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Respiration > Asthma/COPD > Flashcards

Asthma/COPD Flashcards

1
Q

Patient with COPD who has never smoked

A

Alpha 1 anti trypsin deficiency

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2
Q

what is cor pulmonae

A

right sided hypertrophy and heart failure due to increased vascular resistance

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3
Q

difference between obstructive and restrictive disease

A

Obstructive-airways

Restrictive- lungs

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4
Q

examples of obstructive lung disease

A

Asthma, COPD (chronic bronchitis, emphysema)

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5
Q

what is asthma COPD overlap syndrome

A

Asthma and COPD

smokers with COPD who are eosinophilic and show reversibility with bronchodilators and are steroid responsive

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6
Q

Cause of airway obstruction in COPD

A

invagination of mucosa
smooth muscle constriction
alveolar wall attachments to bronchioles break away
in emphysema

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7
Q

Extrinsic vs Intrinsic asthma

A

extrinsic-identifiable cause

intrinsic-unknow cause

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8
Q

Type II Inflammation - what this involves and what types of asthma is this associated with

A

TH2 cells, type II lymphoid cells, B cells which produce IgE, type II cytokines (IL4, IL5, IL13)
Effector cells- eosinophils, basophils, mast cells

associated with allergic asthma, exercise induced asthma and late-onset eosinophilic asthma

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9
Q

Asthma triad

A 
T2 airway inflammation (eosinophils)
Airway Hypersensitivity (twitchiness)
Reversible airflow obstruction
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10
Q

Dynamic evolution of asthma

A
  1. Bronchoconstriction
  2. Chronic airway inflammation
  3. Airway remodelling
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11
Q

Hallmarks of asthma remodelling

A

BM thickening, collagen deposition in the submucosa and smooth muscle hypertrophy

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12
Q

key cytokines in asthma

A

IL4, IL5, IL13

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13
Q

Influence of Leukotriene D4

A

attracts eosinophils, makes goblet cells secrete mucous

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14
Q

Endotypes which indicate type II high asthma

A

present cytokines IL4, IL5, IL13
raised total or specific IgE
Eos >300
Raised FeNO

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15
Q

why should asthmatics never be treated with B2 agonists alone

A

Doesn’t get rid of problem

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16
Q

how do we measure airflow obstruction

A

peak flow or spirometry

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17
Q

how do we measure bronchiole hypersensitivity

A

challenge testing

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18
Q

how do we measure airway inflammation

A

invasive bronchoscopy

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19
Q

Presentation of asthma

A

Episodic S+S i.e. there is a trigger
Diurnal variability-worse at night and early morning
non-productive cough
wheeze
TH2 comorbidities
Responsiveness to steroids and beta2 agonists
FHX of asthma

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20
Q

Presentation of asthma

A 
Episodic S+S i.e. there is a trigger
may be atopic
Diurnal variability-worse at night and early morning
non-productive cough
wheeze
TH2 comorbidities 
Responsiveness to steroids and beta2 agonists 
FHX of asthma
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21
Q

Investigations in Diagnosis of asthma

A

the diagnosis of asthma is a clinical one
should have at least 1 of the 4 symptoms and have variable airflow obstruction
History and examination
Diurnal variability of peak flow rate
Spirometry/peak flow-reduced FER OF <0.75
Reversibility to inhaled salbutamol of >0.15
Provocation testing- exercise, histamine, methacholine, mannitol
FeNO
Blood eosinophils
Blood IgE

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22
Q

Signs and Symptoms of COPD

A 
Usually smoker
Chronic, not episodic
non-atopic
FER <0.7
usually no reversibility to bronchodilators 
Respiratory failure (paO2 down, PaCO2 up)
pulmonary hypertension
RV failure

Productive cough, wheeze, Breathlessness
Exacerbations
Reduced breathing sounds (emphysema)

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23
Q

Treatment of asthma (SIGN GUIDELINES)

A
  1. Low dose ICS with SABA
  2. Add LABA
  3. stop LABA, increase ICS or just increase ICS or add LTRA, theophylline or LAMA
  4. increase ICS or add on 4th drug (LTRA, theo, LAMA)
  5. low dose oral steroid

Step 4 and 5-refer to specialist care

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24
Q

Treatment of COPD

A

Non-Pharmacological

exercise, smoking cessation, vaccines (flu, pneumococcal), pulmonary rehab, o2

Pharmacological

LABA/LAMA (non-eosinophilic)
ICS/LABA
ICS/LABA/LAMA

PDE4 inhibitors- Roflumilast
Mucolytics- Carbocisteine
Antibiotics

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25
Q

What type of inflammation is asthma associated with

A

eosinophilic

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26
Q

Two conditions that make up COPD and their features

A

Neutrophils release protease which cause alveolar wall destruction (emphysema) and mucus hypersecretion (bronchitis)

Emphysema- alveolar wall destruction therefore a loss of bronchiole support, impaired gas exchange (irreversible)

chronic bronchitis- chronic neutrophilic inflammation, mucus hypersecretion, impaired mucocilary function, change in lung microbiome (more G-), smooth muscle spasm and hypertrophy (partially reversible)

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27
Q

Diagnosis of COPD

A

Assess symptoms
Spirometry-FER <0.75
assess risk of exacerbations assess comorbidities

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28
Q

Which COPD patients are ‘high risk’

A

2 or more exacerbations in 1 year, FEV1 <0.5

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29
Q

how stop further decline in COPD

A

smoking cessation

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30
Q

What does spirometry measure

A

forced expiratory volumes, rates

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31
Q

what is helium and N2 washout used for

A

static lung volume, residual volume, TLC, FC

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32
Q

whole body plethysmography

A

measuring changes in volume within an organ or whole body

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33
Q

when would you have reduced CO transfer factor

A

interstitial lung disease, COPD (emphysema), anemia, pulmonary oedema

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34
Q

Spirometry for asthma

A

normal FVC, reduced FEV1

FER <0.75

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35
Q

spirometry of COPD

A

reduced FVC and FEV1

FER <0.7

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36
Q

spirometry of COPD

A 
reduced FVC (emphysema, gas trapping) and FEV1
FER <0.7
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37
Q

PEFR in obstructive vs restrictive

A

reduced in obstructive

normal in restrictive

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38
Q

FEV1 in obstructive vs restrictive

A

both reduced

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39
Q

FVC in obstructive vs restrictive

A

o-asthma normal, COPD reduced

r- reduced in proportion to FEV1

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40
Q

FER in obstructive vs restrictive

A

normal in Restrictive
<0.75 asthma
<0.7 in COPD

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41
Q

FEV1 response to B2 agonists

A

> 0.15 asthma
<0.15 COPD
no effect in restrictive

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42
Q

Bronchiole challenge testing

A

Concentration of allergen to reduce FEV1 by 20%

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43
Q

Two types of drugs for airflow obstruction

A

preventer- anti inflammatories

relivers- bronchodilators

44
Q

Corticosteroids

uses, oral form, inhaled from

A

Used in asthma and COPD
may cause Pneumonia in COPD
Oral=Prednisolone (exacerbations)
Inhaled= Beclomethasone

beclomethasone is used as monotherapy or in combo in asthma, only used in combo in COPD

Targets eosinophils

45
Q

Practical management of asthma

A

induce remission with oral steroids then maintain with inhaled steroids- never use inhaled steroids in acute unstable asthma

46
Q

Actions of spacer device

A

reduces particle size to less than 5 micrometres so can get past carina

reduces velocity therefore gag
reduced systemic absorption
reduced oropharyngeal and laryngeal S/E

47
Q

Cromones

A

eg cromoglicate
mast cell stabilisers (anti-inflammatory)
only used in asthma, affective in atopic children (EIB)
inhaled only

poor efficacy

48
Q

Anti-Leukotriene

example drug, use ect

A

eg Montelukast- 1/ day tablet

only used in asthma as an add on-best drug for EIB and allergic rhinitis

49
Q

Name the three monoclonal antibodies used in severe asthma and examples of each

A

Anti-IgE: Omalizumab
Anti-IL5/Anti-IL5R alpha: Mepolizumab, Benralizumab
Anti-IL4R alpha: Duplimab

50
Q

Anti-Leukotriene

example drug, use ect

A

eg Montelukast- 1/ day tablet

only used in asthma as an add on-best drug for EIB, allergic asthma and allergic rhinitis

51
Q

short acting B2 agonists

A

salbutamol

52
Q

long acting b2 agonists

A

salmeterol, formoterol

53
Q

side effects of b2 agonists

A

tachycardia, fine tremor, hypotension, hypokalaemia

54
Q

Action of muscarinic antagonists

A

Block M3 receptors

mostly used in COPD

55
Q

short acting muscarinic antagonist

A

ipratropium

56
Q

long-acting muscarinic antagonist

A

tiotropium
Glycopyrronium
aclidinium
umeclidinium

57
Q

Examples of methylxathines

A 
Theophylline
Aminophylline (acute attacks)
non-selective phosphodiester inhibitor is an adenosine antagonist
used in asthma, sometimes COPD
P450 interactions
58
Q

Examples of methylaxthines

A

Theophylline (add on in asthma, SE limit therapy)
Aminophylline (acute attacks)
non-selective phosphodiester inhibitor is an adenosine antagonist
used in asthma, sometimes COPD
P450 interactions

59
Q

Mucolytics

A

Carbocisteine, erdosteine
add on in COPD
increased sputum viscosity

60
Q

Mucolytic

A

Carbocisteine, erdosteine
add on in COPD
increased sputum viscosity

61
Q

Treatment of acute asthma

A 
Oxygen
Salbutamol (nebulised)
Hydrocortisone (IV) or Oral prednisolone(40mg, 5/7 days)
Ipratropium (nebulised)
Theophylline, aminophylline
Magnesium 
ANaesthetists
62
Q

Treatment of acute COPD

A

Oxygen
Salbutamol (neb)
Ipratropium (neb)

Antibiotic (amoxicillin/doxy)
Prednisolone
physio for sputum exportation

NIV, ITU

63
Q

GOLD

A

looks at FEV1

1 OVER 80
2 50-79
3 30-49
4 LESS THAN 30

64
Q

Symptoms of asthma

A

Non-productive cough, wheeze, tight chest, breathless

65
Q

SIGN diagnosis of asthma

A

start treatment then test
start on SABA- if good response diagnose with asthma
if poor response test spirometry + bronchodilator reversibility+ other tests

66
Q

when should asthma patients be referred to secondary care+red flags

A
  • all occupational asthma
  • up to stage 4
  • severe/life threatening asthma
  • fever, myalgia, weight loss
  • crackles, clubbing, stridor
67
Q

Inaudible laryngeal obstruction

A

inappropriate abduction of vocal cords

Sensitivity to strong smells, exercise- severe breathlessness- stridor- cant breathe in-feeling of something stuck in the throat

not an allergic phenomenon

68
Q

Drugs that won’t work with smoking

A

steroids

macrolides

69
Q

Allergic Broncho-pulmonary Aspergillosis
symptoms
pathology
treatment

A

allergic response to aspergillus, involves mucus plugging and proximal bronchiectasis
Total IgE >1000, elevated aspergillus IgE

Treatment: Steroids and Itraconazole

70
Q

Atopic triad of allergic asthma and treatment options

A

Asthma, eczema, rhinitis

allergy avoidance
anti-histamines
montelukast
Omalizumab (binds to Fc of IgE)

71
Q

Eosinophilic asthma aetology

treatment

A

late onset, mostly women
steroid resistant
Mepolizumab, Benralizumab

72
Q

why is normal co2 is acute asthma worrying

A

Should have low co2 due to hyperventilation- a normal co2 is very bad-phone intensive

73
Q

should be use CPAP in acute asthma

A

CPAP not indicated for acute asthma

74
Q

moderate acute asthma

A

increasing symptoms
PEF >50-75%
no symptoms of acute severe asthma

75
Q

acute severe asthma

A

any 1 of:

  • PEF >33-50%
  • RR >25/min
  • HR >110/min
  • inability to complete full sentences in 1 breath
76
Q

life-threatening asthma

A
  • altered consciousness (PEF<33%)
  • Exhaustion (SpO2 <92%)
  • Arrhythmia (PaO2 <8KPa)
  • Hypotension (normal PaCo2 4.6-6KPa)
  • Cyanosis
  • Silent chest
  • Poor respiratory effort
77
Q

Near fatal asthma

A

Raised PaCo2 and/or requiring mechanical ventilation with increased ventilation pressures

78
Q

effect of ACh on airways

effect of VIP and NO on airways

A

ACh causes bronchoconstriction and mucus hypersecretion via M3 receptors

VIP and NO cause bronchodilation

79
Q

effect of sympathetics on airways

A

no direct innervation, but will stimulate adrenal gland which releases adrenaline

  • bronchodilation due to adrenaline acting on B2 adrenoceptors
  • decreased mucus
  • increased mucocilary clearance
  • vascular smooth muscle contraction (a1)
80
Q

gold square

A

x axis=symptoms

y axis=exacerbations

81
Q

criteria for bullectomy

A

bullae occupying for than 50% of thoracic cavity

82
Q

Two types of NIV

A

expiratory positive airways pressure-lowers work of breathing, reduced pCo2

inspiratory positive airways pressure- increased TV and Pco2

83
Q

process of contraction in ASM

A

ACh stimulates M3 ACh GCRP, activating Gq/11 which activates PLC.
PLC causes conversion of PIP to IP3.
IP3 activates the Ca2+ channels in the SR to release calcium from SR
causes depolarisation of other calcium channels and more calcium enters
increased intracellular calcium-contraction

84
Q

Describe how calcium causes the contraction of ASM

A

calcium and calmodulin make calcium-calmodulin
calcium-calmodulin activates MLCK
Active MLCK will phosphorylate cross bridges

Phosphorylated MLC

85
Q

What causes relaxation of ASM

A

Dephosphorylation of MLC by myosin phosphorylase

Adrenaline activates GPCR which activates GS which causes conversion of ATP to cAMP
cAMP activates PKA which phosphorylates and stimulates myosin phosphotase and inhibits MLCK

86
Q

how is cAMP deactivated

A

by PDE-turned into 5AMP

87
Q

Immediate and delayed phases of an asthma attack

A

immediate- bronchospasm-Type I hypersensitivity

delayed- type IV hypersensitivity

88
Q

response to allergen by non-atopic individual

A

TH1 response, cell mediated response involving IgG and macrophages

89
Q

Atopic individual

A

Strong TH2 response, antibody mediated IgE response

90
Q

what response predominates in mild-moderate asthma

A

TH2

91
Q

what response predominates in severe asthma

A

TH2 and TH1 contributes

92
Q

cascade of events with cells in Asthma

A
  • Allergen presented to T CD4+ cell by APC
  • T CD4+ cell converts to TH0 which differentiates to TH1 and TH2
  • TH2 will activate B cell via IL4 and B cells will form plasma cells which secrete IgE antibodies
93
Q

Influence of TH2 cells on effector cells

A

TH2 produces IL4, IL5, IL13

IL4 activates B cells to make more plasma cells which secrete IgE
IL5 activates eosinophils which express IgE receptors
IL4 and IL13 activate mast cells to degranulate

94
Q

Effect of IgE binding to mast cell

A

stimulates calcium entry into mast cells and the release of intracellular calcium stores

  • Smooth muscle contraction: release of histamine and leukotrienes
  • Attracting inflammatory cells: release of chemotaxins, prostaglandins ect
95
Q

two types of steroid hormone secreted by adrenal cortex

A

not stored, synthesised on demand
Glucocorticoid-cortisol which reduced inflammatory responses
mineralocorticoid-aldosterone (unwanted in treatment of inflammatory conditions)

96
Q

Mechanism of glucocorticoids

A

enter cells by diffusion across cell membrane
combine with GRa so it dissociates from inhibitory shock proteins
activated receptor translocates to nucleus via importins
with nucleus, homodimers form
transcription of specific genes is switched on or off

97
Q

effect of glucocorticoids on inflammatory and anti-inflammatory genes

A

Glucocorticoids increase anti-inflammatory genes by recruiting histone deacylase

Glucocorticoids decrease inflammatory genes by aceylation of histones

98
Q

Effect of glucocorticoids on inflammatory cells

A

TH2-apoptosis
Eosinophils-apoptosis
mast cells-reduced no and reduced Fce expression

99
Q

What component of asthma does glucocorticoids supress

A

Inflammation

100
Q

Most common side effects of ICS

A 
Dysphonia (weak and hoarse voice)
oropharyngeal candidiasis (thrush)
101
Q

which phase of breathing fails in COPD

A

Expiration

102
Q

Systemic effects of SAMA and LAMA

A

Quaternary ammonium group (atropine) reduces absorption and systemic effects of SAMA/LAMA

103
Q

Location of muscarinic ACh receptors in airways and types of receptors

A

M1-ganglia (fast, nicotinic receptors)
M2-postganglionic neuron terminals- reduce release of ACh (inhibitory autoreceptors)
M3-ASM-contraction due to ACh

104
Q

what type of muscarinic antagonists are preferred for asthma treatment

A

selective-we don’t want to block M2- preference for agents which prefer M3 signalling

SAMA, ipratropium is non-selective
LAMAs are selective

105
Q

Management of an acute exacerbation of asthma within community setting

A

40mg Prednisolone 5/7 days
smoking cessation, allergy avoidance
2 day f/u safety net

106
Q

investigation for patient with 3 or more COPD exacerbations in 6 months

A

HRCT to check for bronchiectasis

Respiration (6 decks)

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