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The Patient - Semester 2 > Patient Sem 2 RESPIRATORY > Flashcards

Patient Sem 2 RESPIRATORY Flashcards

1
Q

Is sympathetic innervation involved in airways?

A

No, parasympathetic nerves cause bronchoconstriction and mucus secretion via the release of acetylcholine which acts on M3 receptors
Sympathetic nerves innervate tracheobronchial blood vessels and glands, but not human airway smooth muscle

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2
Q

What is the muscarinic airway path?

A

CNS –> Parasympathetic ganglion (via vagus nerve) on trachea –> Smooth muscle via post ganglionic fibres

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3
Q

How can you treat asthma using M3 receptors?

A

Block M3 receptor which produce acetylcholine.

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4
Q

Why does blocking the Muscarinic 3 receptor treat asthma?

A
  • Prevents production of acetylcholine.
  • Ach increases intracellular Ca2+ which forms a Ca2+ calmodulin complex
  • which activate MLCK (myosin light chain kinase)
  • Kinase phosphorylates myosin = CONTRACTION

The drugs that stop this process are Muscarinic antagonists

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5
Q

How do B2 agonists treat asthma?

A
  • B2 agonists increase production of adenyl cyclase.
  • Increases cAMP
  • Activates protein kinase A
  • Phosphorylates proteins that decrease Ca2+ such as SERCA and PMCA - these pump calcium out of cell.
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6
Q

Give an example of a muscarinic antagonist.

A

Ipratropium (LAMA)

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7
Q

What is asthma?

A
  • Airway inflammation which is reversible.
  • Hyper-responsiveness to stimuli
    which cause bronchoconstriction and increases mucus secretion.
  • Leads to recurrent airway obstruction.
  • Inflammatory cell = eosinophil.
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8
Q

What is COPD?

A
  • Chronic inflammation of the airways, lung tissue and pulmonary blood vessels as a result of exposure to inhaled irritants such as tobacco smoke.
  • Irreversible
  • The inhaled irritants cause inflammatory cells such as neutrophils, CD8+ T-lymphocytes, B cells and macrophages to accumulate.
    When activated, these cells initiate an inflammatory cascade that triggers the release of inflammatory mediators such as tumour necrosis factor alpha (TNF-α)
  • This can lead to tissue damage.
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9
Q

Advantages of B2 agonists?

A
  • Administered by inhalation; mostly well-tolerated
  • Rapid onset (minutes), short-acting forms (last 3-6 hrs) SABA’s.
  • Long-acting forms (onset 10-20 min; last 8-12 hr) LABA (preventative use)
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10
Q

Disadvantages of B2 agonists?

A
  • May stimulate b1 adrenoceptors (adverse effects)

- Increased risk of asthma-related death (unusual genotype)

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11
Q

What are phosphodiesterase inhibitors and how do they work?

A
  • Prevent breakdown of adenylcyclase by blocking phosphodiesterase.
  • Increase cAMP so enhance B2 adrenoceptor effects.
  • AKA Methlxanthines (also present in coffee and tea)
    E.g. Theophylline, aminophylline and roflumilast.
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12
Q

Disadvantages of PDE inhibitors (methylxanthines)

A
  • Less effective than beta adrenoceptor agonists
  • Stimulate heart
  • Stimulatory effect on CNS (increase alertness, tremor, nervousness and sleep disturbance)
    Small therapeutic window.
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13
Q

Disadvantages of Antimuscarinic bronchodilators (M3 Antagonists).

A

Numerous adverse effects - Arrhythmias;cough;dizziness;dry mouth;headache;nausea

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14
Q

What is ipratropium bromide and what is it used for?

A
  • M3 antagonist

- Alternative therapy for asthma –> short-acting : inhaled : maximal effect in 30-60 min; lasts 3-6 hr

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15
Q

Use of tiotropium bromide?

A
  • For severe asthma or maintenance treatment for COPD
  • long-acting : inhaled : onset 30-40 min; last >24h
    not suitable for acute bronchospasm*
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16
Q

Structure of tiotropium bromide and ipratropium bromide.

A

Both are quaternary nitrogen compounds:

  • highly polar
  • not well absorbed into the circulation
  • essentially affect only the bronchi.
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17
Q

What are glucocorticoids?

A

inhibit transcription of genes for interleukins

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18
Q

What do corticosteroids do?

A
  • Inhibit transcription of genes for COX2, iNOS, cytokines, interleukins and cell adhesion molecules
  • Stimulate synthesis and release of annexin-1
  • Reduce airway inflammation
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19
Q

Treatment regime for asthmatic adults:

A

1) SABA – reliever for adults with new diagnosis (with infrequent, short-lived wheeze + normal lung function)
2) Maintenance (low dose ICS) therapy - if uncontrolled on ICS, add LTRA (leukotriene antagonists e.g. motelukast)
3) Add LABA +/- LTRA
4) Change ICS/LABA to MART* (ICS + LABA in single inhaler for daily maintenance/ relief of symptoms)
5) Inc maintenance dose of ICS from low to moderate
6) Inc maintenance dose of ICS from moderate to high + SABA + add LAMA or theophylline

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20
Q

COPD therapy:

A
  1. SA b2 agonist or SA mAChR antagonist
  2. FEV1/ FVC ratio >50% = LA b2 agonist
    LA mAChR antagonist
    FEV1/ FVC ratio <50% = LA b2 agonist +
    inhaled corticosteroid*

3) Long-acting mAChR antagonist
+ long-acting b2 agonist
+ inhaled corticosteroid

Final step of treatment – add roflumilast (Methylxanthine PDE inhibitor)

21
Q

What is roflumilast?

A
  • PDE4 and is cAMP-specificRofumilast
  • Enhances β2-adrenoceptor effects (improves FEV1)
  • Adverse effects : diarrhoea, nausea, abdominal pain, headache and unexplained weight loss
22
Q

Other treatment options for COPD?

A
  • Mucolytic drugs* (e.g. i.v. N-acetylcysteine, oral carbocisteine)
  • Prophylactic antibiotics (need specialist advice)
  • Oxygen therapy
23
Q

Other treatments for asthma:

A
  • Leukotriene antagonist e.g montelukast = block release of allergic reaction mediators such as histamine
  • Cromones e.g. nedocromil = mast cell stabilisers
  • Anti IgE monoclonal antibodies e.g. omalizumab = prevents binding of IGE to mast cell receptors
  • Immunosupressants = e.g. methotrexate
24
Q

What is the pharynx?

A

throat

25
Q

What is the larynx?

A

voice box

26
Q

What is the anatomic dead space?

A

Where there is no transport of CO2 or O2 in airways.

27
Q

Do the lungs have muscles?

A

No

28
Q

What is cystic fibrosis?

A

Mucus inhibits capillary action therefore mucus stays in airway leading to infection.

29
Q

When does Patm = Pav = 0mmHg

A

Between breaths

30
Q

How does a collapsed lung occur?

A

Pleural sac breaks and air rushes in - lungs are no longer tightly attached to sac.

31
Q

What is the volume of dead space?

A

150ml

32
Q

What causes reduced compliance in the lungs?

A

Reduced surfactant in alveoli.

33
Q

Asthma triggers:

A
  • Allergen (pollen)

- Dust mites (faeces, casts, saliva) = immune response = overproduction of IgE

34
Q

Beclametasone mode of action:

A
  • Glucocorticoids are masked by heat shock proteins
  • Beclametasone = lipophilic therefore will diffuse through membrane and bind to glucocorticoid.
  • Changes shape of receptor and HS proteins dissociate.
  • Receptor with steroid moves to nucleus and sits on gene for promotion of IL1 and TNFa therefore DNA polymerase can’t bind.
35
Q

Omilazumab (Xoliar) mode of action:

A

It is a monoclonal antibody which bings to IgE region and prevents attachment to mast cells

36
Q

Is a SABA a reliever or controller?

A

Reliever

37
Q

How can asthma be prevented?

A
  • Breast feeding

- Allergen detection and avoidance

38
Q

Risk factors/ symptoms of COPD:

A
  • Current or ex smoker
  • Persistent cough
  • Recurrent bronchitis in winter
  • Wheezing
39
Q

Symptoms of asthma:

A
  • Frequent chest infections
  • Persistent cough
  • Children - recurrent wheezing
  • Chest tightness = shortness of breath
40
Q

What is the NCSCT?

A

National Centre for Smoking Cessation + training

41
Q

Examples of Smoking cessation drugs?

A

Bupropion–> has been used as an antidepressant

Varenciline –> a selective nicotine receptor partial agonist

Stopping for 7 days = extra 28 days of life

42
Q

How to obtain Nebulisers and advice:

A

Determine local policy: borrow from surgery/hospital? purchase from pharmacy?

Advice:

  • increased SE’s
  • Servicing once a year
43
Q

General monitoring for respiratory disease:

A
  • Changes in Rx
  • Symptoms
  • Inhaler technique
  • Adherence
  • Interactions
  • Asthma- annual flu vaccine
  • COPD - pneumococcal vaccine and annual flu vaccine, sputum
44
Q

Patient problems with MDI’s:

A
  • Not shaking inhaler before use.
  • Inhaling too sharply or at wrong time
  • Not holding breath for long enough after breathing.
45
Q

How long is the course of oral steroids for asthma?

A

5 days

  • continue with inhaled steroids
  • Take all tabs in morning
46
Q

How long is the course of oral steroids for COPD?

A

7 days

  • continue with inhaled steroids
  • Take all tabs in morning
47
Q

What is the aim for PEF?

A

Aim >70%
Normal >80%
Acute severe asthma = <50%

48
Q

Advantages of spacers:

A
  • avoids need for coordination
  • increases lung deposition
  • decreases deposition in throat.
49
Q

Are ICS preventers or relievers?

A

Preventers.

The Patient - Semester 2 (4 decks)

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