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COPD Flashcards

1
Q

how do muscarinic antagonists work?

A

SAMA/ LAMA mechanism: competitive inhibition of muscarinic receptors on bronchiole smooth muscle. By antagonising Ach action, this prevents increase for intracellular calcium which causes bronchodilation.

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2
Q

why are SAMA/ LAMA used more in COPD than asthma?

A
  • More benefits in COPD
  • Can be nebuliser in severe exacerbations of asthma
  • Only by inhalation (dry powder/ aerosol) or nebuliser (caution for glaucoma)
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3
Q

how long does LAMA effect last?

A

24hrs

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4
Q

what are the side effects of LAMA?

A
  • Side effects: dry mouth, in men- difficulty passing urine
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5
Q

why are LAMA and LABA used together?

A

further benefits – better lung function, improved symptoms, better exercise tolerance.

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6
Q

what therapy is not recommended as monotherpay within COPD?

A

ICS - modest effect in relieving breathlessness/ lung function

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7
Q

what are the side effects of corticosteroids?

A

glaucoma, central fat deposition, osteoporosis, increased risk of infection, hirsutism, peptic ulcer, increased appetite, emotional disturbances, hypotension, hypokalaemia

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8
Q

what is the action of theophylline/ aminophylline?

A

vasodilator, anti-inflammatory, contributes to immunomodulatory actions

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9
Q

what is aminophylline hydrolysed to?

A

rapidly hydrolysed after absorption from gut to theophylline

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10
Q

what are the side effects of theophylline/ aminophylline?

A
  • GI- nausea, vomiting, diarrhoea
  • CNS stimulation – insomnia, irritability, occasional seizures at high plasma concentrations
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11
Q

what does theophylline/ aminophylline react with?

A

many antibiotics

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12
Q

before nebulising a breathlessness patient who isnt responding to therapy what should you check?

A

inhaler technique

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13
Q

when are mucolytic used?

A

used in patients with chronic productive cough with thick vicious sputum

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14
Q

what is contra indicated with mucolytic medication?

A

history of peptic ulcer

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15
Q

define acute exacerbating COPD?

A

sustained or worsening symptoms from usual stable state, which is beyond day to day variations with acute onset

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16
Q

what are the non defining symptoms of acute exacerbating asthma?

A
  • symptoms may include: increased SoB, increased cough, increased sputum production and change in sputum colour
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17
Q

what is the management of exacerbated COPD?

A
  • oxygen
  • steroids – 30mg for 7-14mg
  • bronchodilators- salbutamol/ ipratropium
  • antibiotics – purulent sputum – amoxicillin, doxycycline, clarithromyocin
  • aminophylline
  • consider rescue packs on discharge – personal care plan
  • end stage – opioids/ benzodiazepines
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18
Q

which COPD can take prophylatic AB?

A

those who do not smoke

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19
Q

what primarily causes COPD?

A

smoking

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20
Q

describe COPD

A

COPD: predominately caused by smoking and characterised by airflow obstruction that is not fully reversible, does not change markedly over several months and is usually progressive
- Exacerbations often occur where there is rapid and sustained worsening of symptoms beyond normal day to day variations and require change in treatment.

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21
Q

what are the symptoms of COPD?

A

wheezing, lip pursing, chronic productive cough, barrel chest, dyspnoea, prolonged expiratory time, bronchitis – increased sputum, digital clubbing

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22
Q

what are the clinical features of COPD?

A

Clinical features: easily fatigued, frequent resp infections, use of accessory muscles for normal breathing, orthopneic, cor pulmonale (later in disease), thin appearance

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23
Q

what is emphysema?

A

alveolar destruction - alot bigger hence less SA

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24
Q

how quick can hypoxia occur?

A

seconds/ minutes

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25
Q

how long does it take to have respiratory acidosis?

A

hours

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26
Q

how long does it take for metabolic compensation?

A

days

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27
Q

what is normal Pa of O2?

A

10.6-13.4

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28
Q

what is normal PaCO2?

A

4-6kPa

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29
Q

what is normal bicarbonate levels?

A

22-26mmol/L

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30
Q

how do you assess an ABG reading?

A
  1. Look at pH – acidosis or alkalosis
  2. What caused it? Resp first. If high CO2 – more acidic (lower pH – respiratory acidosis). If low CO2 – more alkaline (higher pH – respiratory alkalosis)
  3. Is there any compensatory? Check bicarb – higher – metabolic alkalosis, if lower than metabolic acidosis
    - Compensatory takes time to occur – so can judge how long this has occurred for
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31
Q

how many hospital beds are occupied by patients with smoking related illnesses?

A

1 in 20

32
Q

what are the 5As in smoking cessation?

A

ask (regularly ask all patients if they smoke), advise (advise all smokers to quit in unambiguous way), assess (tailor to patients own needs), assist (offer help), arrange (follow ups are essential and likely to increase long term abstinence)

33
Q

out of the 5As what As does the UK focus on for smoking cessation?

A
  • UK mainly focuses on ASK, ADVISE and ASSIST
34
Q

what can nicotine dependence be a predictor for within smoking cessation?

A
  • Nicotine dependence is a predictor of withdrawal symptoms and intensity of symptoms required. Reliable indicator – smoking within 30 mins if waking. Severe dependence – smoking within 5 mins of waking
35
Q

what can nicotine dependence be a predictor for within smoking cessation?

A
  • Nicotine dependence is a predictor of withdrawal symptoms and intensity of symptoms required. Reliable indicator – smoking within 30 mins if waking. Severe dependence – smoking within 5 mins of waking
36
Q

what are pharmacotherapies used in smoking cessation?

A

used in those with nicotine dependence – nicotine gum, patchy, lozenge, nasal spray, inhaler, bupropion and varenicline

37
Q

what is varenicline?

A

partial nicotine agonist that relieves cravings and withdrawal symptoms and reduces rewarding feeling when you smoke.

38
Q

what is bupropion within smoking cessation?

A

– originally an antidepressant – reduces urge to smoke and symptoms of nicotine withdrawal.

39
Q

what differentials of COPD does a CXR rule out?

A

congestive Hf, bronchiectasis, TB, pnuemonia

40
Q

what causes bronchitis?

A
  • Caused mainly by smoking – can be infection caused (viral/ bacterial), air pollution and occupational exposure (more in cities with coal fires – mining etc)
41
Q

what is the pathophysiology of chronic bronchitis?

A
  • It is the enlargement of mucus secreting glands in trachea and bronchi – hypersecretion. There is also immobilisation and damage to cilia. There is bronchial inflammation and progressive airflow limitation – the tar from cigarettes is not moved and hence causes blocking.
42
Q

how might a patient with chronic bronchitis may feel after waking up?

A
  • Might wake up feeling better and cilia has been able to move (the cigarette paralyses the cilia) but then cough up all the rubbish
43
Q

what is emphysema?

A
  • Long term progressive disease of lungs in which there is a loss of alveolar walls and reducing surface area for exchange of gases
  • Obstructive – because airflow on exhalation is slowed and stopped
44
Q

what are the two main types of emphysema?

A
  • Two main types – centrilobular (associated with smoking) and panlobular (inherited)
45
Q

how does smoking contribute to emphysema?

A
  • Tobacco products release inflammatory products from white cells – neutrophils and this breaks down elastic tissue and circulating a-1 antitrypsin has anti-elastase activity.
  • Tobacco products inhibit a-1- antitrypsin
46
Q

the air spaces in emphysema are decreased what is the consequence?

A

less efficient gas exchange
- The airspaces are at least2x diameter of normal reduce area of wall by 16 fold

47
Q

what can cause pulmonary fibrosis?

A
  • Lots of causes – some diffuse some local. Idiopathic PF – most common form of smoking related interstitial lung disease
  • Other causes: some infectious agents (Epstein barr virus), certain medications, pollution, gastro- intestinal reflux (highly acidic HCL from stomach escapes and then could go to pharynx and larynx in tiny amounts which can then enter trachea and into lungs) – could be a combination of many things? COVID?
48
Q

what is the pathophysiology of pulmonary fibrosis?

A

Loss of type 1 pneumocytes – failure of normal maturation. There is an excessive deposition of collagen

49
Q

what are the clinical features of pulmonary fibrosis?

A

dry cough on exertion, progressive SoB with exercise, crackles on auscultation – Velcro sound, finger clubbing, inexorable progression. Not much mucus brought up

50
Q

what are the causes of lung cancer?

A

tobacco, air pollutants (car fumes), radiation including gases, occupational risks (asbestos, chromates, arsenic, mustard gas)

51
Q

what is a primary lung cancer?

A

starts in lungs

52
Q

why is secondary lung cancer so common?

A

blood flows through lungs - to get oxygen

53
Q

what are clinical features of lung cancer?

A

weight loss, cough, haemoptysis, dsypnoea, finger clubbing, voice changes, metastases in other organs and non-metastatic distant effects

54
Q

how many types of primary lung cancer are there?

A

4

55
Q

what can cause acute resp infections?

A

lower resp tract infection – acute bronchitis, infective exacerbation of chronic lung disease, pneumonia

56
Q

what can cause a chronic lung infection?

A

COPD, asthma, bronchiectasis, TB

57
Q

what are signs of pneumonia?

A

infection of lung interstitum, alveoli and airways – cough, sputm, SoB, fever, pleuritic, chest pain. Signs of consolidation and CXR changes

58
Q

how do you classify pneumonia?

A
  • Pneumonia gets classified by source, localisation and pathogen
59
Q

what are the defence mechanisms within the respiratory system?

A

nose (filters, warms, humidifies), larynx (coughing), lungs (mucociliary clearance), cellular and humoral immunity

60
Q

what causes pleural rub?

A

– inflamed tissue extending to pleura (visceral and parietal) – very painful. Creaking

61
Q

why would you get coarse crackles?

A

liquid surface

62
Q

what would cause a wheeze?

A

asthmatic
polyphonic due to airway narrowing

63
Q

what is a genetic risk factor of COPD?

A

alpha -1 anti trypsin deficiency

64
Q

when does alpha 1 anti trypsin deficiency present?

A

younger patients (20-40)

65
Q

what is the result of anti-1 antripysin?

A
  • Alpha-1 antitrypsin – protease inhibitor. Actions – prevent neutrophil elastase breaking down alveolar structures.
  • Deficiency leads to increased destruction of alveolar structures – early onset emphysema
  • Some cases involve impaired secretion of alpha 1 antitrypsin in the liver – causing a uild up of it there which leads to cirrohosis
66
Q

what is alpha 1 antitrypsin deficiency?

A
  • elastase breakdown elastin
    (elastin maintains structural integrity of alveoli)
    alpha 1 antitrypsin stops elastase
    deficiency causes emphysema
67
Q

where is the emphysema seen in A1AT?

A

panlobular in lower zone

68
Q

how do the cells differ between asthma and COPD?

A

asthma - eosinopjils, CD4+, T cells
COPD: neutrophilic infilitration, CD8+, T cells and macrophages

69
Q

what is seen within chronic bronchitis?

A

goblet cell hyperplasia, mucus secretion, chronic inflam and fibrosis, narrowing of small airways

70
Q

what can cause cor pulmonale?

A

COPD
PE
ILD
primary pulmonary HTN

71
Q

what is the pathology of cor pulmonale?

A

right ventricular impairment
chronic hypoxia causing vasoconstriction in pulmonary arteries

72
Q

what are signs of cor pulmonale?

A

raised JVP, cyanosis, oedema, parasternal heave, hepatomegaly
pursed lip breathing
coarse crackles
CO2 retention

73
Q

what are symptoms of COPD?

A

chronic cough - usually productive
sputum production
SoB- usually on exertion
frequent bronchitis

74
Q

how is breathless measured and assessed?

A

MRC dyspnoea scale - measuring SoB
1. SoB on strenuous activity
5> SoB on minimal activity

75
Q
A

respiratory (10 decks)

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