COPD Flashcards

1
Q

what does COPD stand for?

A

chronic obstructive airway disease

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

what is the cardiopulmonary system?

A

Need abundant O2 and glucose – cellular respiration
•Need to ‘clear’ waste products of ATP metabolism – CO
- relies on diffusion of the skin

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

what is a limitation of the cardiopulmonary system and how is it overcome?

A

To overcome these limitations
•Respiratory system
•Cardiovascular system
–Provides a large surface area for gas exchange
–Allows gases to be dissolved in the blood and transported
•O2 (from atmospheric air) to respiring cells
•CO2 to the lungs (into atmospheric air) from respiring cells

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

is pulmonary circulation oxygenated or deoxygenated?

A

deoxygenated

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

what is tidal movement?

A

total movemet of air in and out of lungs
- generated by strexhing lung tissue - impression in airways as expand and allowing to collapse back
as pressure rises/ falls it equalises

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

is ventilation a voluntary or involuntary control?

A

autonomic pressure/ voluntary control

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

what happens in inhilation when PH falls?

A

h ion increases- drive to increase respiratory rate- accumulation by co2

  • Alveoli are separated by alveoli septum
  • Air moves predom by diffusion
  • High co2- low o2
  • O2 is bound by deoxygenated haemoglobin
  • The blood vessels and resp epithelial surfaces shares
  • Combined wall thickness being less than 2 microns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the respiratory function tests for COPD?

A

Blood gas analysis, spirometry(ESSENTIAL IN DIAGNOSIS AND MANAGMENT) and imaging help to assess lung function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are ABG andhow do we measure?

A

ABG= arterial blood gases
- differ between similar conditions
assess lung function

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

how does spirometery work?

A

using volume/ time graphs

it can either be obstrictive or restrictive

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

how do obstuctive and restrictive present on a chart?

A

Obstructive–Loss of flow greater than proportional loss of volume
•Restrictive–Loss of volume greater than proportional loss of flow

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

what are the related conditions to COPD that may be confused for/ overlap?

A

Chronic bronchitis
•Emphysema–These may (often) co-exist – both diseases at same time
•May exist with other respiratory conditions e.g. asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what condition would obstructive spirometery show?

A

Asthma–COPD–Cystic fibrosis–Bronchiectasis

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

what conditions would restrictive spirometry show?

A

Fibrosis–Sarcoidosis–Neuromuscular (ALS)–Scoliosis / kyphosis

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

how would you differenciate COPD from similar diseases?

A

Obstructive
•Progressive (worsen over time)
•Irreversible (unlike asthma)
•Similar risk factors (smoking)•Overlap between the conditions
•Treatment is ostensibly the same
PEFR is reduced and FEV1 is lower than expected

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

what would and fev1 <0.7 indicate?

A

COPD

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

can something be done about the airflow limitation in COPD?

A

Preventable
•Inflammatory: secondary to an avoidable environmental ‘pollutant’ (extrinsic risk factors)•Host factors (intrinsic) may be important in some–Progressive
•Punctuated with exacerbations

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

what kind of preventable risk factors are there?

A

pollutanat- environmental
Demographic risk factors–Low socio-economic status»Housing (indoor pollution and outdoor pollution) and overcrowding»Poverty (co

ntrinsic risk factors–Low birth weight and poor early nutrition–Respiratory disease in development–Gestational problems inhibiting lung development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what effect does inflamation of the airways have?

A
causes increase mucous production by:
Enlargement of mucus secreting glands
–Increased goblet cell number
–Inflammatory cell proliferation
–Poor correlation to severity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the things that happen once airways are inflamed?

A
mucous secretion
Inflammatory mediators
•Complex (both innate and adaptive changes)
local effects
systemic 
consequences
Loss of airway patency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how do the lungs longs lose airway patency?

A

–Reduced lumen diameter
–Loss of ciliated epithelial function
–Loss of airway elastic fibres
»Collapse during expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is Emphysema?

A

Loss of elasticity
Reduced ᵳ1-anti-trypsin [anti protease] resulting in destruction of elastic fibres–Acquired – tobacco smoking–Intrinsic – ᵳ1-anti-trypsin deficiency (associated with liver dysfunction)

collapse of alveoli
loss of reticular structure
•Loss of associated vasculature

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

how would you diagnose COPD?

A

Loss of matching air flow to physiological requirements–Breathlessness – often first reason for presentation to a practitione

24
Q

how is the airflow affected in COPD?

A

inspired volume relatively unchanged
•Flow at expiration diminished
inspired tidal volume relatively unchanged
•Flow at expiration diminished

25
Q

what happens when air is trapped?

A

Air trapping – lung hyperinflation
•Dynamic – major cause of hyperinflation
•Static – increased compliance associated with emphysema

26
Q

what is Dyspnoea and how can it be measured?

A

Breathlessness may be associated with functional loss; it is subjective and difficult to quantify
•Exercise tolerance – MRC modified dyspnoea scale

27
Q

what is a classic sign of COPD?

A

Classic symptom of COPD is productive cough

28
Q

what does speutum production tell us about a cough?

A

–Mucus plus cell fragments and inflammatory mediators–Appearance of mucus can be useful in clinical assessment»Mucoid – clear appearance to purulent – green

29
Q

what is a wheeze?

A

Generally expiratory–Secondary to turbulent flow in the smaller airways•Narrowing / partial blocking of airway•May be audible or heard using stethoscope

30
Q

what do most COPD patients die from?

A

Most patients with COPD die from CV disease–Hypercholesterlaemia–Hypertension–Myocardial infarctio
it is a systemic as well as local disease

31
Q

what other symotoms can you get from COPD?

A

Malnutrition and altered fat metabolism
•Muscular weakness/deconditioning
•Increased inflammatory markers
•Increased risk of osteoporosis

32
Q

what would be visual features of COPD?

A

Intercostal indrawing
•Use of accessory muscles
•Pursed-lip breathing

33
Q

what guidlines do COPD follow?

A

UK – predominantly NICE

•Pan-national – GOLD

34
Q

what does each guidelines focus on?

A

GOLD
•Focus on symptomology to drive choice–Level of symptoms–Rate of exacerbations–Asthmatic contribution–

NICE
•Focus on outcomes and overall cost effectiveness–Element of symptom control (mild disease) and progression–Asthma

35
Q

irrespective of which guideline what are the therapeutics preformed?x

A

Importance of diagnosis – history, assessment and clinical diagnostics–Smoking cessation( method doesnt matter)–Vaccination
•Single one-off pneumococcal vaccine•Annual influenza vaccine–? Covid-19 and impact on recommendations

36
Q

what is the scoring tool used for COPD?

A

CAT
Scoring system
•More objective assessment–Severity of disease–Important for GOLD

37
Q

when do we use inhaled bronchodilators?

A

SABAs and SAMAs•Short acting beta agonists–Salbutamol, terbutaline,
•Short acting muscarinic antagonists–Ipratropium
•Immediate relief from dyspnoea – not as effective as in asthma, but provide symptomatic control

38
Q

what are the long acting beta/muscarinic antagonists?

A

LABAs and LAMAs
•Long acting beta agonists–Salmeterol, formoterol, indacaterol and olodaterol •Long acting muscarinic antagonists–Tiotropium, glycopyrronium, acaldinium bromide, umeclidinium

39
Q

what effects do Corticosteroids have?

A

exogenous semi-synthetic analogues of cortisol
•Anti-inflammatory–Suppression of nuclear transcription–Inhibition of phospholipase A2
•Suppress immune cell activation–Macrophages, lymphocytes, eosinophils, dendritic
•Upregulation of beta 2 receptors–Increased response to SABAs (salbutamol, terbutaline etc.)

40
Q

what are the s/e corticosteroids?

A
  • Skin–Acne, Cushing’s appearance, hirsuitism
  • CV–Hypertension, Na retention
  • Bone–Osteoporosis
  • Eyes–Glaucoma, cataracts
41
Q

what is the dose and managment of Azithromycin?

A

250 mg tds–Patient assessment•Frequent exacerbations resulting in hospitalisation•Large volumes of sputum–TB, bnronchiectasis, pseudomonas etc. ruled out•Non-smoker•Check ECG – QTc prolongation

42
Q

how does Theophylline work?

A

Acts through inhibition of phosphodiesterase (non-specific) and causes cAMP-dependent bronchodilatation

43
Q

what are the problems associated with yheophylline?

A
  • Relatively little evidence that it is generally effective–Patients unable to tolerate inhaled therapies, for example
  • Narrow therapeutic index–
44
Q

what are mucolytics?

A

Oral therapies intended to reduce the viscosity of sputum – help with mucus clearance

45
Q

what does the Roflumilast – PDE4 inhibitor do?

A

–Acts by increasing cytoplasmic cAMP
•Bronchodiltation–Inhibits immune cell response
•Macrophages, T and B lymphocytes
Severe COPD where FEV1 < 50% of predicted

46
Q

what is oxygen considered as in the treatment of COPD?

A

O2 is a PoM and should be considered and treated as a medicine–There are risks associated with O2 therapy•Clinical risks•Physical – supports combustion–Hazard in smokers (have been deaths secondary to burns)–Long-term O2 Therapy (LTOT)

47
Q

COPD can cause hypoxia, what is this?

A

Hypoxia (reduced ventilation and reduced transfer of O2 into the blood)•If this occurs slowly over time – adaptation

48
Q

what are the types of respiratory failure and what happens in each?

A

–Type I respiratory failure•Hypoxic hypoxia
•Low circulating levels of arterial (Pa)O2•Occurs without changes to other gases

–Type II respiratory failure•Hypercapnic hypoxia•Low circulating levels of arterial (Pa)O2, but raised PaCO2

49
Q

what are the 3 potential problems in type 2 failure?

A

Three potential problems–O2-induced acidaemia»Displacement of CO2 and H+ from RBCs–Respiratory arrest»Loss of hypoxic drive–Paradoxic hypercapnia»Give O2 get large increase in PaCO2

50
Q

what causes an exacerbation of COPD?

A

•Different causes–Bacterial–Viral–Smoking
–Antibiotics
•C&S or empirical–Steroids–

•Commonly–Increased cough–Increased sputum, change in sputum colour (to green often)

51
Q

how do you control exacerbation of COPD?

A

Symptom control
•Bronchodilators–Nebuliser / MDI via spacer–IV theophylline (in hospital if no response to standard)
•O2 (assuming assessed for risk)–Hypercapnia–Acidaemia

52
Q

depending on severity- how else may COPD exacerbation be treated?

A

If needed – depending on severity
•Mechanical ventilation (ICU)–NIV if difficult to wean from ventilator
•Non-invasive ventilation (NIV)–Air supplemented often with O2

53
Q

what is a Cor pulmonale and what is it used for?

A

–Essentially right ventricular failure–Desaturation – loss of O2
–Effect of chronic pulmonary dysfunction of COPD
•Hypoxia – pulmonary hypoxic vasoconstriction•Right sided afterload

54
Q

how do you treat Cor pulmonale?

A
  • Continuous O2–Reduced R CO reduces O2 transfer–Reverses PHV (O2 vasodilator in lungs)
  • Treat PH–Diuretics (also treats oedema) – loop (furosemide)»Improves CO / cardiac dynamics•Hypokalaemia – may alter respiratory drive–Vasodilators»Prostacylin analogues (epoprostenol)»Et-A antagonsists (bosentan)
55
Q

what would they do in surgery to treat COPD?

A

ung volume reduction – hyperinflation–Lung transplantation–Bullectomy•Large bulla – occupying > 1/3 of hemithorax

56
Q

how do you reduce distress during palative care?

A

Ensuring distress is minimised
•Use of opiates to reduce distress of dyspnoea•O2 therapy
•Benzodiazepines / anxiolytics