Medicine 1 > COPD > Flashcards

COPD Flashcards

(57 cards)

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1
Q

1.2 million people in the UK have Asthma in 2019

a. Incidence
b. Prevalence

A

b. Prevalence

(the bathtub)

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2
Q

760,000 new cases of Asthma were diagnosed annually

a. incidence
b. prevalence

A

a. incidence

(coming out of the tap)

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3
Q

Symptoms

A

a manifestation of the disease apparent to the patient themselves

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4
Q

Signs

A

a manifestation of the disease that the physican perceives (more objective)

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5
Q

Symptoms of COPD

A
  • Cough productive of sputum
  • Dyspnoea
  • Wheeeze
  • Progressive* and not fully reversible
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6
Q

Risk factors for COPD

A
  • smoking
  • pollution
  • occupational exposures
  • genetics (aplha 1 antitrypsin deficiency)
  • poor lung growth in childhood
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7
Q

Complications of COPD

A
  • Cor pulmonale (Right sided HF)
  • Type 2 respiratory failure
  • Secondary Polycythaemia
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8
Q

Type 2 respiratory failure

complication of COPD

A

*HYPOXIA with HYPERCAPNIA
* Respiratory system cannot remove Carbon Dioxoide
* Increased resistance to breathing (COPD, Asthma)
* Area of lung not available for gas exchange (COPD - emphysema)

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9
Q

Type 1 Respiratory failure

A
  • Hypoxia WITHOUT hypercapnia
  • Respiratory system cannot adequetely supply oxygen to the body
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10
Q

what type of respiratory failure is COPD associated with

A

Type 2

Hypoxia WITH hypercapnia

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11
Q

Polycythaemia is a complication of COPD

a. true
b. false

A

a. True

Having a high concentration of RBCs - makes the blood thicker and less able to travel through the organs

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12
Q

Non-drug treatments for COPD

A
  • Smoking cessation
  • Pulmonary rehabilitation (MDT)
  • Dietition
  • Pychological
  • Vaccinations (pnrumococcal vaccine and influenza)
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13
Q

What vaccinations should patients with COPD be offered?

A
  • Pneumococcal
  • Influenza (flu)
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14
Q

How does smoking damage healthy lungs

A

Toxins are engulfed by inflammatory cells which release elastase in response to infection/cigarette smoke

Elastase damages healthy lungs

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15
Q

A rare inherited cause of emphysema

A

Alpha 1 anti- trysin enzyne deficiency

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16
Q

What happens in Alpha 1 anti- trysin enzyne deficiency

A
  • Early onset of COPD/emphysema <45 years
  • Alpha-1-trypsin is a anti-elastase (elastase inhibitor) which limits the damage caused by activated inflammatory cells releasing elastase
  • When absent/low - alveolar damage and emphysema
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17
Q

When would you suspect someone to have alpha-1-trysin deficiency as cause of COPD

A
  • very young with COPD features
  • non-smoker
  • Basal predominance to emphysema
  • Liver fibrosis or cirrhosis
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18
Q

Chronic bronchitis is defined as

A

having a cough productive of sputum in at least 3 months
in 2 consecutive years

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19
Q

what chest wall deformity is associated with COPD

A

due to hyperinflation of the chest

“barrel chest”

the anterior/posterior distance is larger than expected

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20
Q

what objective signs might you discover on examination of COPD patient

A
  • Chest wall deformities (barrel)
  • Pursed lip breathing (trying to increase expiratory pressure)
  • Cyanosis (tongue, lips, peripherals) - hypoxia
  • Raised JVP (later , right HF)
  • peripheral oedema
  • Cachexia - severe weight loss
  • Expiratory whistling
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21
Q

Modified medical research councils (mMRC)

breathlessness scale

A

0-4

0= strenous exercise
1 = hurrying on level/slight hills
2 = walking slow, stopping
3 = few mins or 100m
4 = dressing/undressing

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22
Q

Pulmonary Acinus refers to

A

gas exchange tissue of the lung (everything distal to the terminal bronchiole)

(Respiratory bronchioles, alveolar ducts, sacs)

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23
Q

Centriacinar emphysema

Study These Flashcards
A
  • Loss of tissue is concentrated in CENTRE of acinus
  • affects upper lobes in both lungs (apical)
  • associated with smoking/COPD - smoking inhalation damages the top of the lungs
24
Q

Panacinar emphysema

Study These Flashcards
A
  • Lower lobes/zones
  • Takes out Large AREAs (all of the acinus is wiped out/not just the centre)
  • Associated with Alpha -1- trysin deficiency -> basal predominance/or heavy smokers
25
Periacinar emphysema
* EDGES of acinus * against the pleura * usually where it abuts against pleura or vessel * can cause spontaneous pnuemothorax
26
What would a CXR in COPD possibly show
* hyperinflation (Flattened diaphragm) * Air trapping * Narrow/elongated heart * Bullae * > 10 posterior ribs (see all 12) due to increased Lung volume, more than 8 * destruction of lung (bulla) * prominant hila areas (hypertension)
27
Treatable part of COPD
*** smooth muscle tone and inflammation ** * inflammation leads to an increase in smooth muscle tone * (air flow limitation caused by chronic bronchitis)
28
Cor pulmonale is
* hypertrophy of the right ventricle due to high pressure in pulmonary circulation * eventually Right ventricle HF
29
What causes cor pulmonale
* Pulmonary vessel vasoconstriction * Right ventricle has to work against higher pressures * Leads to hypertrophy * The intimal surface becomes fibrotic , leading Right sided HF
30
COPD inhaled treatment steps for patients who are predominantly breathless
1. SABA 2. SABA + LAMA 3. SABA + LABA + LAMA
31
COPD step wise treatment for patients with exacerbations AND breathlessness
1. SABA + LAMA 2. SABA + LABA + LAMA 3. SABA + LAMA + LABA and ICS (if FEV <50% + continued exacerbation)
32
When would you offer LTOT (long term oxygen therapy in COPD)
* Pa02 < 7.2 OR * Pa02 > 7.3 -8 with (polythaemia, nocturnal hypoxia, peripheral oedema, pulmonary hypertension) * signs of RVHF
33
When would you offer LTOT (long term oxygen therapy in COPD)
If in respiratory failure * Pa02 < 7.2 OR * Pa02 > 7.3 -8 with (polythaemia, nocturnal hypoxia, peripheral oedema, pulmonary hypertension) * signs of RVHF
34
What might an AECOPA (acute exacerbation of COPD look like?)
* sudeen worsening in respiratory symptoms (SOB, worsening cough, increased sputum volume, purulent sputum, wheezy, chest tightness) * using SABA more frequently
35
GOLD staging of COPD severity
FEV1 predicted = GOLD 1 - mild: ≥80% predicted. GOLD 2 - moderate: 50% - 80% predicted. GOLD 3 - severe: 30% - 50% predicted. GOLD 4 - very severe: <30% predicted.
36
what steriod is used to treat AECOPD
* prednisolone * 40mg for 5-7days
37
treatment for AECOPD
* nebulised SABA * Prednisolone (steriods) * Antibiotics (mosif purulent sputum) but most due to viral infections
38
oxygen target saturation in hospital for COPD
88-92% as COPD patients are on hypoxic drive (and oxygen therapy can supress their respiratory drive)
39
What tests would you carry out in the hospital for COPD
* FBC (RBC, Hb, iron, WBC, platelets, B12) * Haematocrit (% of blood that is RBC) * Biochemistry and glucose * Arterial blood gas (ABG) - oxygen, co2, ph * ECG * CXR * blood culutures * sputum microscopy
40
How would you manage COPD on ward
1. oxygen saturation of 88-92% 2. nebulised bronchodilators 3. corticosteriods (oral prednisolone) 4. antibiotics (IV if unwell) 5. ABG to assess for evidence of respiratory failure 6. non-invasive ventilation
41
Bronchial asthma is a type 1 hypersensitivity response a. true b. false
a. true related to the degranulation of MAST CELLS in airways which release chemical factors
42
Type 1 hypersensitivty response in bronchial asthma
- degranulation of mast cells - chemical factors released - 1. inflammation - inflammatory cells come to airway (swelling and oedema) - 2. bronchial smooth muscle constrict
43
GOLD stages of COPD severity
(mild, moderate, severe, very severe) FEV% ( >80%, , 50-80%, 30-50%, < 50%)
44
COPD patients will lack reversibility . what do this mean for their spirometry
score will be < .7 post-bronchodilator
45
Obstrutive spirometry shows
FEV1 reduced FVC reduced to lessor extent FEV1/FVC ratio reduced <0.7
46
Normal peak flow range
400-600ml (height/gender dependent) 80-100% of best value is NORMAL
47
Residual volume and total lung capacity increase in emphysema a. true b. false
a. true
48
There will be reduced gas transfer in COPD due to
* emphysema effects alveoli - there is a loss of alveoli
49
What would RR be in severe COPD exacerbation
> 25/min
50
flapping tremor in COPD is caused by
hypercapnia due impaired gas exchange in lung parenchyma, worsens with exercise, and is suggestive of respiratory failure.
51
Type one respiratory failure is caused by
hypoxia due to decrease in P02 (no hypercapnia)
52
Type two respiratory failure
Hypoxia (low 02) WITH increases in PC02 *hypercapnia* - ventilatory drive failure occurs in severe COPD - oxygen difficult to get in/C02 difficult to get out (squeezing neck of bottle)
53
signs of hypercapnia (increased C02 in blood - C02 retention)
* flapping tremor * drowsy * acidotic * hypoxic drive (reliant on peripheral chemoreceptors) aim for 88-92% 02 sats
54
Signs of cor pulmonale
* tachycardiac * oedmaa * raised JVP * congested liver * right axis deviation * Echo - pulmonary hypertension/tricuspid regurgitation * ECG - right pulmonary deviation, t-wave inversion
55
Secondary polycythaemia
* the body increases erythropoietin (made in kindey) in response to low 02 * raised Hb/ Haematocrit * increased vicosity -> increased BP
56
COPD is a cause of clubbing a. true b. false
b. false not a cause (which is result of low oxygen in blood) - found in lung cancer, bronchiectasis, cystic fibrosis
57
when to offer LTOT (long term oxygen therapy)
Pa02 < 7.3 kPa OR Pa02 7-.3-8 Kpa and -> secondary * Polycythaemia * Peripheral oedema (Swelling) * Pulmonary hypertension/Raised JVP
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