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Resp > Asthma > Flashcards

Asthma Flashcards

1
Q

Definition?

A

Chronic respiratory condition linked to airway inflammation and hyper-responsiveness.

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2
Q

Risk Factors?

A
  • Family history of atopic disease
  • Male -pre-pubertal
  • Female-childhood to adulthood
  • Respiratory infections in infancy
  • Exposure to tobacco smoke
  • Premature birth and associated low birth weight
  • Obesity
  • Social deprivation
  • Exposure to inhaled particulates
  • Workplace-flour dust and isocyanates
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3
Q

Differentials and key signs?

A
  • Bronchiectasis-copious sputum, frequent chest infections, a history of childhood pneumonia, and coarse lung crepitations
  • COPD-Clinical features of COPD include a productive cough anddyspnoea on exertion in a person over 35 years of age whois a current or previous smoker
  • Ciliary dyskinesia-clinical features include persistent moist cough present from birth.
  • CF-moist coughandgastrointestinal symptoms that are often present from birth, finger clubbing, and failure to thrive in children.
  • Dysfunctional breathing-breathlessness, dizziness, light-headedness, and peripheral tingling.
  • Foreign body aspiration-suggested by sudden-onset cough, stridor (upper airway) or reduced chest wall movement on the affected side, bronchial breathing, and reduced or diminished breath sounds
  • GORD-cough, postural and food-related symptoms, andvomiting.
  • HF- orthopnoea, oedema, a history of ischaemic heart disease, and fine lung crepitations.
  • Interstitial lung disease-dry cough and fine lung crepitations
  • Lung cancer-persistent cough, haemoptysis, weight loss, or persistent hoarse voice.
  • Pertussis-vomiting after coughing, or an inspiratory whoop
  • PE-acute-onset breathlessness, pleuritic pain, haemoptysis, crackles, and sinus tachycardia.
  • TB-persistent productive cough, which may be associated with breathlessness and haemoptysis
  • Upper airway cough syndrome-frequent throat clearing and associated symptoms of chronic sinusitis and allergic rhinitis
  • Vocal cord dysfunction-dyspnoea andstridor.
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4
Q

Epidemiology?

A

Prevalence: over 8 million
Age: children
Sex: male in childhood, reversed in adulthood
Ethnicity: N/A

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5
Q

Aetiology?

A
  • Multi gene association interacting with environment (multifactorial)
  • Viral, bacterial and allergens and occupational exposures can generate hypersensitivity reactions due to some pre-disposing genes.
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6
Q

Clinical Presentation?

A
  • Presence of risk factors
  • Recent upper resp tract infection
  • Dyspnoea
  • Cough
  • Expiratory polyphonic wheeze
  • Nasal polyposis
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7
Q

Pathophysiology?

A

• Bronchial hyperresponsiveness
• Inflammation-
• More eosinophils, thicker mucus and basement membrane and increased goblet cells and mast cells, neutrophils and t helper cells
• Smooth muscle cell hypertrophy
• Asthma-more t helper 2 cells not normally found in lungs-more humoral immunity
• Allergen binds to dendritic cell in lamina propria
• Columnar cells secrete thymic stromal lymphopoietin that conditions the dendritic cell to produce chemokines for Th2
• This stimulates IgE production via IL-13 and IL-4 to plasma cells
• Also promotes mast cells via IL-9 and eosinophils via IL-5
IgE antibodies form complexes with mast cells that detect allergens and release histamine prostaglandins and leukotrienes
• Bronchoconstriction, mucus secretion and more inflammation

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8
Q

first line Investigations?

A

resp exam

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9
Q

2nd line investigations?

A
  • FeNO (confirms eosinophil inflammation- 40 ppb if no corticosteroids and 35 ppb if on),
  • FEV1 /FVC ratio(<80%),
  • Bronchodilator reversibility test if obstructive (demonstrate reversibility of airflow obstruction to short-acting bronchodilator, usually defined as improvement in FEV₁ by >12% and >200 mL from baseline)
  • PEFR-flow rate as a comparison to patient’s personal best or normal values for height and gender
  • FBC-raised neutrophils or eosinophils
  • CXR-normal or hyperinflated
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10
Q

3rd line investigations?

A
  • bronchial challenge test-agents stimulating hyper-responsiveness
  • immunoassay for allergen-specific IgE-positive for allergen
  • skin prick allergy testing-positive for allergen
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11
Q

Management of infrequent?

A

• Low dose ICS and formoterol
• Or
• Low dose ICS (beclomethasone) and SABA/salbutamol
Review after 3-6 months

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12
Q

Management of >twice a month first line?

A
  • Low dose inhaled corticosteroid
  • SABA
  • Low dose ICS and formoterol
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13
Q

Management of >twice a month second line?

A
  • Low dose ICS (beclomethasone) and SABA/salbutamol

* Leukotriene receptor antagonist (montelukast)

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14
Q

Management of Uncontrolled?

A
  • High dose inhaled corticosteroid
  • Short course oral corticosteroid
  • SABA
  • Or
  • Medium dose corticosteroid and LABA (maintenance and reliever therapy-in one inhaler)
  • Short course oral corticosteroid
  • SABA
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15
Q

Ongoing first line?

A
  • Low dose ICS and formoterol

* Management of exercise-induced bronchoconstriction

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16
Q

ongoing second line?

A
  • Low dose ICS and SABA
  • Management of exercise induced bronchoconstriction
  • SABA
17
Q

ongoing third line?

A

• Add leukotriene receptor antagonist

18
Q

ongoing fourth line?

A
  • Sub-lingual allergen immunotherapy for patients sensitised to house dust mite
  • Theophylline
19
Q

ongoing fifth line?

A
  • Tiotropium/LAMA, then biological agents then azithromycin

* Note as steps increase, dose of ICS/oral CS does too

20
Q

What two types of inhalers are there?

A
  • Metered dose- Medicine in aerosol form and each puff is a certain dose-have to coordinate breathing and pushing down can be hard if arthritis
  • Dry powder-Need to take a deep breath in -expensive
21
Q

What is a spacer?

A

Spacers help to get all of the metered dose into the lungs without having to coordinate breaths, and increases bioavailability

22
Q

Complications?

A 
• Severe exacerbation
• Moderate exacerbation
• Airway remodelling
• Oral candidiasis secondary to use of inhaled corticosteroids
• Dysphonia-ICS
• Oesophageal candidiasis-ICS
• Death
• Fatigue
• pneumonia, 
• pulmonary collapse (atelectasis caused by mucus plugging of the airways), 
• respiratory failure, 
• pneumothorax, 
Status asthmaticus
23
Q

Prognosis?

A

• Early airway remodelling in childhood can cause airway obstruction, but remains stable in adulthood
• Accelerated decline in lung function can cause severe exacerbations
• Need ICS for life
• Life expectancy similar to those without it
• Most episodic cases in childhood resolve
pattern of asthma during childhood tends to predictoutcome in later life

24
Q

Definition-acute exacerbation?

A

Acute progressive worsening of symptoms in asthma, marked by decreased pulmonary function

25
Q

Risk factors-E?

A
  • Viral infection
  • Uncontrolled symptoms
  • High use of SABAs
  • Not enough use of ICS
  • Incorrect inhaler technique
  • Low forced FEV1/high FeNO
  • High BDR
  • Smoking
  • Allergen exposure/air pollution
  • Atopic eczema
  • Obesity/GORD
  • Chronic rhinosinusitis
  • Pregnancy
26
Q

Differentials?

A
  • Foreign body obstruction
  • Vocal cord dysfunction
  • Cardiac dysfunction
  • Anaphylaxis
  • Emphysema/COPD
  • Carcinoid syndrome
  • PE
  • Allergic bronchopulmonary aspergillosis
  • Pneumothorax
27
Q

Epidemiology-E?

A

Age: N/A
Sex: Females
Ethnicity: N/A
Prevalence-300 million worldwide

28
Q

Aetiology?

A

Exposure to irritant, allergen or infection

Sensitisation after repeated exposure triggers acute exacerbation

29
Q

Clinical Presentation-E?

A
  • Risk factors
  • Cough
  • Wheeze
  • SOB
  • Chest tightness
  • Sleep disturbance
  • Accessory muscle use
  • Tachypnoea
  • Tachycardia
  • Diminished breath sounds
  • Can’t speak
  • Stridor
  • Cyanosis
30
Q

First line investigations-E?

A

ABCDE/resp exam, peak expiratory flow rate and oxygen sats

31
Q

Second line investigations-E?

A

ABG and CXR

32
Q

First line management-E?

A
  • ICU admission
  • Inhaled SABA
  • Inhaled anti-cholinergic (ipratropium)
  • Controlled oxygen-reach 93-95% then titrate off
  • IV/I CS
33
Q

Adjunct management -E?

A

• IV magnesium-bronchodilator
• Antibiotics-if evidence of infection
mechanical ventilation

34
Q

Complications-E?

A
  • Delayed response to therapy
  • Pneumonia
  • Pneumothorax
  • Pneumomediastinum
  • Resp failure
35
Q

Prognosis-E?

A

Deaths per yr-preventable

Use of ICS decreases hospital admission and mortality rates

Resp (16 decks)

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