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The development of cardiorespiratory disease > PBL 47 > Flashcards

PBL 47 Flashcards

1
Q

Asthma is characterised by…

A
  1. Reversible airflow obstruction
  2. Airway inflammation
  3. Airway oedema
  4. Increased airway responsiveness
  5. Airway remodelling
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2
Q

Give some triggers of an allergic asthma exacerbation

A
  1. House pets
  2. Dust mites
  3. Mould
  4. Pollen
  5. Cold air
  6. Occupational triggers
  7. Infections
  8. Aspirin and NSAIDs
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3
Q

Which T-lymphocytes are involved in asthma?

A

Th2 and Th1

But Th2 involvement > Th1

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4
Q

Explain the pathophysiology of asthma

A
  1. Allergen intake
  2. Dendritic cells present the allergen antigen to Th2-type T cells
  3. Th2-type T cells will produce IL-4, IL-5 and IL-13
  4. These interleukins will signal B cells to produce IgE (allergic antibody)
  5. IgE binds to mast cells in the airway and causes degranulation
  6. Degranulation of mast cells causes pro-inflammatory mediator release such as histamines and leukotrienes which promote airway inflammation and bronchoconstriction
  7. Histamine and leukotrienes will mediate cytokine action (IL4,5,10) which activate T and B cells, causing further eosinophil attraction
  8. Eosinophils attract more inflammatory mediators to cause airway inflammation and asthma-type symptoms
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5
Q

Signs & symptoms of asthma

A
  1. Wheezing
  2. Dyspnoea
  3. Chest tightness
  4. Cough
  5. Tachypnoea
  6. Tachycardia
  7. Pulsus paradoxus (Fall of systolic BP >10mm/Hg during inspiration)
  8. Visible efforts to breathe: accessory muscle use, pursed lips, inability to speak
  9. Cyanosis
  10. Low O2 sats <90%
  11. Pa CO2 >45mm/Hg
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6
Q

True or false, asthma symptoms may be diurnal?

A

True, they worsen in the morning and at night but get better throughout the day

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7
Q

Risk factors for asthma

A
  1. Household allergens have been seen to be involved in development
  2. Diets low in Vit C and E
  3. Perinatal factors such as young maternal age, poor maternal nutrition, low birth wt, prematurity and lack of breastfeeding
  4. Born with a predisposition towards pro-allergic and pro-inflammatory Th2 immune response
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8
Q

Diagnosis of asthma

A
  1. Spirometry
  2. RECURRENT EPISODES of wheeze and chest tightness
  3. History of atopy
  4. Pulmonary function testing/reversibility testing
  5. Bronchial challenge testing
  6. Blood test for IgE - shows evidence of atopy
  7. Sputum eosinophilia = GOLD STANDARD
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9
Q

Explain pulmonary function tests AKA reversibility testing

- What constitutes a positive test?

A

STOP BRONCHODILATORS BEFORE THE TEST (4hrs for SABA, 15hrs for LABA)

  1. Perform spirometry
  2. Administer SABA
  3. Look at spirometry again
  • Positive test if FEV1 increases by 200mls and 12&
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10
Q

Explain bronchial challenge testing

A
  • The mannitol challenge
    1. Perform spirometry
    2. Inhalation of incrementally increased concentration of mannitol
    3. At the point where FEV1 decreases by 15% compared to baseline, this is the concentration required to cause the decline
    4. This can define degree of bronchial hyper-reactivity
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11
Q

What is the gold standard for asthma diagnosis, what are the disadvantages?

A
  • Sputum eosinophilia

- Very labour intensive and therefore use is limited to academic centres

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12
Q

Medications used in treatment of asthma

A
  1. B2 agonists: SABA and LABA
  2. Corticosteroids
  3. Leukotriene receptor antagonist
  4. Anti-muscarinic agents
  5. Methylxanthine
  6. Bronchial thermoplasty
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13
Q

Examples of B2-agonists

A

Salbutamol (SABA)
Salmeterol (LABA)
Formoterol (LABA)

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14
Q

Mechanism of salbutamol

A

Mechanism1: B2-agonist

  1. Binds to GPCR
  2. cAMP activation
  3. PKA activation
  4. Decreased MLCK activity due to PKA phosphorylating MLCK
  5. Modulation of myosin phosphorylation
  6. Lowers int. calcium concentrations
  7. Smooth muscle relaxation and bronchodilation

Mechanism 2
1. Increased cAMP inhibits broncho-constricting agent release in the airway such as basophils, eosinophils, and mast cells

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15
Q

Side effects of salbutamol

A
  1. Hand tremor
  2. Tachycardia
  3. Headaches
  4. Inability to sleep
  5. Cough
  6. Dry mouth
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16
Q

How long does salbutamol last?

A

Quick onset
4-6 hours
- RELIEVER

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17
Q

Mechanism of salmeterol

A
  • LABA
    1. Lipophilic side chain binds to exosites near the B2-AR in the lungs and bronchial smooth muscle
    2. This allows the active portion of the molecule to remain at the receptor site, continually binding. Hence it is called long acting
    3. Otherwise the same mechanism as SABA
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18
Q

Side effects of salmeterol

A
  1. Hand tremor
  2. Headache
  3. Dizziness
  4. Cough
  5. Ear pain
  6. Stuffed/runny nose
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19
Q

Which of salbutamol or salmeterol is used for relief of asthma symptoms?

A

Salbutamol

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20
Q

What is the use of salmeterol?

A

Decreases the number and severity of asthma attacks

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21
Q

Difference between salmeterol and formoterol

A

Formoterol has a faster action and is more potent

22
Q

Which drug is in the blue, reliever inhaler?

A

SALBUTAMOL

23
Q

Which drug is in the brown, preventer inhaler?

A

BECLOMETHASONE

24
Q

Mechanism of beclomethasone

A

Mechanism 1:

  1. Binds to glucocorticoid receptor
  2. Receptor dimerises and translocates to the nucleus where it binds to glucocorticoid response elements on glucocorticoid-responsive genes
  3. Increases the transcription of genes encoding for anti-inflammatory proteins such as lipocortin-1 and interleukin-10

Mechanism 2:

  1. Inhibits the expression of multiple genes that encode pro-inflammatory factors, such as nuclear factor-kappa B and activator protein-1.
    - Chronic inflammation is often characterised by enhanced expression of these transcription factors which bind and activate co-activator molecules to further amplify the inflammatory process
25
Q

Side effects of beclomethasone (inhaled)

A
  1. Oral thrush
  2. Hoarse voice
  3. Cough
  4. Nausea
  5. Back pain
26
Q

Side effects of beclomethasone (oral)

A
  1. Moon face
  2. Buffalo hump
  3. Proximal muscle wasting
27
Q

Give an example of another corticosteroid, other than beclomethasone, used in asthma treatment

A

Budesonide

28
Q

Give an example of a leukotriene receptor antagonist

A

Montelukast

29
Q

Mechanism of montelukast

A
  1. Antagonises leukotriene D4 at the cysteinyl leukotriene receptor (CysLt1) in the human airway
  2. This prevents airway oedema, smooth muscle contraction, and enhanced secretion of thick, viscous mucus
30
Q

Side effects of montelukast

A
  1. Stomach pain
  2. Diarrhoea
  3. Fever or flu symptoms
  4. Ear pain or full feeling. Trouble hearing
  5. Headache
  6. Cold symptoms –> runny/stuffy nose, sinus pain, cough, sorethroat
31
Q

Example of an anti-muscarinic agent

A

Tiotropium

This is a LONG ACTING ANTI-MUSCARINIC AGENT

32
Q

Mechanism of tiotropium

A
  1. Blocks the activity of mAchR
  2. Results in bronchial dilatation and decreased secretions
    - Causes a 20% improvement in FEV1
33
Q

Example of a methylxanthine

A

Theophylline

34
Q

Mechanism of theophylline

A

Exact mechanism is not well understood but it is thought to involve:

  1. inhibit phosphodiesterase
  2. less degradation of cAMP
  3. PKA activation
  4. Inhibition of TNF-alpha and leukotriene synthesis
  5. Reduction of inflammation and innate immunity
35
Q

Side effects of theophylline

A
  1. Headache
  2. Nausea/vomiting
  3. Disturbed sleep
  4. Tachycardia
  5. Skin rash
  6. Seizures
36
Q

What is bronchial thermoplasty?

A

Endoscopic procedure that reduces the effects of airway remodelling by applying temperature-controlled radio frequency energy to the airway wall.
- This decreases ASM mass

37
Q

What is type 1 respiratory failure?

A

Hypoxia WITHOUT hypercapnia

38
Q

Causes of type 1 respiratory failure

A
  1. Low ambient oxygen e.g. high altitude
  2. Ventilation-perfusion mismatch e.g. pulmonary embolism (parts of lung receive oxygen but not enough blood to absorb it)
  3. Alveolar hyperventilation - decreased minute volume due to reduced respiratory muscle activity
  4. Diffusion problem - O2 cannot enter the capillaries due to parenchymal disease e.g pneumonia
  5. Shunt - Oxygenated blood mixes with non-oxygenated blood from the venous system e.g. left to right shunt
39
Q

What is type 2 respiratory failure?

A

Hypoxia and hypercapnia –> ACIDOSIS

- It is defined as the buildup of CO2 levels that have been generated by the body but cannot be eliminated

40
Q

Causes of type 2 respiratory failure

A

Caused by inadequate alveolar ventilation and both O2 and CO2 are affected, underlying causes include:

  1. Increased airways resistance: COPD, asthma, suffocation
  2. Reduced breathing effort: drug effects, brainstem lesion, extreme obesity
  3. A disease in the area of the lung available for gas exchange e.g. chronic bronchitis
  4. Neuromuscular problems
  5. Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest
41
Q

What is COPD

A

Chronic, slowly progressive disorder characterised by airflow obstruction that does not change markedly over several months, it involves:

  1. Chronic partially reversible poor airflow - AIRFLOW LIMITATION
  2. Inability to breathe out fully - AIR TRAPPING
42
Q

What are the 2 characteristics of COPD

A
  1. Emphysema

2. Chronic bronchitis

43
Q

What is chronic bronchitis?

A

Chronic inflammation and mucus hypersecretion within the airways
- Contributes to airway obstruction

44
Q

What is emphysema?

A

Architectural obstruction, loss of structure of alveoli and enlargement of alveolar spaces, all of which reduces gas transfer capacity and reduces support structure around airways leading to AIRFLOW OBSTRUCTION

45
Q

COPD is a syndrome comprised of which 3 changes? (Pathophysiology)

A
  1. Airway inflammation
  2. Mucociliary dysfunction
  3. Airway structural changes
46
Q

Explain the pathophysiology of COPD

A
  1. Airway inflammation
    - Irritants (smoking) cause inflammatory cells such as neutrophils, CD8+, B cells and macrophages to accumulate
  • These cells initiate an inflammatory cascade, releasing inflammatory mediators = TNFa, IFN-y, IL1, IL6, IL8, fibrinogen, MMP6 and MMP9
  • Inflammatory mediators sustain the inflammatory process and lead to tissue damage as well as a range of systemic effects
  1. Structural changes
    - Airway remodelling is seen as a direct result of inflammatory response and leads to narrowing of the airways. Three main factors contribute to this:
  2. Peribronchial fibrosis
  3. Build-up of scar tissue from damage
  4. Over-multiplication of epithelial cells lining the airways
    - This leads to destruction of the structures supporting and feeding the alveoli (emphysema), meaning that the small airways collapse during exhalation, impeding airflow, trapping air in the lungs and reducing lung capacity
  5. Mucociliary dysfunction
    - Smoking and inflammation enlarge mucous glands that line the airway walls in the lungs, causing goblet cell metaplasia and leading to healthy cells being replaced by more mucous-secreting cells
  • Inflammation also causes damage to the mucociliary transport system which is responsible for clearing mucus from the airways
  • Both of these factors contribute to excess mucus in the airways which eventually accumulates, blocking them and worsening airflow
47
Q

Characteristics of chronic bronchitis

A
  1. Mucous gland hypertrophy
  2. Smooth muscle hypertrophy
  3. Goblet cell hyperplasia
  4. Inflammatory cell infiltrate
  5. Excess mucous
48
Q

Signs and symptoms of COPD

A
  1. SOB
  2. Cough
  3. Wheezing
  4. Sputum production
  5. Chest tightness
  6. Frequent respiratory infection
  7. Lethargy
  8. Unexplained weight loss (later stages)
49
Q

Risk factors for COPD

A
  1. SMOKING is the main risk factor BUT not every smoker will develop COPD so there must be some sort of underlying predisposition
    - Smoking drives the inflammation within the lungs and airways, leading to disease processes seen in COPD (emphysema and chronic bronchitis)
  2. Tobacco
  3. Alpha-1 antitrypsin deficiency
  4. Recreational drug use
  5. Passive smoking
  6. Chronic asthma
  7. FHx
  8. Occupation: biofuels, working with toxic gases etc…
  9. Air pollution
50
Q

What is cor pulmonale?

A

Severe COPD can cause right-sided heart enlargement and failure, this is cor pulmonale

  • Pulmonary hypertension occurs due to hypoxia in the vessels within the lungs due to COPD
  • The excess strain from pulmonary hypertension of the right ventricle can result in right ventricular hypertrophy and consequently heart failure
  • This causes a back log of blood, mostly into the SVC, which will settle in the peripheries (legs, ankles, abdomen, as well as the lungs).
  • You can also get parasternal lift, neck vein distention and hepatomegaly
51
Q

Treatment for COPD

A
  1. Short-acting bronchodilators: salbutamol, ipratropium
  2. Long-acting bronchodilators
    - Salmeterol = LABA
    - Tiotropium = LAMA
    - LAMA and LABA combination therapy
  3. Oxygen therapy
  4. Azithromycin - used to treat GORD associated with chest
52
Q

Would a combination of inhaled steroid and LABA work for COPD treatment? Why?

A

Yes and no, only for severe COPD patients

  • It is associated with higher risk of pneumonia
  • Offers little advantage in terms of exacerbations
  • Reserve for patients with SEVERE COPD

The development of cardiorespiratory disease (23 decks)

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