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Year 3 > Week Two - Case One > Flashcards

Week Two - Case One Flashcards

1
Q

what are the three main characteristics of asthma

A

airflow limitation

airway hyper-responsiveness

inflammation of the bronchi

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2
Q

how many patients in the UK die a year from asthma

A

2000

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3
Q

what is associated with the inflammation of the bronchi

A

with infiltration by eosinophils, T cells and mast cells. there is associated plasma exudate, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage.

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4
Q

what often causes an asthmatic flare and what symptom does this bring

A

often flares up with viral infections which often causes a loud wheeze

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5
Q

who Is most likely to be affected before/after puberty

A

before puberty, boys are more likely to be affected

after puberty, girls are most likely to be affected

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6
Q

is asthma intrinsic or extrinsic

A

the disease can either be intrinsic (aka cryptogenic) where no causatory factor can be found, or extrinsic, where there is a definite external cause

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7
Q

when does intrinsic asthma often start

A

often starts in middle age, and is sometimes called late onset asthma.

no trigger can be identified

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8
Q

when does extrinsic asthma occur

A

in atopic individuals who have positive skin prick test results.

this type of asthma causes 90% of childhood cases, and 50% of adults with chronic asthma.

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9
Q

what is extrinsic asthma often accompanied by

A

eczema

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10
Q

how do non-atopic individuals develop asthma in later life

A

via sensitisation to occupational agents, aspirin, or as a result of taking Beta-blockers for hypertension or angina

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11
Q

what kind of reaction is extrinsic asthma

A

involves a type 1 hypersensitivity reaction to inhaled allergens

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12
Q

what other reaction happens with asthma

A

there is also a delayed phase reaction, type IV hypersensitivity which occurs hours-days after exposure

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13
Q

what does the term atopy describe

A

people who often have allergies/asthma/hayfever and where the trait runs in families

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14
Q

what gene is associated with airway hyper-responsiveness and airway remodelling

A

ADAM33

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15
Q

what gene is associated with increased IgE production

A

PHF11 gene

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16
Q

what antibodies do people have to many common allergens

A

IgE antibodies - these antibodies are present in 35% of the population

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17
Q

what is the hygiene hypothesis

A

this is a theory that states that growing up in a clean environment in the early years of life can cause atopy. if you grow up in a dirty environment and are exposed to various bacteria, this is thought to help direct your immune system away from recognising inert particles as allergens.

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18
Q

what are the allergens for asthma very similar to

A

very similar to the allergens that cause rhinitis.

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19
Q

what is rhinitis

A

is inflammation of the mucosal lining of the upper respiratory tract, particularly affecting areas near the nose

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20
Q

what can rhinitis cause

A

a constant runny nose

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21
Q

how can you test airway hyper-responsiveness

A

asking patient to inhale gradually increasing amounts of methacholine or histamine.

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22
Q

what is this test called

A

bronchial provovation test

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23
Q

what does this test induce

A

will induce transient airflow limitation in 20% of the population - and these are the patients that exhibit airway hyper-responsiveness

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24
Q

what are the features of non-atopic asthma

A

does not appear to be immunologically mediated - i.e there is not T cell involvement

associated with recurrent respiratory tract infection (viral)

skin tests are negative

bronchoconstriction due to airway hyper-responsiveness , not as much due to inflammation and leukocyte infliltration

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25
Q

what is the mechanism of aspirin induced asthma

A

mechanism is unknown but thought to be due to increased leukotrienes and decreased prostaglandins which leads to increased airway irritability

aspirin inhibits COX enzymes. This reduces the production of prostaglandins. However, prostaglandin E2 controls leukotriene production - thus in some patients this allows overproduction of leukotrienes and allows for an abnormal inflammatory reaction.

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26
Q

what kind of drug can this also occur with

A

NSAIDs such as ibuprofen.

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27
Q

what is a relative contra-indication

A

ibuprofen

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28
Q

what is occupational asthma

A

asthma induced by hypersensitivity to an agent at work - probably a combination of types I and IV hypersensitivity reactions

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29
Q

what products can cause asthma via an IgE-independent route

A

paints, varnishes and sprays

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30
Q

what do paints, varnishes and sprays do

A

bind directly to T cells (activating them) and other epithelial cells, without IgE

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31
Q

what kind of food diet can precipitate attacks

A

a high sodium and low magnesium diet

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32
Q

next questions are about pathology

A
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33
Q

what will happen to CD4 T cells when there is exposure to the antigen

A

CD4 T cells will differentiate into T helper cells (Th2 type, as opposed to Th1)

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34
Q

what will these T helper cells begin to secrete

A

IL4 and IL5

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35
Q

what will IL4 cause

A

IL-4 will cause B cells to become plasma cells and begin secreting IgE

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36
Q

what will IL-5 do

A

act on eosinophils and mast cells, making them reactive to the new antigen.

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37
Q

what does this IgE do

A

binds to mast cells in the mucosa

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38
Q

will this initial exposure cause an allergic reaction

A

no

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39
Q

what is this initial exposure

A

the IgE binding to the mast cells in the mucosa.

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40
Q

what does the IgE do on the mast cell

A

it just sits there, waiting to come into contact with the antigen again, perhaps for years

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41
Q

what happens upon re-exposure to the antigen

A

the mast cell will be activated, and will degranulate.

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42
Q

what does this degranulation do

A

causes the release of inflammatory mediators

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43
Q

what are there increased numbers of in both the airway secretion and epithelial lining of lungs in asthmatics

A

increased numbers of mast cells.

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44
Q

what does this increased number of mast cells lead to

A

increased response to any antigens

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45
Q

what does this cause

A

the initial asthma attack

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46
Q

what is this initial asthma attack a result of

A

histamine and prostaglandin (as well as leukotrienes; particularly LTC4) release by mast cells.

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47
Q

what is responsible for the early attack

A

mast cells

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48
Q

what does histamine cause

A

smooth muscle contraction, increased bronchial secretions, and increased vascular permeability

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49
Q

what is the late phase reaction and when does it occur

A

occurs several hours after the initial reaction.

it is causes by the accumulation of eosinophils at the site

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50
Q

which phase is a more sustained inflammation

A

the late phase. the initial phase is more bronchoconstriciton without much underlying inflammation

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51
Q

what are good at treating the initial phase reaction

A

bronchodilators (beta-adrenergics)

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52
Q

what are good at preventing the inflammation that causes the late phase reaction

A

steroids and other anti-inflammatories

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53
Q

what may also happen in the late phase reaction

A

there may also be activation of platelets

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54
Q

what does activation of platelets lead to

A

micro thrombi in the lumen

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55
Q

what are the effects of bronchoconstriction on the distal airway

A

there will be distal airway hyperinflation and collapse (and reduced gaseous transfer to these regions)

56
Q

what will happen in the bronchi

A

mucus plugging

57
Q

what is this mucus plugging in the bronchi due to

A

increased number of goblet cells

58
Q

what are Curschmann’s spirals

A

these are bits of epithelium that have been shed, and can be seen on histology of the mucous plugs

59
Q

what are Charcot-Layden crystals

A

crystals that are formed as a result of eosinophil aggregation

60
Q

what occurs via the process of remodelling

A

thickening of the bronchial basement membrane.

the submucosa becomes thickened, which means that when the smooth muscle does contract, there is an excessive narrowing of the airway and response to the contraction.

61
Q

what are the effects of bronchoconstriction and inflammation on the epithelium

A

the epithelium loses many of its columnar ciliated cells, and these are replaced with over-active mucous secreting cells.

62
Q

what does the mucosa release

A

lots of inflammatory proteins

63
Q

what are the effects of bronchoconstriction and inflammation on smooth muscle

A

the smooth muscle is hypertrophied and also undergoes changes which make it more likely to contract, and more likely to stay contracted for longer

64
Q

what does cold air and exercise do to the mucosa of the lungs

A

these both dry out the mucosa of the lung, which makes the lining hyperosmolar

65
Q

what does this hyperosmolar lining lead to

A

causes mast cells to release histamine and prostaglandins, thus causing inflammation

66
Q

what does atmospheric pollution do to asthma

A

large amounts of dust, cigarette smoke, car fumes and other allergens can trigger asthma in some individuals.

ozone has been a trigger in the past

67
Q

what kind of diet is protective from asthma

A

high intake of fruit and vegetables possibly due to the large amounts of anti-oxidants

68
Q

what its the ADAM33 gene thought to be responsible

A

for the release of factors by eosinophils

69
Q

what are some of the factors released by eosinophils and what do they cause

A

MBP, ECP

these factors cause remodelling of the epithelium and stimulate growth of fibroblasts.

this increases the amount of smooth muscle present

70
Q

what is the end result of these factors being released

A

increased airway hyperresponsiveness

71
Q

what does the normal process of bronchoconstriction occur in response to

A

occurs in response to direct parasympathetic stimulation

72
Q

what is antagonism to this effect produced by

A

freely circulating adrenaline that acts upon beta-receptors

73
Q

what have been known to induce attacks in asthmatic patients

A

beta-blockers because they prevent adrenaline from doing its job

74
Q

what are the 7 clinical features of asthma

A

Wheezing attacks

Periodic shortness of breath

Symptoms often worse during the night

Cough is frequent – and often misdiagnosed as bronchitis

Nocturnal cough alone can be a presenting feature

Some patients can have chronic symptoms

Attacks precipitated by a very wide range of triggers

75
Q

what is thought to be the most useful test for asthma

A

twice daily measurements of PEF is probably the most useful test

76
Q

what is PEF

A

the peak expiratory flow.

patients should take two readings per day, to show the variability of the disease

77
Q

what should you get patients who have suspected asthma to do

A

get them to take two weeks worth of measurements whilst at work, and 2 weeks whilst at home, to prove the cause of the disease

78
Q

what is the spirometry test you can do to show the presence of asthma

A

demonstrate a 15% improvement in FEV1 or PEF following the inhalation of a bronchodilator

79
Q

what will the picture be of

A

an obstructive disease

80
Q

what would the carbon monoxide transfer test show in an asthmatic

A

nothing, it would be normal

81
Q

what happens to nitrous oxide levels in asthmatic’s breath

A

levels of NO are raised

82
Q

what test is often used to diagnose children with asthma

A

the exercise test

83
Q

describe how to perform an exercise test

A

the child should run on a treadmill for a max of 6 minutes
- enough to increase the heart rate till at least 160bpm

then test the peak flow before and after

test every 15 minutes after, again looking for a 15% difference

84
Q

does a negative test rule out asthma

A

no

85
Q

what does the histamine or metacholine bronchial provocation test indicate

A

hyper-responsiveness - which is found in most asthmatics

86
Q

what is the histamine or metacholine bronchial provocation test most useful for

A

diagnosing patients who’s main or only symptom is a cough

87
Q

what does the dose of the drug in the histamine or metacholine bronchial provocation test need to produce

A

needs to produce a 20% drop in FEV1 and is called the PD20 FEV1

patients with airway hyperresponsiveness require only a very small dose to achieve this

88
Q

who should the histamine or metacholine bronchial provocation test not be performed on

A

those with brittle asthma, or those who have an FEV1<1.5L

89
Q

what improvement in the FEV1 always demonstrates the presence of asthma

A

> 15% improvement

90
Q

what test is not diagnostic on its own but may help form your diagnosis

A

blood and sputum tests that you can test for high number of eosinophils

91
Q

what will a CXR of an asthmatic show

A

this will be normal, unless they are having a particularly bad exacerbation, in which case, overinflation may be present

92
Q

what is the CXR good at doing

A

excluding the possibility of a pnevumothorax

93
Q

when should you perform skin prick tests

A

should perform these on all newly diagnosed asthmatics to help find a cause

94
Q

what is an absolute contra-indication for asthmatics

A

taking beta-blockers in any form

95
Q

what is step one, mild intermittent and exercise induced asthma defined as (6 things)

A

Symptoms ≤2 times a week

Asymptomatic and normal peak expiratory flow (PEF) between attacks

Attacks are brief with varying intensity

Night-time symptoms ≤2 times a month

Forced expiratory flow at 1 second (FEV1) or PEF ≥80% of predicted

PEF variability <20%.

96
Q

what is sufficient alone to treat mild intermittent asthma or exercise induced asthma (step1)

A

the use of a SABA as required is sufficient alone.

97
Q

what is step 2, mild persistent asthma defined as (5 things)

A

Symptoms >2 times a week but <1 time a day

Exacerbations may affect activity

Night-time symptoms >2 times a month

FEV1 ≥80% of predicted

PEF variability between 20% and 30%.

98
Q

what are added if control is not achieved with SABA in type 2, mild persistent asthma

A

low dose inhaled corticosteroids are added.

99
Q

what can be used in step 2 asthma (mild persistent) instead of inhaled corticosteroids

A

either sodium cromoglicate, leukotriene receptor antagonists (LRTA), nedocromil or theophylline.

100
Q

what is step 3, moderate persistent asthma defined as (7 things)

A

Daily symptoms

Use of short-acting beta agonists daily

Attacks affect activity

Exacerbations ≥2 times a week and may last for days

Night-time symptoms >1 time a week

FEV1 greater than 60% to less than 80% of predicted

PEF variability >30%.

101
Q

what is added in treatment for step 3, moderate persistent asthma

A

adds LABA to step 2 therapy (SABA and low-dose ICS)
OR
increase low dose ICS to medium dose ICS.

102
Q

what are second line alternatives to either increasing ICS dose or adding a LABA

A

combine SABA as needed and ICS with either LRTA’s, theophylline or zileuton

103
Q

what is step4-6, severe persistent asthma defined as (6 things)

A

Continual symptoms

Limited physical activity

Frequent exacerbations

Frequent night-time symptoms

FEV1 ≤60% of predicted

PEF variability >60%.

104
Q

what is the preferred combination of treatment for step 4, severe persistent asthma

A

medium-dose ICS plus LABA plus SABA as needed.

105
Q

what can LABA be substituted for

A

either LRTA, theophylline or zileuton

106
Q

what happens in step 5

A

changes medium-dose ICS to high-dose ICS

107
Q

what can also be considered in stage 5 for patients with allergies

A

immunodilators such as omalizumab

108
Q

what happens in step 6

A

adds oral corticosteroids to existing treatments

109
Q

what may be added to the use of beta2 agonists in an acute asthma attack

A

theophylline and aminohpyline (aminophyline is metabolised to theophylline)

110
Q

what is omalizumab

A

a drug that forms completes with free IgE, and prevents it binding to inflammatory cells

111
Q

what is status asthmatics

A

this is asthma that has failed to resolve within 12 hours of therapy use

we now use the term acute severe asthma

112
Q

what are the features of acute severe asthma

A

inability to complete a sentence in one breath

RR>25

tachycardia >110bpm

PEF<50% predicted

113
Q

what are the features of a life threatening attack

A

silent chest

feeble respiratory effort

cyanosis

exhaustion

bradycardia

hypotension

confusion or coma

PEF <30% predicted normal or best (approx 150L/min in adults)

114
Q

what is pulsus paradoxis

A

on inspiration, the diastolic pressure decreases by 10mmHg. this is present in about 45% of cases

115
Q

what is the hospital management for a severe acute asthma attack

A

(Do an ABG – it may be life-threatening if:
CO2 > 5kPa (high)
O2 <8kPa (low)
Low pH

Start on 100% O2 (non-rebreathing mask) with the patient sat upright in bed

Give 5mg salbutamol with 0.5mg ipratropium bromide via nebulizer on 100% O2

Give hydrocortisone 100mg IV or 50mg prednisolone orally. Give both if very unwell

Do CXR to exclude pneumothorax

116
Q

what are the 4 steps if life threatening steps are present

A

Inform ITU and seniors

Give magnesium sulphate 1.2-2g IV over 20 minutes

Change the nebulized salbutamol every 15 minutes, or give 10mg continuously per hour. Only give more ipratropium every 4-6 hours

Repeat PEF every 15-30 minutes to assess the situation. If improving then gradually reduce O2 and nebs. If not, try and find senior, keep giving nebs, and consider aminophyline.
Check pulse oximetry – aiming for sats >92%
Check blood gases every 2 hours, and definitely within 2 hours of admission
Record PEF’s and β-agonists when given / carried out
A maximum of 60mg/day of prednisolone can be given (orally)
You can give 200mg hydrocortisone every 4 hours for a max of 24 hours
Give oral prednisolone for 5 days after they are starting to recover
Ventilation is an option – you would have to call an anaesthetist
Patients have to have >75% predicted PEF for discharge

117
Q

what should be continued after a severe asthma attack

A

oral corticosteroids should be continued until the PEF rate is at least 80% of the patient’s previous best

118
Q

what is brittle asthma

A

catastrophic sudden severe asthma

119
Q

what do steroids cause an increased risk for

A

peptic ulcers

120
Q

can anaemia cause breathlessness

A

yes, especially in younger patients including young females who may have menorrhagia leading to anaemia which can cause breathlessness

121
Q

what tests do you run to confirm diagnosis of asthma as demonstrated in NICE guidelines

A

-peak flow
- peak flow diary
- exhaled nitric oxide
- spirometry

122
Q

how are patients predicted peak flows calculated

A

you need to know the gender, age, and height to calculate the Patient’s predicted peak flow

123
Q

what do normal adult peak flow scores range between

A

400-700 litres per minute

124
Q

how long before exercise should you use a SABA (salbutamol - blue inhaler)

A

15 mins

125
Q

if someone is waking frequently at night what also may a GP prescribe as well as a SABA

A

a low dose ICS inhaler

126
Q

what is in a low-dose corticosteroid inhaler

A

beclomethasone diproprionate

127
Q

what does beclomethasone dipropriate do and how fast does it work (QVAR)

A

QVAR (beclomethasone dipropionate) is an inhaled corticosteroid and acts to reduce inflammation in the airways. As a result it is classed as a preventer medication as it doesn’t have an immediate effect and may take weeks to work and is used to prevent ongoing asthma symptoms, by reducing airway inflammation and thereby bronchial hyperreactivity to stimuli like cold air.

128
Q

what are two examples of SABAs (short acting)

A

salbutamol
terbutaline

129
Q

what is an example of a LABA (long acting)

A

salmeterol

130
Q

what are 4 examples of inhaled corticosteroids

A

beclometasone
fluticasone
ciclesonide
budesonide

131
Q
A
132
Q

what are the 3 types of inhaler devices

A

metred dose inhalers (MDI)
- inhale slow and steady

dry powdered inhalers (DPI)
- inhale quickly and deep

breath actuated inhalers (BAI)

133
Q

look up video on how to perform spirometry

A
134
Q

In what other medical conditions can you hear a wheeze in

A

cardiac failure
eosinophilic lung disease
COPD
foreign body aspiration
OPD

135
Q

define the term Peak Expiratory Flow Rate

A

the PEFR is the rate of maximal volume of air that a person can exhale during a short maximal expiratory effort after a full inspiration

136
Q

how do you record serial readings of PEFR and for how long

A

for diagnosis 2-4 weeks, twice daily

for occupational asthma it may require 2-4 hourly readings over several weeks

137
Q
A

Year 3 (63 decks)

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