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Respiratory System > Asthma > Flashcards

Asthma Flashcards

1
Q

What is asthma?

A

Chronic inflammation of airways which causes narrowing

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2
Q

Causes of asthma

A

Genetic factors (family history)
Environmental factors

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3
Q

Triggering substance of asthma

A
  • air pollution: cigarette smoke, car fumes
  • allergens: dust, animals, mould, pollen
  • medication: aspirin (NSAIDs), beta blockers
  • cold air
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4
Q

Symptoms of asthma

A
  • dry cough (often at night)
  • chest tightness
  • dyspnoea
  • wheezing/high pitched whistling on exhalation on
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5
Q

Why is a dry cough in asthma more common at night?

A

Increased vagal activity at night

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6
Q

What investigations can be used to diagnose asthma?

A
  • Peak flow + diary
  • Spirometry (<70%) + reversibility testing
  • FeNO
  • direct bronchial challenge test
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7
Q

diagnosis of asthma

A
  • spirometry with bronchodilator reversibility: <70% + improvement of >12% with bronchodilators
  • FeNO: >40ppb
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8
Q

Outline the fractional exhaled nitric oxide test for investigation of asthma
What result would support diagnosis?
Why could it be unreliable?

A
  • measures the conc. of NO exhaled (marker for airway inflammation)
  • steady exhale for around 10s into device
  • > 40ppb is a positive test
  • smoking lowers FeNO so could be unreliable in smokers
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9
Q

Management of asthma

A
  • education
  • up to date vaccinations
  • avoid triggers
  • drug treatment: bronchodilators + steroids
  • inhalers
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10
Q

Stepwise approach of medications in chronic asthma

A

Only move onto next step if current step isn’t working:
- SABA e.g. salbutamol, terbutaline PRN
.
- ICS e.g. beclomethasone
- LABA e..g salmeterol, formoterol
- higher dose ICS, leukotriene receptor antagonists
- referral to specialist care

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11
Q

Difference in NICE + BTS guidelines for asthma management

A
  • low dose ICS first for both
  • NICE: add LTRA
  • BTS: add LABA
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12
Q

How do you grade asthma exacerbation severity?

A

mild:
- no features of severe asthma
- PEFR >75% of best or predicted
moderate:
- no features of severe asthma
- PEFR 50-75%
severe: (any one of)
- PEFR 33-50%
- cannot complete sentences in 1 breath
- RR >25
- HR >110
life threatening: (any one of)
- PEFR <33%
- sats <92% or ABG pO2 <8kPa
- cyanosis, poor resp effort or near/fully silent chest
- exhaustion, confusion, hypotension or arrhythmias
near fatal:
- all of above but raised pCO2

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13
Q

How do you manage an acute asthma exacerbation?

A
  • oxygen (aim for 94-98%)
  • 2.5-5mg nebulised salbutamol (repeat after 15mina if needed)
  • 40mg oral prednisolone
    .
  • if severe, 500mg nebulised ipratropium bromide
    .
  • if life threatening or near fatal:
  • urgent ITU, portable CXR + anaesthetist assessment
  • IV aminophylline
  • consider IV salbutamol if nebulised route ineffective
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14
Q

What class of drug is aminophylline + what is its mechanism of action?

A

Methylxanthine class
- it inhibits phosphodiesterase > increased cAMP in smooth muscle cells > bronchodilation
- also has anti-inflammatory effects

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15
Q

What does the term controlled oxygen refer to?
Who typically needs it?

A
  • the administration of O2 at specific conc. or flow rate to achieve a target O2 saturation
  • key in patients with COPD (risk of CO2 retention)
    Key aspects:
  • precise control of O2 delivery
  • monitoring O2 sats
  • prevention of complications e.g. hypercapnia
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16
Q

Criteria for safe asthma discharge post exacerbation

A
  • PEFR >75%
  • stop regular nebulisers 24hrs prior to discharge
  • reassess inhaler technique + adherence
  • written asthma action plan
  • at least 5 days oral prednisolone
  • GP follow up within 2 days
  • resp clinic follow up within 4 weeks
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17
Q

What is an asthma management plan?

A

A written document designed for each individual with asthma to help control their symptoms + reduce exacerbations
Components:
- daily treatment instructions
- monitoring + symptoms tracking e..g peak flow diary
- action plan for exacerbations

18
Q

Blue vs brown inhalers

A

Blue: bronchodilator acts a reliever (short term)
Brown: anti inflammatory (corticosteroids) to reduce risks of asthma attacks (longer term)

19
Q

Describe how asthma attacks happen and what process take place in the body

A
  • triggered by something in th environment
  • picked up by dendritic cells
  • present to type 2 helper cells - CD4+
  • cytokines releases (IL-4+IL5)
  • IL-4: production of IgE antibodies > coat mast cells and stimulate the release of histamines, leukotrienes + prostaglandins
  • IL-5: act on eosinophils > release more cytokines + leukotrienes
  • causes smooth muscle spasm + increased mucous secretion
  • also increased vascular permeability > immune cells from blood > eosinophils damage endothelium of lung
  • airways become even narrower
20
Q

What immune cells are in involved asthma?

A

Type 2 helper cells
B cells > plasma cells > antibodies

21
Q

What is the atopic triad?

A

Asthma
Atopic dermatitis
Allergic rhinitis

22
Q

What type of reaction do IgE antibodies cause?

A

Type 1 hypersensitivity

23
Q

What cytokines are released in asthma?

A

IL-4
IL-5

24
Q

What does the release of IL-4 cause?

A
  • production of IgE antibodies (type 1 hypersensitivity reaction)
  • IgE coat mast cells
  • histamines, leukotrienes + prostaglandins are released
25
Q

What does the release of IL-5 cause?

A
  • act on eosinophils
  • release leukotrienes + more cytokines
26
Q

What does chronic asthma cause?

A

Airways remodelling - irreversible changes
- hypertrophy + hyperplasia of smooth muscle
- hypertrophy of mucous glands
- thickening of basement membrane

27
Q

What three processes affect the airways in an asthma attack?

A
  • smooth muscle spasm
  • increased mucous secretion
  • increased vascular permeability > immune cells from blood > eosinophils damage endothelium of lung

Makes airways even narrower

28
Q

What is asthma characterised by?

A

A triad of:
- bronchial smooth muscle contraction
- airways inflammation
- increased secretions

29
Q

What are the two phases of immune response in asthma?

A

Immediate response: type 1 hypersensitivity (IgE) > bronchial smooth muscle contraction
Late phase response: type IV hypersensitivity (eosinophils) > airways inflammation

30
Q

Outline the immediate response to asthma triggers

A
  • type 1 hypersensitivity
  • production of IgE antibodies
  • coat mast cells
  • histamine, prostaglandins + leukotrienes released
  • causes bronchoconstriciton
31
Q

Outline the late phase response in asthma triggers

A
  • type IV hypersensitivity
  • includes inflammatory cells e.g. eosinophils, mast cells, lymphocytes, neutrophils
  • release leukotrienes + cytokines
  • causes airway inflammation
32
Q

What features of airway inflammation cause reduced airflow?

A
  • mucosal swelling (oedema)
  • thickening of bronchial walls
  • mucous over production
  • smooth muscle contraction
  • epithelium is shed + incorporated into thick mucous
    .
  • triggers airway hyper-responsiveness
33
Q

What are the effects of airway narrowing on gas exchange?

A

reduced ventilation > V/Q mismatch

34
Q

How can asthma cause type 1 respiratory failure?

A
  • in unmanaged mild asthma
  • airways narrowing > reduced ventilation
  • hyperventilation can’t compensate for hypoxaemia but can compensate for CO2 retention
  • low pCO2 + low pO2
35
Q

How can asthma cause type 2 respiratory failure?

A
  • in severe attacks
  • complete blockage of some airways + exhaustion which limits amount of CO2 which can be breathed out
  • this leads to a rise in CO2 in body
  • high pCO2 + low PO2
36
Q

Why might a normal pCO2 level on ABG be concerning in a patient having a acute asthma exacerbation?

A
  • initially the patient is hypocapnic
  • the asthma attack continues + severity of airflow obstruction increases
  • the hypocapnia becomes normocapnia before becoming hyercapnia
  • normocapnia is a step in the progression from type 1 respiratory failure to type 2
37
Q

Describe airway hyperresponsiveness

A
  • inflammation makes airway more ‘reactive’ to triggers
  • triggers can cause bronchoconstriction
38
Q

What type of countries is asthma more prevalent in?

A

High income countries

39
Q

Describe an asthmatic’s airway when they are well/symptom free

A

Inflamed + thickened walls

40
Q

Describe an asthmatic’s airway during an attack

A
  • inflamed + thickened wall
  • increased mucous
  • tightening smooth muscle
  • air trapped in alveoli
41
Q

What is atropy?

A

Genetic tendency to develop allergic diseases

42
Q

What is rhinitis?

A

Inflammation of mucous membrane inside nose

Respiratory System (25 decks)

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