Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > Asthma > Flashcards

Asthma Flashcards

1
Q

What is the definition of asthma?

A

chronic inflammatory airway disease characterised by intermittent airway obstruction and hyper-reactivity.

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

What are the 2 types of asthma?

A
  • Allergic/ eosinophilic: allergens and atopy
  • Non-allergic/ non-eosinophilic: e.g. exercise, cold air and stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Epidemiology of asthma

A
  • 3 deatsh a day in the UK
  • Commonly starts in childhood between the ages 3-5 years and may either worsen or improve during adolescence
  • Peak prevalence between 5-15 years
  • 60k hospital admissions a year
  • 160k diagnosed a year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

RFs for asthma

A

Eczema
Allergic rhinitis
Family history
Allergens
Viral upper respiratory tract infection
Occupational exposure

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

What is there an excessive reaction from in asthma?

A

Th2 cells against specific allergens

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

What do allergens from environmental triggers get picked up by?

A

picked up by dendritic cells and presented to Th2 cell. This leads to production of cytokines e.g. (IL-3, IL-4, IL-5, IL-10, IL-13)

leads to the production of IgE antibodies which coat mast cells and stimulate them to release granules containing histamines, leukotrienes and prostoglandins

Results in activation of eosinophils which promote immune response by releasing more cytokines and leukotrienes.

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

What happens minutes after the exposure to allergen?

A
  • Bronchospasm
  • leads to constriction of the airway as more mucus is produced in response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is there an increase of in asthma?

A
  • Vascular permeability + addition of immune cells from the blood.
  • A few hours after exposure immune cells release chemical mediators that physically damage the endothelium of lungs.
  • Initially inflammatory changes reversible - but over years become irreversible - thickens epithelial basement mebrane reducing airway diameter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What cytokines do the T cells release?

A

Allergens + microbes and pollutants attack airway epithelial cells releasing dendritic cells
Th17 - IL-17, CXCL8
Th1 - IFNg, TNFa
Both activate neutrophils
Th2 - IL-4, IL-13 (Activates B cells), IL-5
ILC2 - IL-5 (which activates Eosinophil), IL-13 which activates airway smooth muscle cells

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

What activates TH2 and ILC2 cells?

A

Cytokines IL-33, 25 and TSLP from airway epithelial cells

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

Genetic factors of asthma

A
  • Genetic susceptibilitypredisposes patients toairway hyper-responsiveness, triggered by environmental factors such as viral infection, allergens (the main cause in children), cold and exercise
    • Genes controlling the production of cytokines IL-3,-4,-5,-9 & -13
    • ADAM33 is associated with airway hyper-responsiveness and tissue remodelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Asthma ages

A

causes of childhood asthma diagnosed before age 12 are thought to be due to a stronger genetic influence, whereas later onset asthma is more likely to be largely due to environmental factors.

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

Signs of asthma

A
  • Diurnal PEFR variation: worse at night and early morning
  • Dyspnoea and expiratory wheeze due to change from laminar to turbulent flow
  • Samter’s triad
    • Nasal polyps
    • Aspirin insensitivity
    • Asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Symptoms of asthma

A
  • Episodic shortness of breath: diurnal variation (worse at night and early morning)
  • Dry cough
  • Wheeze and ‘chest tightness’
  • May be sputum
  • History of exposure to a trigger
  • Nocturnal symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Primary investigations of asthma:

A
  • Fractional exhaled nitric oxide (FeNO):>40 ppb is positive in adults
  • Spirometry:FEV1/FVC <70% suggests obstruction. If obstruction is found, BDR should be carried out
    • Bronchodilator reversibility (BDR): improvement of FEV1 by ≥12%andincrease ≥200ml in volume post-bronchodilator
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What other investigations should you consider for asthma?

A

Peak flow rate
Allergy testing
Chest X-ray

17
Q

Key drugs in asthma

A
  • SABA(short-acting beta-agonist); e.g. salbutamol
  • ICS(inhaled corticosteroid); e.g. beclomethasone.
  • LTRA(leukotriene receptor antagonist); e.g. montelukast
  • LABA(long-acting beta-agonist); e.g. salmeterol
  • MART(maintenance and reliever therapy); this iscombinedfast-acting LABA and ICS for symptomatic relief and maintenance in a single inhaler.
18
Q

Management of Asthma

A
  1. SABA
  2. SABA + low dose ICS
  3. SABA + ld ICS + LTRA
  4. SABA + ld ICS + LABA - consider stopping LTRA depending on response
  5. SABA +/- LTRA - switch ICS/LABA to MART
  6. SABA+/-LTRA - increase dose of ICS within MART
  7. SAVA +/- LTRA + one of the following - increase ICS to high dose or trial and additional drug
19
Q

Treatment step down and monitoring

A
  • Aim is to use lowest effective doses of medication to manage symptoms
  • BTS guidelines recommend stepping down treatment approximatelyevery 3 months
  • Patients withstable asthmaare usually reviewed formally on anannual basis, whilst those with recenttreatment escalationor frequent exacerbationsshould be reviewedmore frequently
  • A specific step-down regimen isnotdescribed (e.g. step 4 to step 3), but step-down requires consideration of factors such as patient preference, treatment duration and side-effect profile
  • Reduction of inhaled corticosteroids: 25-50% at a time
20
Q

Other things to do with asthma

A
  • Each patient should have an individual asthma self-management programme
  • Yearly flu jab
  • Yearly asthma review
  • Advise exercise and avoid smoking
21
Q

Complications of asthma

A
  • Asthma exacerbations:typically triggered by an upper respiratory tract infection, pneumonia, or exposure to a trigger, e.g. an allergen or occupational exposure
  • Pneumothorax
  • Oral thrush: due to steroid medication
22
Q

What is an asthma exacerbation?

A

acute or subacute episode of progressive worsening of symptoms of asthma, including shortness of breath, wheezing, cough, and chest tightness.

23
Q

Epidemiology of asthma

A

Asthma is responsible for 60,000 admissions in the UK every year

24
Q

Key triggers of an asthma exacerbation

A
  • Known diagnosis of asthma
  • Allergen exposure:pollen, dust mite, pets
  • Occupationalexposures:plastics, foam, glue, flour
  • Viral infection
  • Smokingexposure
  • Pollution
  • Exercise
25
Q

General clinical manifestations of asthma exacerbations

A
  • Progressively worsening shortness of breath
  • Use of accessory muscles
  • Fast respiratory rate (tachypnoea)
  • Symmetrical expiratory wheeze on auscultation
  • The chest can sound “tight” on auscultation with reduced air entry
26
Q

Moderate asthma exacerbations

A

PEFR 50-75%

27
Q

Severe asthma exacerbation

A
  • PEFR 33-50%
  • Respiratory rate ≥ 25
  • Heart rate ≥ 110
  • Inability to complete sentences in one breath
28
Q

Life-threatening asthma exacerbation

A
  • PEFR < 33%
  • SpO2< 92%
  • PO2< 8 kPa
  • PCO2normal (4.0-6.0 kPa)
29
Q

Near fatal asthma exacerbations

A

High pCO2 (> 6.0 kPa) and/or requiring ventilation with raised inflation pressures.

30
Q

Investigations of asthma

A
  • Peak flow expiratory rate (PEFR)
  • ABG:patients will initially have respiratory alkalosis. Abnormal or high PCO2is an extremely concerning sign as it implies patient is tiring.
  • Inflammatory markers:raised CRP and WCC may suggest an infective trigger
  • CXR:hyperexpansion +/- a focus of infection
31
Q

Management of asthma exacerbations

A
  • Moderate asthma: treated in primary care with
    • Inhaled salbutamol
    • 5-day course of prednisolone
  • Severe or life-threatening exacerbation: treatment in hospital
32
Q

Immediate management of asthma exacerbations

A

Oxygen:
Nebulised bronchodilators: salbutamol 5mg first line
Ipratropium bromide 0.5mg can be given additionally every 4-6 hours

Corticosteroids:
Prednisolone 40mg
100mg hydrocrotisone IV

33
Q

If patient does not respond to treatment in asthma what do you do?

A
  • IV bronchodilator:magnesium sulphate (first-line)
  • ICU admission:if the patient is not responding to the above therapy, they may need ICU admission for further IV bronchodilation (salbutamol or aminophylline) and possible intubation
34
Q

Complications of asthma exacerbations

A
  • Intubation:those who fail to respond to medical therapy will require ICU admission and intubation
  • Death:respiratory failure can lead to death. Three people die from asthma everyday in the UK
35
Q

OSHITME for asthma exacerbation

A

Oxygen
Nebulised salbutamol
IV hydrocortisone/ prednisolone
Ipratropium bromide
IV theophylline
IV MgSO4
E escalate

Respiratory (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions