Resp: Asthma, COPD, Brochiestasis, CF Flashcards

1
Q

What is Asthma?

A

A chronic inflammatory disorder of the airways

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

What are the defining characteristics of asthma?

A
  • Susceptibility
  • Variable airflow obstruction
  • Chronic inflammatory process
  • Reversibility
  • Airway hyperreposniveness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the symptoms of asthma?

A
  • Expiratory wheeze
  • Cough
  • Difficulty breathing
  • Chest tightness
  • Exercise induced wheeze
  • Atopic history (allergies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What differentiates asthma and COPD?

A
  • Airway obstruction in asthma is often reversible with bronchodilators(>15% improvement with treatment)
  • Airway obstruction in COPD is not fully reversible (<15% improvement with treatment)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What should an asthma diagnoses be made on?

A
  • History of characteristic symptom patterns

- Evidence of variable airflow limitation, from bronchodilator reversibility testing or other tests

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

What present with a severe asthma exacerbation?

A

Silent chest

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

What is the frequent finding on physical examination of asthmatic patient?

A
  • Often normal

- Wheezing may be absent during severe asthma exacerbation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are common triggers for asthma?

A
  • Allergens
  • Cold air
  • Exercise
  • Fumes
  • Cigarette smoke
  • Perfumes
  • Chemicals
  • Drugs
  • Emotional distress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What cells primarily drive asthma?

A

TH2 cells

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

What are the main points in the pathophysiology of asthma?

A
  • Presentation of antigen to T lymphocytes
  • TH2 release cytokines which attract and activate inflammation cells including mast cells and eosinophils
  • Activation of B cells occurs as well which produce IgE
  • In a sensitised atopic asthmatic exposure to antigen results in a 2 phase response.
  • Immediate response and late phase response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the immediate response for asthma pathophysiology?

A
  • Interaction of allergen and specific IgE antibodies

- Leads to mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the late phase response?

A
  • Type 4 hypersensitivity
  • Involves inflammatory cells including eosinophils, mast cells, lymphocytes and neutrophils which release mediators and cytokines
  • This causes airway inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the result inflammatory cells in asthma on the bronchioles?

A
  • Reduced airway calibre
  • Mucosal swelling (oedema) due to vascular leak
  • Thickening of bronchails wall due to inflammatory cell infiltration
  • Mucus overproduction (sticky, thick, tenacious)
  • Smooth muscle contraction
  • Epithelium shed and incorporated into thick mucus
  • Hyper responsiveness of the airway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the effect of long term poorly controlled asthma on the respiratory organs?

A
  • Hypertrophy and hyperplasia of smooth muscle
  • Hypertrophy of muccus glands
  • Thickening of the basement membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What type of respiratory failure normally occurs in severe asthma attacks?

A
  • Type 2 respiratory failure

- Hyperventilation cannot compensate due to extensive effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What type of respiratory failure occurs in mild asthma?

A
  • Type 1 respiratory failure

- Compensation of hyperventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What test are used to assess the condition of a patient with suspected asthma?

A

Airflow limitation - FEV1/FVC reduced

Variation in lung function greater than normal

Spirometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How can eosinophilic inflammation be measured?

A
  • Induced sputum
  • Peripheral eosinophil count
  • FeNO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the principles of asthma treatment?

A
  • Patient education (SIMPLE)
  • Drug treatment involves brochodilators (beta2) and steroids such as prednisone . Inhalers are used to deliver in aerosol form.
  • Long acting reliever is prescribed with corticosteroid inhaler. B2 agonist is also given
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do we treat acute severe asthma?

A
  • Oxygen, high flow –aim to keep O2 94-98% sat
  • Nebulised salbutamol
  • Oral prednisolone
  • If moderate exacerbation not responding, or acute severe/life threatening, add nebulised ipratropium bromide
  • Consider iv magnesium and/or iv aminophylline if no improvement and life-threatening features not responding to above treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the characterises of acute severe asthma?

A
  • Respiratory rate >25
  • Heart rate >110/min
  • Inability to complete sentences in one breath
22
Q

What are the features of life threatening asthma?

A
  • Altered conscious level
  • Exhaustion
  • Arrthymia
  • Hypotension
  • Cyanosis
  • Silent chest
  • Poor respiratory effort
  • PEF <33% best or predicted
  • SpO2 <92%
  • PaO2 <8 kPa
  • Normal PaCO2
23
Q

What is COPD?

A

A disease state characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis.

24
Q

What is the aetiology of COPD?

A
  • Tobacco (90% of cases)
  • Air pollution
  • Occupational exposure
  • Alpha-1 antitrypsin deficiency
25
Q

What are the pathological changes in COPD?

A
  • Enlargement of mucus-secreting glands of the central airways
  • Increased number of goblet cells (which replace ciliated respiratory epithelium)
  • Ciliary dysfunction
  • Breakdown of elastin leading to destruction of alveolar walls and structure, and loss of elastic recoil.
  • Formation of larger air spaces with reduction in total surface area available for gas exchange
  • Vascular bed changes leading to pulmonary hypertension.
26
Q

What are the effects of the pathological changes in COPD?

A

-Progressive hypoxia leading to Cor Pulmonale

27
Q

What is the pathophysiology of the COPD?

A
  • Host repose to to inhaled cigarette or other noxious substances
  • Chronic inflammation process and oxidative injury which affects central and peripheral airways, lung parenchyma, alveoli and pulmonary vasculature.
28
Q

What are the symptoms of COPD?

A
  • Cough that is productive of sputum

- Shortness of breath initially on exertion but can progress to at rest

29
Q

What are the sign of COPD on physical examination?

A
  • Tachypnoea
  • Use of accessory muscles of respiration
  • Barrel chest
  • Hyper resonance on percussion
  • Reduced intensity breath sounds
  • Wheezing may be present
30
Q

What are some late features of COPD?

A
  • Central cyanosis
  • Flapping tremors
  • Signs of right sided heart failure second to pulmonary hypertension
31
Q

What the specific features of emphysema?

A
  • Elastin breakdown
  • Loss of alveolar integrity
  • Permanent destructive enlargement of the airspaces distal to terminal bronchioles
32
Q

What are the specific feature of chronic bronchitis?

A
  • Excessive mucus secretion
  • Impaired removal of section due to ciliary dysfunction
  • Chronic productive cough
  • Chronic respiratory infections
33
Q

What are some lung function tests in COPD?

A
  • Spirometry (FEV1/FVC <70%)
  • Chest X-ray show hyper inflated lungs
  • Pulse oximetry
  • ABG analysis
  • Alpha-1 antitrypsin level checked
34
Q

What is the management of COPD?

A
  • Smoking cassation
  • Bronochdilatos
  • Pulmonary rehabilitation
  • Long term oxygen management
  • Surgical interventions
35
Q

What vaccinations are recommended for COPD patients?

A

Pneumococcal vaccinations

36
Q

How are patient with acute exacerbations of COPD managed?

A
  • Montor for hypoxia and hypercapnia
  • Appropriate antibiotics to account for pneumococcus and haemophilia influenza
  • Nebulised bronchodilators
  • Oral steroids
  • 24 or 28% oxygen therapy
37
Q

What are the complications of COPD?

A
  • Recurrent pneumonia
  • Pneumothorax
  • Respiratory failure
  • Cor Pulmonale
38
Q

What is bronchiestasis?

A

Bronchiectasis is the Chronic dilatation of one or more bronchi. The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection

39
Q

What is the Gold standard diagnostic test for bronchiestasis?

A

High resolution CT

40
Q

What are the symptoms of bronchiectasis?

A
  • Chronic cough
  • Daily sputum production
  • Breathless on exertion
  • Intermittent haemopytisis
  • Nasal symtoms
  • Chest pain
  • Fatigue
41
Q

What is the pathophysiology of bronchiestasis?

A
  • Post infective
  • Immune deficiency
  • Genetic/Mucocilliary clearance defect
  • Obstruction
  • Toxic insult
42
Q

What are the common organisms to cause bronchiestasis?

A
  • Haemophilus influenza
  • Pseudomonas aeruginosa
  • Moraxella catarrhalis
  • Stenotrophomonas maltophilia
  • Fungi (aspergillus, candida)
  • Non-tuberculous mycobacteria
  • Staph aureus (think about CF)
43
Q

What is the management for bronchiestasis?

A
  • Treat underlying cause
  • Physiotherapy
  • Antibiotics according to sputum cultures
  • Supportive
  • Pulmonary rehabilitation
  • Management plan for infective exarcerbations
44
Q

What is Cystic fibrosis?

A

CF is an autosomal recessive disease leading to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR).

-No longer able to push chloride out of the cells

45
Q

What is the pathophysiology and organs affected in Cystic fibrosis?

A
  • Chromosome 7 defect
  • Leads to Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) mutation
  • Leads to ineffective cell surface chloride transport
  • Leads to thick, dehydrated body fluids in organs which have CFTR (Mucus)
  • Affects Pancreas, Skin, GI tract, Vas deferens, Lungs, Reproductive Organs.
46
Q

What are the presentations of CF?

A
  • Meconium Ileus (delay in passing first stool)
  • Intestinal malabsorption
  • Recurrent chest infections
  • Newborn screening
47
Q

How is CF diagnosis made?

A

A history of CF in a sibling
Or a positive newborn screening test result

And
-An increased sweat chloride concentration
(> 60 mmol/l) – SWEAT TEST
-Or identification of two CF mutations – genotyping
-Or demonstration of abnormal nasal epithelial ion transport (nasal potential difference)

48
Q

What is the management of CF?

A
  • Agressive therapy with respiratory infections with physio and antibiotics
  • Monitoring of body weight
  • Pancreatic enzyme supplements (Can present with distal intestinal obstruction syndrome)
49
Q

How does distal intestinal obstruction syndrome present?

A

-Palpable right iliac fossa mass

50
Q

Examples of lifestyle advice for CF patients

A
  • No smoking
  • Avoid other CF patients
  • Avoid friends / relatives with colds / infections
  • Avoid Jacuzzis (pseudomonas)
  • Clean and dry nebulisers thoroughly
  • Avoid stables, compost or rotting vegetation – risk of aspergillus fumigatus inhalation
  • Annual influenza immunisation
  • Sodium chloride tablets in hot weather/vigorous exercise