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EXAM 1 > Asthma & COPD > Flashcards

Asthma & COPD Flashcards

1
Q

What is NANC?

A

Non-adrenergic, non-cholinergic (nerves)

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2
Q

How does the autonomic nervous system cause bronchodilation?

A
  1. Sympathetic impulse generated
  2. Received by adrenal glands
  3. Secretion of epinephrine
  4. Stimulates adrenergic receptors on airway smooth muscle
  5. Causes smooth muscle relaxation (increase in diameter and decrease in airway resistance)
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3
Q

How does the autonomic nervous system cause bronchoconstriction?

A
  1. Cholinergic fibres innervate airway smooth muscle (surround)
  2. Vagus post-ganglion transmits acetylcholine
  3. ACh binds to M3 receptor on airway smooth muscle
  4. Causes bronchoconstriction & increase in mucous production
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4
Q

Specifically, what does the stimulation of M3 do?

A
  1. M3 stimulates Gq protein complex
  2. Gq complex causes the up-regulation of phospholipase C
  3. Causes the release of IP3
  4. Increase in intracellular Calcium

= Smooth muscle contraction

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5
Q

What is extrinsic asthma and what can trigger it?

A

Extrinsic asthma is an allergy reaction which is mainly caused by increased levels of IgE antibodies.

Triggers:
* Dust
* Pollen
* Mites

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6
Q

What is intrinsic asthma and what causes it?

A

Non-allergy and non-atopic asthma. Has a late onset and is less common.

Causes: Obesity, Exercise, Food additives (chemicals), stress, infections, drugs

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7
Q

What are asthma symptoms?

A
  • Wheezing (especially on expiration)
  • Breathlessness
  • Chest tightness
  • Diurnal coughing (Morning/Night)
  • Commonly overweight
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8
Q

What are emphysema symptoms?

A
  • Increasing dypsnea even at rest
  • Bronchial infection less common
  • Hyperventilation
  • Commonly thin body
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9
Q

What are chronic bronchitis symptoms?

A
  • Frequent winter infections
  • Wheeze
  • Dypsnea during physical exertion
  • Productive cough
  • Lose ability to increase rate & depth of ventilation
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10
Q

COPD clinical features

A
  • Smoker/Ex-smoker
  • Chronic productive cough
  • Persistant breathlessness
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11
Q

Asthma clinical features

A
  • Night-time waking with breathlessness
  • Episodic breathlessness
  • Symptoms surface under age 35
  • Duirnal symptoms
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12
Q

What is peak flow?

A

Peak expiratory flow is a person’s maxinum speed and volume of expiration which is measured with a peak flow meter.

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13
Q

What are the red flags for asthma?

A
  • Systemic features (fever, myalgia, weight loss)
  • Crackles, stridor, cyanosis abnormal voice
  • Persistent breathlessness (supposed to be episodic if it is asthma)
  • Chronic sputum production
  • Chest X-ray shows shadows
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14
Q

What are the different stages of obstruction indicated by FEV1 results

A

Stage 1: FEV1>80%
Stage 2: FEV1 50-79%
Stage 3: FEV1 30-49%
Stage 4: FEV1<30%

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15
Q

What is an Asthma control test?

A

A quiz that patients can take at home ofwhich the score should indicate how well controlled theit asthma has been over the past 4 week.
Scores:
* 25 - Under control
* 20-24 - On target
* < 20 - Off target

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16
Q

Describe the early pathophysiology of asthma

A
  1. Dendritic cells capture allergen and present to T-cell
  2. B-cell activated and production of antibody IgE occurs
  3. IgE binds to FcεRI on mast cells
  4. Degranulation & release of histamines, leukocytes, prostaglandins
  5. Mediators (such as Histamine, PGD2 etc) cause vasodilation and increase in vascular permeability resulting in oedema
  6. Mediators also stimulate goblet cell hyperplasia -> Increased mucous secretion
  7. Mediators cause bronchoconstriction

Minutes to hours of the reaction

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17
Q

Describe the late phase pathophyiology of asthma

A
  1. Leaked plasma proteins from blood vessel cause injury to the epithelial layer
  2. Mediators recruit eosinophils which further cause endothelial shedding
  3. Nerves exposed ->Bronchial hyperresponsiveness
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18
Q

What is the identifying process when asthma is suspected

A

A test for airway obstruction is conducted. This includes a spirometry combined with a bronchodilator reversibility test.

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19
Q

Give examples of COPD red flags

A
  • Haemoptysis (coughing blood)
  • Chest pain
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20
Q

Describe the Asthma histopathology

A
  • Globlet cell hyperplasia -> Increased mucous secretion
  • Increase in blood vessels surrounding -> Oedema
  • Increase in smooth muscle layer thickness = Narrower lumen
  • Collagen deposition leads to subepithelial fibrosis
  • Increased volume of submucosal glands results in increased mucous production.
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21
Q

What is cyanosis?

A

Cyanosis is the turning blue of the skin which is caused by insufficiently oxygenated blood in the arteries.

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22
Q

Explain hypercapnia

A

Hypercapnia is when there is excess amounts of CO2 in the artierial blood

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23
Q

Explain Hypocapnia

A

When there is a below-normal level of CO2 in the arterial blood

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24
Q

Explain Hypoxia

A

When there is insufficient level of oxygen in body tissues

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25
Q

Describe chronic bronchitis histopathology

A
  • Thickening of smooth muscle
  • Collagen deposits under epithelial layer -> Subepithelial fibrosis
  • Goblet cell hyperplasia -> Increased Mucous secretion
  • Structural remodelling of the airways
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26
Q

Describe Emphysema histopathology

A

Alveolar membranes collapse due to elastin breakdown resulting in large holes in which air gets trapped in.
* Causes breating problems
* Hyperventilation

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27
Q

What should be checked prior to changing asthma therapy?

A
  • Patient adherence
  • Inhaler technique
  • Eliminate triggers
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28
Q

Name some ICS (Inhaled corticosteroids)

A
  • Beclometasone dipropionate
  • Budesonide
  • Fluticasone propionate
  • Mometasone furoate

In the case of COPD, they are only ever given IN COMBINATION with LABA or LAMA

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29
Q

Examples of SABA and their characteristics

A

Salbutamol,Terbutaline
* Onset: ~30 mins
* Duration: 4-6hrs

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30
Q

What is the up-step regime for asthma treatment?

A
  1. Preventer added immediately - Low dose ICS
  2. Add inhaled LABA (Salmeterol 50mcg BD)
  3. If no respone to LABA -> Terminate LABA
  4. Increase ICS to medium-dose OR add LTRA (Montelukast 10m ON)
  5. Refer patient for specialist care

Check adherence and inhaler technique before stepping up treatment.

Reliever (Salbutamol) is present at all time of the regime (salbutamol)

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31
Q

What amount of reliever use in a week indicates that asthma is not well controlled ?

A

More than 3 times a week

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32
Q

Examples of LABA drugs and doses

A
  • Formoterol 12mcg BD|MAX: 24mcg BD
  • Salmeterol 50mcg BD (COPD max) |MAX: 100mcg BD
33
Q

What are some long-acting beta-2 agonists and their characteristics?

A

Also known as LABA. This is a preventer therapy
* Salmeterol
* Formoterol
* Bambuterol
* Indacaterol^
* Olodaterol^
* Vilanterol^

The last three are only used for COPD
Action time: 12-24 hours
No rapid onset of bronchodilation effects with LABAs

34
Q

What are some the characteristics b2 agonists

A

Onset: ~30 minutes
Action time: 4-6 hours

35
Q

What are the Beta-2 agonist side effects

A

SABAs and LABAs can cause any of the following…
* Termors
* Headaches
* Nervous tension
* Palpitations (B1 agonistic effects)
* Tachycardia (B1 agonistic effects)
* Hypokalemia (High-doses of B2 agonists)

36
Q

What is MART therapy (asthma)

A

Maintenance and reliever therapy.

Includes the use of Formoterol in combination with a corticosteroid. Acts as both a reliever and a preventer as the formoterol has both SHORT acting and LONG acting components.

37
Q

Why are Qvar and Clenil not interchangable medicines

A

This is because Qvar has extra fine particles and is therefore twice as potent as Clenil.
Ergo prescribe by brand even though they are the same Active ingredient (Beclometasone)

38
Q

Clenil (Beclometasone) doses

A
  • Very low dose (children) = 50mcg, 2 puffs BD
  • Low dose (starting adult dose) = 100mcg, 2 puffs BD
  • Medium dose = 200mcg, 2 puffs BD
  • High dose = 250mcg, 2-4 puffs BD
39
Q

Ciclesonide doses

A
  • Medium dose = 80mcg, 2 puffs OD
  • High dose = 160mcg, 2 puffs OD
40
Q

Qvar (Beclometasone )doses

A
  • Low dose (starting adult dose) = 50mcg, 2 puffs BD
  • Medium dose = 100mcg, 2 puffs BD
  • High dose = 100mcg, 4 puffs BD
41
Q

Fluticasone doses

A
  • Very low dose(children) = 50mcg, 1 puff BD
  • Low dose(starting dose) = 50mcg, 2 puffs BD
  • Medium dose = 125mcg 2 puffs, BD
  • High dose = 250mcg 2 puffs BD
42
Q

Corticosteroid side effects

A
  • Hoarseness
  • Throat irritation
  • Dysphonia (change of the voice)
  • Candida
43
Q

Non-pharmaceutical interventions for asthma

A
  • Reduce exposure to triggers (dust, mites, pollen)
  • Stop or reduce smoking
  • Lose weight
  • Practise breathing exercises
  • Annual influenza vaccination
44
Q

What are some non-pharmaceutical interventions for COPD

A
  • Offer treatment & support to stop smoking
  • Offer pneumococcal & influenza vaccinations
  • Offer pulmonary rehabilitation
  • Treat other comorbidities
45
Q

Describe the treatment regime for COPD

A
  1. Considered non-pharmaceutical interventions
  2. SABA or SAMA | Reliever
  3. Non-asthmatic features -> LABA+LAMA (cannot have SAMA so change to SABA for reliever)
  4. Asthmatic features -> LABA+ICS
  5. LABA + LAMA + ICS
46
Q

What treatment is the go-to for late phase asthma

A

Corticosteroid treatment (E.g. Clenil [Beclometasone])

47
Q

What is the go-to treatment for early phase asthma

A

B2 agonist such as Salbutamol or Formoterol

48
Q

Explain what anti-alpha trypsin deficiency is

A

An autosome recessive condition inwhich the individual lacks anti-alpha trypsin which are proteins that inhibit neutrophil elastase from breaking down extracellular matrix leading to lung and alveolar damage which eventually leads to emphysema COPD

49
Q

What are the important inflammatory cells in Asthma and what mediators do they release

A
  • Mast cells (Histamine, PGD, Leukotrines)
  • Basophils (IL-4)
  • CD4+ Th2 lymphocytes (IL-4, IL-5)
50
Q

What are the important imflammatory cells in COPD and what mediators do they secrete

A
  • Neutrophils (IL-8, Elastase, )
  • Macrophages (MCP1)
  • CD8+ Th1 cells (IFN-γ, TNF)
51
Q

What compound attracts and recruits neutrophils and T-cells to the site of inflammation

A

Leukotriene B4

52
Q

Describe the COPD pathogenesis

A
  1. Cigg smoke or other noxious agents
  2. Activate alveolar macrophages & epithelial cells
  3. Release of chemokines & cytokines (TNFa, IL-6, MCP1) that recruit CD8+ lymphocyte (Th1) and neutrophils
  4. Inflammatory agents + proteases released

Causing…
* Increase mucous secretion
* Breaking down alveolar walls
* Activating fibroblast ->Fibrosis

53
Q

Counselling points for the use of SABA

A
  • Use as necessary
  • Carry with you at all times
  • Use ahead of exercise
  • Salbutamol max: 8
54
Q

Why is B2 agonist monotherapy strongly discouraged

A

There are studies that show monotherapy leads to hospitalisation frequently as receptors and immune cells rapidly desensetize with the frequent use of SABA and therefore has a decreasing therapeutic effect by itself.

55
Q

Explain receptor desensitisation in asthma

A
  • β2 receptor repeated stimulation
  • GPCR phosphorylated
  • Becomes a substrate for other protein binding
  • Internalisation
  • Receptor downregulation {Increase in receptor lysosomal degradation and a decrease in β2 receptor mRNA}
56
Q

Aside from the relaxatory effects of β2 agonists, what else does it do

A
  • Decrease mediator release in mast cells
  • Reduce plasma exudation = Reduce oedema
  • Reduce cholinergic neurotransmission thereby reducing parasympathetic effects in the lungs
57
Q

Describe how β2 agonists cause smooth muscle relaxation

A
  1. Bind to β2 receptor coupled with Gas
  2. Gas dissociates from GPCR complex and stimulates adenylyl cyclase
  3. ATP converted to cAMP
  4. cAMP inhibit MLCK
    * Inhibits Ca2+ release from intracellular stores
    * Reduces Ca2+ entry into cells
    * Induces Ca2+ sequestration into ER

Decrease in Calcium causes airway smooth muscle relaxation.

58
Q

Why is ephedrine not as effective as other β2 agonists

A

Ephedrine stimulates other β receptors causing unwanted systemic effects ∴ not as effective

59
Q

Complication with introducing LABA to treatment

A
  • Not everyone reacts well with LABA
  • It is started on a low dose
  • Monitored and trialled for 6 weeks
  • Removed if no significant improvement or worsening of symptoms occurs
60
Q

Counselling points for ICS in COPD

A
  • Use regularly- has no effect if missing doses
  • Brush teeth after taking in morning (reduces likelyness of candida)
  • Do not suddenly stop taking it
61
Q

What do corticosteroids do in asthma

A
  • Reduce IL-2 transcription preventing clonal expansion of Th cells and subsequently decreasing the amount of cytokines that promote eosinophils.
  • Less IgE antibody production
  • Upregulate β2 receptors (good for combination therapy)
  • Inhibit leukotriene production
  • Inhibit prostaglandins ∴ reducing vasodilation and subsequent oedema
62
Q

Explain the only SAMA and its characteristics

include its brand name

A

Ipratropium bromide (Atrovent)
* Non-selective antagonist
* Onset: 30 mins
* Duration: 3-6hrs (taken 3-4 times/day)
* Poorly absorbed ∴ few systemic side effects
* Available as MDI and nebuliser (nebuliser only for severe acute asthma)

63
Q

What are the LAMAs, their brand names and their indication

A
  • Tiotropium OD (Asthma & COPD) -> Spiriva
  • Glycopyrronium OD (COPD)-> Seebri Breezhaler
  • Umeclidinium OD (COPD) -> Incruse Elipta
  • Aclidinium bromide BD (COPD)-> Eklira Genuar
64
Q

What are the side effects of anti-muscarinic drugs

A

Side effects:
* Dry mouth
* Cough
* Constipation
* Headache

65
Q

What are LTRAs and what do they do

A

It blocks the CysLt1 receptor thereby inhibiting leukotrienes and..
* Relaxing airway smooth muscle
* Reducing eosinophil and oedema

66
Q

LTRA side effects

A
  • GI disturbances {Diarrhoea, Vomitting, GI discomfort}
  • Nausea
67
Q

What are the rare reactions that patients and carers should be wary of with LTRAs

A

LTRA has the potential to induce neurophychiatric reactions such as:
* Depression
* Obsessive compulsive symptoms
* Speech impairment (starting as a stutter)

Churg-strauss syndrome
* Inflammation of blood vessels
* Associated with patients who have been on oral steroids

Report any of the above symptoms immediately

68
Q

What are xanthines and what is their indication

A

Aminophylline which is given only intravenously for severy acute exacerbation of COPD and severe acute Asthma.

Theophylline is given orally as an MDR drug and for long-term asthma treatment

Not very useful in exacerbations as it is not fast acting

69
Q

What are some important cautions regarding xanthines

A
  • Xanthines have a very narrow therapeutic index 10-20 mg/L and GI disturbances can still be experienced when in the index range. A blood sample should be taken 4-6 hours after administration and concentration should be measure 5 days after.
  • Smokers require a high dose
70
Q

What are the side effects of xanthines

A
  • CNS stimulation
  • Palpitations
  • Tachycardia
  • Vasodilation
  • Nausea/vomitting
  • Diarrhoea
71
Q

What do xanthines do

A
  • Airway smooth muscle relaxation
  • Reduce endothelial leaks = less migration and less oedema.
  • Reduction of mast cells and eosinophils
  • Reduction in neutrophils
  • Less pro-inflammatory chemokines
72
Q

LAMA + LABA combinations

A
  • Aclidinium + Formoterol
  • Tiotropium + Olodaterol
  • Glycoyrronium + Indacaterol
  • Umeclidinium + Vilanterol
73
Q

ICS +LAMA + LABA

A
  • Fluticasone + Umeclidinium + Vilanterol
  • Beclometasone + Glycopyrronium + Formoterol
74
Q

Suggest ways to improve a B2 selectivity

A
  • Increase side chain length at amine + steric bulk = Increases β2 activity + DoA
  • Including an ether at the long side chain = Increases DoA
  • Adding a carbon at the upper hydroxyl of the catechol = Slows COMT metabolism = Increases DoA
  • Inclusion of an R enantiomer at hydroxyl = Increases β2 activity
75
Q

What are the interactions at the β2 receptor

A
  • TM5: Hydrogen bonding (catechol hydroxyls - serine residues)
  • TM3: Ionic interaction (Protonated amine - Aspartic acid carboxylic group)
  • TM6: Hydrogen bonding (Hydroxyl group - Phenylalanine amide)
  • TM6: π-π stacking (Catechol benzene - Asparagine benzene)
76
Q

Fostair inhaler

A

Beclometasone (ICS) + Formoterol (LABA)

A MART therapy

77
Q

Fobumix inhaler

A

Budesonide + Formoterol

A MART therapy

78
Q

Luforbec inhaler

A

Beclometasone + Formoterol

79
Q

Symbicort inhaler

A

Budesonide + Formoterol

EXAM 1 (10 decks)

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