CT 10 - Airway Disease Flashcards

1
Q

what is asthma

A

chronic inflammatory airway disease characterised by intermittent and reversible (either spontaneously or with treatment) airway obstruction, and hyper-reactivity)

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2
Q

triggers for asthma

A

viral or bacterial infections, allergens, food additives and chemicals, aspirin, occupational exposures etc)
exercise
cold air
strong emotions

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3
Q

what is the pathophysiology in an acute asthma attack

A

Early phase = initiated by IgE antibodies produced by plasma cells. Bind to mast cells and basophils and upon exposure to the trigger the cells release cytokines and degranulate. The chemical mediators released such as histamine, leukotrienes and prostaglandins cause contraction of smooth muscle leading to bronchoconstriction

Late phase = immune cells such as eosinophils, basophils and neutrophils migrate to lungs and facilitate further bronchoconstriction and inflammation.

Alongside this there is hypersecretion of mucous and plasma leakage leading to oedema

(dendritic cells present to T cells and produces IL-4 for differentiation of T cells into Th2 cells. tH2 release cytokines which attract eosinophils and promote B cell proliferation. b cells produce IgE which binds to mast cells to release histamine

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4
Q

what is status asthmaticus

A

severe, prolonged asthma attack that doesn’t respond to standard treatment, and can be life-threatening. Neutrophils are important with this, as they move to the airway, and
change the epithelium, airway tone, and autonomic neural control. This leads to hypersecretion of
mucus, mucociliary function alteration, and increased smooth muscle responsiveness

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5
Q

Risk factors for asthma

A

FHx
atopic triad
obesity
GORD
allergens
occupational exposures (spray painters, nurses, chemical industry workers, handling animals, hairdressers and timber workers at greatest risk)

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6
Q

S + S of asthma

A

Shortness of breath
Chest tightness
Dry cough
Wheeze

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7
Q

what drugs can worsen asthma

A

BB especially non selective like propranolol

NSAIDs

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8
Q

what is FEV1

A

volume that has been exhaled at the end of the first second of forced expiration

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9
Q

what is FVC

A

volume that has been exhaled after a maximal expiration following a full inspiration

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10
Q

what happens to FEV1, FVC AND RATIO

A

FEV1 = reduced

FVC normal

FEV1/FVC = <70%

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11
Q

what investigations for asthma

A

1) spirometry

2) FeNO ( >50ppb in adults and >35 in children older than 5)

3) reversibility testing: measure baseline. give salbutamol. remeasure, greater than 12% increase in FEV1 is positive

4) peak flow variability diary

5) direct bronchial challenge testing with inhaled histamine or methacholine.

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12
Q

Example of SABA

A

salbutamol

Normally binding of adrenaline to B2 receptors in the lungs causes smooth muscle relaxation. SABA works as an agonist at b2 receptors.

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13
Q

SE of SABAs

A
  • tremor
  • nervousness
  • headaches
  • palpitations
  • muscle cramps
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14
Q

Example of inhaled corticosteroid

A

beclometasone

Used in patients whose asthma is not controlled by SABA alone
Taken everyday, regardless of whether the patient has symptoms

Side effects include oral candidiasis and stunted growth in children

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15
Q

Example of LABA

A

salmeterol
formeterol

act in same fashion as SABA but have longer half life.

  • taken everyday regardless of symptoms (preventative)
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16
Q

LTRA’s

A

montelukast

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17
Q

muscarinic antagonists

A
  • tiotropium
  • ipratropium

ACh normally binds to M3 receptors within the airway causing SM contraction and secretion of mucus. these drugs act as antagonists at M3 receptors providing relief

18
Q

what is MART

A

combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required

19
Q

1st line management for asthma

A

1) low dose ICS/formoterol combination
OR if severe exacerbation low dose MART

2) Low dose MART

3) mod dose MART

4) if feno or eosinophil count raised refer to specialist.
if not consider LTRA or LAMA in addition to mod dose MART

5) specialist if not under control despite above steps

20
Q

management of asthma in children aged 5-11

A

First step
twice-daily paediatric low-dose inhaled corticosteroid (ICS) + short-acting beta2 agonist (SABA) as needed

2nd:
MART pathway or conventional pathway

21
Q

COPD

A
  • chronic bronchitis = long-term symptoms of a cough and sputum production due to inflammation in the bronchi
  • emphysema = involves damage and dilatation of the alveolar sacs and alveoli, decreasing the surface area for gas exchange.
22
Q

investigations for COPD

A

The following investigations are recommended in patients with suspected COPD:
post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%
chest x-ray: hyperinflation, bullae, flat hemidiaphragm. Also important to exclude lung cancer
full blood count: exclude secondary polycythaemia
body mass index (BMI) calculation

23
Q

management of COPD without asthmatic involvement

A

> smoking cessation advice: including offering nicotine replacement therapy, varenicline or bupropion
annual influenza vaccination
one-off pneumococcal vaccination

a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is first-line treatment

add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)

24
Q

signs of severe COPD

A

very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
cyanosis
polycythaemia
peripheral oedema
raised jugular venous pressure
oxygen saturations less than or equal to 92% on room air

25
Treatment of asthma exacerbation
O SHIT ME (M BEFORE T) oxygen target sats are 94-98% salbutamol nebs hydrocortisone IV or oral pred Ipratropium nebs Magnesium sulfate IV (calcium antagonist that relaxes SM - bronchodilation) theophylline escalate care: intubation, ventilation etc
26
most common cause of exacerbation in COPD
- infection with haemophilus influenzae - or strep pneumoniae - or moraxella catarrhalis
27
treatment of acute COPD exacerbation
increasing the frequency of bronchodilator use (i.e. SABA, and consider giving via a nebuliser), giving oral prednisolone 30mg daily for 5 days, and giving oral antibiotics only if sputum is purulent or there are signs of pneumonia (first line are amoxicillin, clarithromycin, or doxycycline)
28
whats TII RF
- hypoxia - hypercapnia
29
what are examples of non invasive ventilation used in severe COPD
- CPAP - continous positive airway pressure - IPAP inspiratory positive airway pressure - BIPAP Bilevel positive airway pressure
30
O2 sats target in COPD patients
- 88 to 92%
31
does improvement in FEV1/FVC ratio following reversibility testing indicate asthma or copd
asthma
32
features of obstructive disease
- reduced FEV1 - slightly reduced or normal FVC - reduced ratio
33
features of restrictive disease
- reduced FEV1 - reduced FVC - normal ratio: as both factors are equally affected
34
causes of obstructive disease
- Asthma - COPD - CF - bronchiectasis
35
causes of restrictive lung disease
pulmonary: - pulmonary fibrosis - pulmonary oedema -parenchymal lung tumours - pneumoconiosis non pulmonary: - chest wall deformities/skeletal - neuromuscular motor neuron disease, myasthenia gravis, Guillan-Barre syndrome) -Connective tissue diseases -Obesity or pregnancy
36
what is alpha 1 antitrypsin deficiency
Alpha-1 antitrypsin (AAT) is a protein that forms in your liver and moves through your bloodstream to your lungs. It’s the “off switch” for an enzyme called neutrophil elastase. Neutrophil elastase is important for fighting infections in your lungs, but it can also destroy your healthy lung tissue. After elastase has had time to help fight an infection, AAT shuts it off (inhibits) so it won’t damage your lungs. If a gene mutation causes low levels of AAT or creates incorrectly formed AAT, you won’t have enough in your lungs to stop elastase, which will start breaking down the protein elastin in your lungs. Elastin gives strength to the small air sacs of your lungs (alveoli) and allows them to stretch and contract, like a rubber band. Without it, your alveoli lose their shape and become floppy. This makes it so you can’t breathe or get oxygen properly. This is a condition called emphysema.
37
what is cor pulmonale
right-sided heart failure caused by respiratory disease. The increased pressure and resistance in the pulmonary arteries (pulmonary hypertension) limits the right ventricle pumping blood into the pulmonary arteries. This causes back-pressure into the right atrium, vena cava and systemic venous system.
38
causes of cor pulmonale
COPD (the most common cause) Pulmonary embolism Interstitial lung disease Cystic fibrosis Primary pulmonary hypertension
39
Symptoms of cor pulmonale include:
Shortness of breath Peripheral oedema Breathlessness of exertion Syncope (dizziness and fainting) Chest pain
40
acute exacerbation of COPD results in what..
respiratory acidosis Low pH indicates acidosis Low pO2 indicates hypoxia and respiratory failure Raised pCO2 indicates CO2 retention (hypercapnia) Raised bicarbonate indicates chronic retention of CO2