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CP2 - CBM > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is asthma?

A

Respiratory disorder characterised by recurrent episodes of dyspnoea, cough and wheeze caused by reversible airway obstruction

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2
Q

Describe the aetiology of asthma?

A

Children
occupational
HRT
Drug related

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3
Q

What are the common symptoms of asthma?

A

intermittent dyspnoea
wheeze
cough - often nocturnal
sputum

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4
Q

What are the precipitants of asthma?

A 
cold air
exercise
emotion
allergence
infection 
smoking and drugs (NSAIDs)
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5
Q

When is asthma worst?

A

morning

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6
Q

what are the other symptoms of asthma?

A

reduced exercise tolerance
disturbed sleep
acid reflux
other atopic diseases: eczema, hay fever, allergy or FHx

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7
Q

What are the signs of asthma?

A 
tachypnoea
audible wheeze
hyper inflated chest
hyperresonant percussion note
decreased air entry
widespread, polyphonic wheeze
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8
Q

Describe the three factors that contribute to the pathophysiology of asthma

A

bronchial muscle contraction - triggered by a variety of stimuli

mucosal swelling/inflammation - caused by mast cell and basophil degranulation resulting in release of inflammatory mediators

Increased mucus production

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9
Q

What are the associated risks of asthma?

A

Acid reflux
Polyarteritis nodosa
Churg-Strauss syndrome

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10
Q

What investigations are done for asthma?

A

PEFR monitoring

Spirometry

CXR

Skin prick test

Histamine or methacholine challenge

Aspergillus serology

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11
Q

What is step 1 in the tx of asthma?

A

SABA PRN

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12
Q

What is step 2 in the tx of asthma?

A

Add ICS

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13
Q

What is step 3 in the tx of asthma?

A

SABA + ICS + LTRA

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14
Q

What is step 4 in the tx of asthma?

A

SABA + ICS + LTRA + LABA

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15
Q

What is step 5 in the tx of asthma?

A

Switch ICS/LABA for MART

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16
Q

What is step 6 in the tx of asthma?

A

Increase MART
Add theophylline
Refer to specialist

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17
Q

What are the differentials of asthma?

A 
Pulmonary oedema - 'cardiac asthma' 
COPD 
Large airway obstruction - FB/tumour 
SVC obstruction - wheeze/dyspnoea, not episodic 
Pneumothorax
PE
Bronchiectasis 
Obliterative bronchiolitis - suspect in elderly
18
Q

What is COPD?

A

Progressive disorder; airway obstruction with little or no reversibility

chronic bronchitis and emphysema

Disease state characterised by airflow limitation - which is usually both progressive and associated with an abnormal inflammatory response to the lungs to noxious particles of gases

19
Q

What are the symptoms of COPD?

A

Cough - productive, white/clear sputum/haemoptysis

SOB on exertion
Wheeze, breathlessness following years of smoker’s cough
frequent infection

fatigue

20
Q

What are the signs of COPD?

A

Crepitations
Accessory mm use
poor chest expansion
hypercapnia - bounding pulse

21
Q

What are the systemic effects of COPD?

A 
Hypertension
Osteoporosis 
Depression
Weight loss
Loss of muscle mass
Cor pulmonale
Peripheral oedema
Low mood
Anxiety - closely affected with ability to breathe

CVD, peripheral vascular disease

22
Q

What are pink puffers

A

Breathless but not cyanosed

slim

23
Q

What is a bloater?

A

those with lower alveolar ventilation, lower PaO2 and a high PaCO2.
cyanosed but not breathless

may go on to develop cor pulmonale

24
Q

What is the main pathological finding of COPD?

A

Increased number of mucus secreting goblet cells in the bronchial mucosa, particularly larger bronchi

Infiltration of bronchi and bronchioles with inflammatory cells

Squamous, not columnar epithelial layer

Scarring and thickening of

25
Q

What does failure of respiratory effort result in in COPD?

A

Results in increased CO2 levels - short term leads to an increased RR but long term leads to loss of sensitivity to CO2 - patients will rely on the hypoxic drive to stimulate breathing

26
Q

What is emphysema?

A

dilation and destruction of lung tissue distal to the terminal bronchiole

27
Q

How does emphysema occur?

A

lack of inactivation of alpha-1-antitrypsin, leading to destruction of lung tissue

This happens as a result of increased inflammation or decreased anti-protease deficiency

28
Q

How does emphysema manifest?

A

loss of elasticity and increased TLC - loss of alveoli leads to decreased gas exchange and V/Q mismatch

Leads to fall in PaO2 and increased respiratory work demand. Patients become hyper expanded and find it difficult to blow off their CO2 and begin to retain it.

Patients have a prolonged expiratory period - they find it difficult to breathe out because their lungs are less elastic

29
Q

What are the risk factors for COPD?

A

smoking and inhalation of smoke
air pollution
individual susceptibility, alpha-1-antitrypsin deficiency
occupation

30
Q

What investigations are done for COPD?

A

Lung function tests - decreased FEC and FVC1 and reduction in ratio <70%

CXR - normal or may outline bulla

Hb and CRP may be raised

ABG may be normal at rest
ECG and echo

31
Q

Why is too much oxygen in exacerbation bad in COPD?

A

too much oxygen may cause worse inspiratory failure

patients rely on hypoxic drive

32
Q

What does ‘shunt’ refer to in COPD?

A

lung will optimise the parts of the lung that are still able to do their job (not the emphysema alveoli) - oxygen will make the damaged alveolar smaller and the working alveoli bigger.

When giving too much O2, ‘awakens’ the damaged alveoli to get bigger and get blood - BF distributed which then means not enough blood to alveoli which can do gas exchange properly - this increases CO2 retention - Haldane effect

33
Q

What is the management of COPD?

A

Smoking cessation

Inhalers and steroids

34
Q

How is smoking cessation achieved?

A

NRT - provides a low level of nicotine without the chemicals present in tobacco

Varencline - reduces cravings and blocks the rewarding and reinforcing effects of smoking

Bupropion - nicotine agonist

E-cigarettes (electronic device that delivers nicotine in a vapour thus inhaling nicotine without most of the harmful effects of smoking

35
Q

What are the mainstay of inhalers for COPD?

A

regular bronchodilators - B2 agonist and short acting muscarinic - ipratropium)

36
Q

How is exacerbation of COPD managed?

A

Oxygen 24-28% MAX - COPD patients rely on hypoxic drive
Salbutamol - 2-5mg
+/- ipratropium w/ salbutamol - 500 micrograms
Prednisolone - 30mg for 7-14 days

37
Q

How is long term oxygen therapy used for COPD?

A

when used for 15 hours daily

caution in acute setting - aiming for 88-92% sats

38
Q

How is NIV used in COPD?

A

Administration of ventilator support without using an invasive artificial airway

used in ICU and ward environments in patients with decompensated respiratory acidosis when medical help has not helped after 1 hour.

39
Q

What other management should be considered in COPD?

A

Vaccinations e.g. flu
pulmonary rehabilitation
surgery - bullectomy, lung volume reduction surgery or transplant

40
Q

What is the first step in treating COPD?

A

SABA / SAMA

41
Q

What is the second step in treating COPD?

A

If any asthmatic features:

SABA/SAMA +
LABA
+ ICS

If not:
SABA/SAMA + LABA

42
Q

What is the third step in treating COPD?

A

SABA + LAMA + LABA + ICS

CP2 - CBM (5 decks)

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