10. COPD Flashcards

1
Q

What is COPD

A

non-reversible, long term deterioration in air flow through the lungs caused by damage to the lung tissue

almost always a result of smoking

causes an obstruction to the flow of air through the airways making it difficult to ventilate the lungs and making them prone to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is COPD different to asthma

A

the obstruction is not significantly reversible with bronchodilators such as salbutamol

does not change markedly over several months

asthma has reversible airway obstruction (ie by more than 15%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

COPD clinically is a triad of which 3 things traditionally

A

emphysema
chronic bronchitis
small airway fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

History:

what are the risk factors for COPD

A

tobacco smoking
indoor air pollution (ask about asbestos)
alpha-1 antitrypsin deficiency (leads to increased destruction of alveolar structures resulting in early onset emphysema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

History:

what is the usual presenting complaint in COPD

A

progressive dyspnoea and chronic productive cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

History:

what would your typical stereotypical patient present with

A

Suspect COPD in a long term smoker presenting with chronic shortness of breath, cough, sputum production, wheeze and recurrent respiratory infections, particularly in winter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

History:

name symptoms of COPD

A

dyspnoea: initially exertion but can progress to resting dypneoa
chronic productive cough: usually colourless but may be green during LRTIs
recurrent LRTIs
fatigue
headache (due to Co2 retention)
wheeze
impact of symptoms on daily life and occupation
previous exacerbations or hosptialisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

History:

what things would be significant in the patients PMH in relation to dyspnoea

A
anxiety and depression 
cardiovascular disease 
lung or liver disease 
osteoporosis 
asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

History:

what major thing in the patents FH would you ask in particular

A

if they have had any lung or liver disease but consider underlying causes such as alpha-1-antitrypsin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why could liver disease cause symptoms of dyspnoea

A

Ascites elevates the diaphragms and causes basilar atelectasis, which contributes to dyspnea and mild hypoxia

also

AAT, the alpha-1 protein, is mainly produced by the liver. The main function of AAT is to protect the lungs from inflammation caused by infection and inhaled irritants such as tobacco smoke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what medication in particular could cause a patient to have a dry cough

A

ACEi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examination:

name some examination findings

A
tachypnoea 
wheeze onausculation 
pursed lips breathing 
barrel chest
tar staining of fingers 
central cyanosis (if hypoxic or polycythhaemic) 
palpable liver edge 
cor pulmonate signs - signs of RHF such as peripheral oedema, hepatomegaly and raised JVP 
CO2 retention flap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

why would a patient have tachypnoea

A

due to increased neural respiratory drive to breathe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why would a patient have a wheeze on auscultation

A

due to inflammatory airway oedema and mucus obstructing the airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why would a patient have pursed lips breathing

A

to increased airway resistance and therefore reduce expiratory flow limitation (and could have use of accessory muscles as well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why would a patient have a palpable liver edge

A

due to hyper expansion so the liver is pushed down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

name some signs of RHF

A

peripheral odema, hepatomegaly and raised JVP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

name the important differential diagnosis for dyspnoea and a productive cough

A
Asthma 
bronchiectasis 
congestive heart failure 
lung cancer 
tuberculosis 
PE 
angina 
anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what features differentiate asthma from COPD

A

asthma has;
diurnal variation in symptoms and peak flow
history of atopy
eosinophilia (blood and sputum)
lung function test would show bronchodilator reversibility

*note that COPD and asthma can co-exist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what features differentiate bronchiectasis from COPD

A

expect larger volumes of sputum
more frequent lower respiratory tract infections often starting in childhood
high resolution chest CT would show bronchial dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what features differentiate congestive heart failure from COPD

A
orthopnoea 
paroxysmal nocturnal dyspnoea
history of cardiovascular disease 
final basal inspiratory crepitations 
elevated BNP in bloods 
echocardiogram would show reduced ejection fraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what features differentiate lung cancer from COPD

A

weight loss
haemoptysis
chest X-ray and bronchoscopy would show the presence of tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what features differentiate TB from COPD

A

drenching night sweats
weight loss
positive sputum culture and microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what features differentiate anaemia from COPD

A

would present more with fatigue and palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

during an acute exacerbation what differentials is it important to consider along COPD

A
pneumonia 
PE
pneumothorax
acute heart failure 
pleural effusion 
cardiac ischemia or arrhythmia 
lung cancer 
upper airway obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Dyspnoea is graded using the medical research council (MRC) dyspnoea scale. What does grades 1-5 mean

A

grade 1- breathless on strenuous exercise
grade 2- breathless on walking up a hill
grade 3- breathless that slows walking on the flat
grade 4- stop to catch their breath after walking 100m on the flat
grade 5- unable to leave the house due to breathlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how is COPD diagnoses

A

through clinical presentation plus spirometry

28
Q

what would spirometry show in someone with COPD

A

it would show an obstructive picture
their FEV1 would be limited as being able to blow air out is limited by the damage to their airways causing airway obstruction. Therefore in COPD:

FEV1/FVC ratio <0.7

(carried out 15-20 minutes after a SABA)

29
Q

where post-bronchodilator FEV1/FVC ratio is less than 0.7, the severity of the airflow obstruction is graded in what way

A

Graded using the gold staging (global strategy for obstructive lung disease) according to reduction in FEV1 compared to appropriate reference value

Stage 1, mild — FEV1 80% of predicted value or higher.
Stage 2, moderate — FEV1 50–79% of predicted value.
Stage 3, severe — FEV1 30–49% of predicted value.
Stage 4, very severe — FEV1 less than 30% of predicted value or FEV1 less than 50% with respiratory failure.

30
Q

describe the FEV1 and FVC in someone with COPD

A

the FEV1 is reduced a lot more significantly because there is obstruction of air escaping from the lungs
FEV1/FVC ratio is reduced

31
Q

what other investigations would you order along side spirometry

A
CXR
FBC
BMI
sputum culuture 
ECG and echocardiogram 
CT thorax 
serum alpha-1 antitrypsin 
transfer factor for carbon monoxide (TLCO)
ABG
32
Q

why would you carry out FBC

A

to look for polycythaemia or anaemia

polycythaemia (raised haemoglobin) is a response to chronic hypoxia

33
Q

on an ECG what typical signs would you see if someone had cor pulmonale

A

peaked P waves and right axis deviation

34
Q

describe type 1 respiratory failure

A

type 1 is associated with damage to lung tissue which prevents adequate oxygenation of the blood
low O2 with normal CO2
indicates serious underlying pathology with the lungs such as. infection, odema or shunt

35
Q

describe type 2 respiratory failure

A

this is also known as ventilatory failure and is low oxygen with increased CO2
Reduced ventilatory effect can be a result of gas trapping , such as in severe COPD and severe asthma

36
Q

how can the body try and compensate in type 2 respiratory failure

A

the body can try and use the bicarbonate buffering system and so the kidney are stimulated to reabsorb more bicarbonate

37
Q

what are the clinical features of hypercapnia

A
dilated pupils 
bounding pulse 
hand flap 
myoclonus 
confusion
drowsiness 
coma
38
Q

What can you offer a patient in regards to stopping smoking

A

professional advice
nicotine replacement
anti-depressant (bupropion)
nicotine receptor blocker (varenicline)

39
Q

what medication works for symptom relief and what reduces the exacerbation frequency

A

inhaled bronchodilators - work for symptom relief

LABA and corticosteroids reduce exacerbation frequency

40
Q

what is the initial long term management for COPD

A

it is essential for people to stop smoking
patients should also have the pneumococcal and annual flu vaccination
step 1: short acting bronchodilator, either a SABA (salbutamol or terbutaline) or SAMA (ipratropium bromide)

41
Q

if the patient is still limited by symptoms or having exacerbations whilst using a SABA or SAMA what is the step up in treatment if

a) they have no asthmatic features
b) if they have asthmatic features (such as previous diagnosis of asthma/atopy, increased blood eosinophils, diurnal variation of peak flow, variation of FEV1 over time)

A

a) LABA and LAMA

b) LABA and ICS

42
Q

in what circumstance would you prescribe the patient LABA and LAMA and ICS

A

if they still have symptoms on dual therapy that impacts quality of life OR has 1 severe/2 moderate exacerbations a year

43
Q

in severe cases of COPD what are some additional options for treatment

A

nebulisers (salbutamol and/or ipratropium)
oral theophylline
oral mucoltyic therapy to break down the sputum (eg carbocisteine))
long term prophylactic antibiotics (azithromycin)
long term oxygen therapy at home

44
Q

in what circumstances would home oxygen be considered

A

in Severe COPD that is causing problems such as chronic hypoxia, polycythemia, cyanosis or heart failure secondary to pulmonary hypertension (cor pulmonale)

45
Q
Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler:
SABA
A

salbutamol (aka Ventolin, airomir) - blue MDI

terbutaline (bricanyl)- blue/white dry powder

46
Q
Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler:
LABA
A

salmeterol (serevent) - green/blue MDI

formoterol (oxis)- dry powder

47
Q
Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler:
SAMA
A

ipratropium bromide (atrovent) - clear with green lid MDI

48
Q
Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler:
LAMA
A

tiotropium (Spiriva)

49
Q
Give examples of the following class of inhalers, their common drug company names and the colour of the inhaler:
inhaled corticosteroid
A

beclomethasone (becotide or clenil)- brown MDI
Fluticasone (flixotide)- orange MDI
budesonide (pulmicort)- dry powder

50
Q

give an example of an oral and an IV corticosteroid

A

oral - prednisolone

IV- hydrocortisone

51
Q

give an example of a mucolytic

A

carbocisteine

52
Q

what is the generic name for some of the LABA&corticosteroid dual inhaler

a) salmeterol & fluticasone
b) formoterol & budesonide

A

a) seretide - purple MDI

b) Symbicort - white/red powder

53
Q

what is the main genetic causation of COPD and describe this deficiency

A

alpha-1 antitrypsin deficiency

people with this are more susceptible to damage from smoking
major function is to protect lung tissue elastin from neutrophil elastase-mediated destruction

54
Q

what environmental factors can cause COPD

A

tobacco smoke exposure
cannabis
other smokes
mineral dust (eg coal, cadmium) - quite rare now

55
Q

describe the pathological changes and how this relates to symptoms

A
goblet cell hyperplasia produces mucus - causes cough and sputum 
airway narrowing (partly through inflammatory repsone from toxins in tobacco smoke and also fibrosis/scarring) - causes breathlessness and wheeze 
alveolar destruction - causes breathlessness 

there is a large presence of lymphocytes in the mucosa which mediate the tissue damage

56
Q

how does the pathological changes in COPD lead to hypoxia and hypercapnia

A

there is airflow obstruction which leads to impaired gas exchange
-progressive decline in lung function –> progressive dyspnoea and disability –> right ventricular failure –> exacerbations

57
Q

what is the major complication of COPD

A
cor pulmonale 
 exacerbations 
pneumonia 
pneumothorax 
peripheral neuropathy 
cachexia
58
Q

how can COPD lead to cor pulmonale

A

hypoxia leads to pulmonary arterial vasoconstriction
this leads to increases pulmonary artery pressure
this leads to right ventricular hypertrophy
this leads to right ventricular failure

59
Q

what is the major cause of a COPD exacerbation

A

viral or bacterial infection

mostly due to rhino viruses (no treatment currently) and usually a H influenza

60
Q

how does a COPD exacerbation present

A

acute worsening of symptoms such as cough, SOB, sputum production and wheeze
usually trigged by a viral or bacterial infection

61
Q

what is respiratory acidosis

A

this is where they are retaining CO2 (cant get rid of it) and so their blood has become acidotic

62
Q

what parameter would be raised, suggesting they are chronically retaining CO2 and why is this the cases

A

raised bicarbonate as their kidneys have responded by producing more bicarbonate to balance the acidic CO2 and maintain a normal PH

63
Q

what kind of oxygen mask can you use in a patient with COPD in order to manage their oxygen levels

A

a venturi mask as it can deliver a specific percentage concentration of oxygen

64
Q

medical treatment of an exacerbation:

what is the typical treatment is the patient is well enough to remain at home

A

prednisolone 30mg once daily for 7-14 days
regular Inhalers or home news
antibiotics is there is evidence of infection

65
Q

medication treatment of an exacerbation:

what is the typical treatment options if the patient is in hosptial

A

nebulise bronchodilators (eg salbutamol 5mg/4h and ipratropium 500mcg/6h
steroids (eg 200mg hydrocortisone or 30-40mg oral prednisolone
antibiotics is evidence of infection
physiotherapy can help clear sputum

66
Q

give some medical options in severe cases if the patient doesn’t responding to first line treatment for exacerbation of COPD

A

IV aminophylline
non-invasive ventilation (NIV)
intubation and ventilation with admission to intensive care
doxapram can be used as a respiratory stimulant where NIV or intubation is not appropriate

67
Q

what is pulmonary rehabilitation

A

individually tailored, multidisciplinary care program for people with COPD which aims to optimize physical and psychological condition through exercise training, education, and nutritional, psychological, and behavioural interventions