you would expect more CO2 to be blown off, therefore the pCO2 (measurement of the amount of CO2 dissolved in the blood, shown on a blood gas analysis) should be LOW. If a patient is having an acute asthma attack with a high respiratory rate and their pCO2 is “normal”, this means they are not ventilating adequately, and this is an indication that they require specialist input urgently as their asthma is life-threatening.

195
Q
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Medicine 1 (Year 1) (15 decks)

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