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Phoebe's Resp > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where are cell bodies of the parasyympathetic preganglionic fibres located

A

Brainstem

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2
Q

Where are cell bodies of parasympathetic postganglionic fibres located

A

Bronchi and bronchiole walls

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3
Q

Stimulation of postganglionic cholinergenic fibres causes

A

Bronchial smooth muscle contraction (mediated by M3 ACH on ASM)
Increased mucus secretion (mediated by M3 ACH on goblet gland cells)

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4
Q

Stimulation of postganglionic noncholingergenic fibres causes

A

Bronchial smooth muscle relaxation (mediated by NO and VIP)

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5
Q

In the sympathetic division there is no innervation of

A

bronchial smooth muscle

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6
Q

Parasympathetic postganglionic fibres supply

A

Submucosal glands and smooth muscle of blood vessels

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7
Q

Stimulation of parasympathetic postganglionic fibres causes

A

Bronchial smooth muscle relaxation via B2- adrenoreceptors on ASM
Decreased mucus secretion mediated by B2-adrenoreceptors on goblet cells
Increased mucociliary clearance mediated by B2-adrenoreceptors on epithelial cells
Vascular smooth muscle contraction mediated by A1-adrenoreceptors on vascular smooth muscle cells

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8
Q

Contraction of smooth muscle caused by

A

Myosin light chain kinase phosphorylated

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9
Q

Relaxation of smooth muscle caused by

A

Dephosphorylation of Myosin phosphate

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10
Q

What causes the rate of phosphorylation to exceed rate of dephosphorylation

A

Presence of Ca2+

Relaxation requires Ca2+ to return to normal level

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11
Q

How does Ca2+ return to normal level

A

Active transport

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12
Q

Asthma

A

Recurrent, reversible obstruction of airways

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13
Q

Causes of asthma

A

Allergens
Exercise
Resp infection
Smoke, dust, environmental pollutants

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14
Q

Asthma patients present with

A

Tight chest
Wheeze
Cough
Difficulty breathing

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15
Q

Chronic asthma

A

Pathological changes that result from long standing inflammation:

  1. Increase mass of smooth muscle
  2. Accumulation of interstitial fluid
  3. Increased secretion of mucous
  4. Epithelial damage (exposing sensory nerve endings)
  5. Sub-epithelial fibrosis
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16
Q

Asthma caused FEV1 to

A

decrease

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17
Q

mild asthma displays

A

hypersensitivity

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18
Q

severe asthma displays

A

hypersensitivity

hyper-reactivity

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19
Q

FEV1

A

Forced expiratory volume in 1 second

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20
Q

In atopic individuals, stages of asthma immunity

A
  1. allergen
  2. phagocytosis
  3. Strong Th2 response, IgE
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21
Q

Development of allergic asthma

A
  1. Allergen in airway epithelium
  2. CD4+ express Th0 cells
  3. Th0 cells becomes Th2
  4. Th2 activates B cells
  5. B cells become IgE
  6. Th2 also release IL4 and IL13 causing mast cells to express IgE
  7. Stimulates Ca2+ entry, leukotriene release, contraction of smooth muscle
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22
Q

Stages in late phase of asthma

A
  1. Epithelial damage
  2. Airway hyper-responsiveness
  3. Bronchospasm, wheezing, cough, mucous over secretion
  4. Airway inflammation
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23
Q

2 categories of drugs used in treatment of asthma

A

Relievers (bronchodilators)

Controllers (Anti-inflammatory)

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24
Q

Relievers

A

SABA’s
LABA’s
CysLT1 receptors agonist

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25
Q

Controllers

A

Glucocorticoids
Cromoglicate
Humanised IgE monoclonal antibodies

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26
Q

B2 - adrenoreceptors agoinsts

A

antagonist of all spasmogens

Bronchodilators

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27
Q

SABA’s

A

Short Acting B2-adrenoreceptor Agonist
Salbutamol
Increase mucous clearance and decrease mediator release from mast cells and monocytes

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28
Q

LABA’s

A

Long Acting B2-adrenoreceptor Agonist
Salmeterol
Formaterol
Should not be used as monotherapy, should be used with gluticosteroids

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29
Q

used in nocturnal asthma

A

LABA

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30
Q

CysLT1

A

Cysteinyl Leukotriene Receptor Antagonists
Act competitively at CysLT1 receptor stopping smooth muscle contraction
Montelukast

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31
Q

Methylxanthines

A

Inhibits PDE3
Combine bronchodilator and anti-inflammatory actions
Second line drugs used with B2-adrenoreceptor agonists and glucocorticoids

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32
Q

Corticosteroids

A 
Glucocorticoids
Anti-inflammatory
Reduces immunological response
Prevent inflammation
Resolve established inflammation
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33
Q

Cromones

A

Mast cell stabilisers

Weak anti-inflammatory response

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34
Q

Sodium cromoglicate

A

Reduce phases of asthma attack

More effective in young children

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35
Q

Monoclonal antibodies against IgE

A

Binds to IgE to prevent it binding to cells

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36
Q

Asthma Treatment

A
  1. SABA (salbutamol)
  2. Inhaled corticosteroid (beclomethasone)
  3. LABA + ICS (salmeterol)
  4. Increase glucocorticoid dose, add 4th drug
  5. Oral glucocorticoid (prednisolone)
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37
Q

Synthetic glucocorticoid used to prevent inflammation in chronic asthma

A

Inhaled beclometasone

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38
Q

Synthetic glucocorticoid used in severe or rapidly deteriorating asthma

A

Oral prednisolone

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39
Q

Weak anti-inflammatory used in allergic asthma

A

Inhaled Sodium Cromoglycate

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40
Q

volume of air breathed in and out per minute

A

pulmonary ventilation

41
Q

volume of air exchanged between atmosphere and alveoli per minute

A

Alveolar ventilation

42
Q

Major inspiratory muscle in a sheet, containing crura

43
Q

Palpable reference point used in BEC

A

Xiphoid process

44
Q

Site of oblique fissure anteriorly

45
Q

Most O2 is transported

A

bound to haemoglobin

46
Q

Most Co2 is transported

A

as bicarbonate

47
Q

A small proportion of O2 is transported

A

in solution

48
Q

Carries deoxygenated blood, drains into superior vena cava and arches around right lung root

A

Azygous vein

49
Q

Arise from anterior surface of descending aorta

A

Bronchial arteries

50
Q

Surrounded by vessels and may appear black on dissection

A

Pulmonary lymph nodes

51
Q

Palpable with jugular notch

52
Q

Level where lower respiratory tract begins

A

C6 vertebrae

53
Q

Anatomical landmark for cardiopulmonary resuscitation

A

Xiphoid process

54
Q

Site of horizontal fissure

A

Right 4th rib

55
Q

Level of carina

56
Q

Level of oblique fissure posteriorly

A

T3 vertebrae

57
Q

Factor that most increases pulmonary ventilation

A

tidal volume

58
Q

Methylxanthine used as add-on therapy in asthma. Serum levels must be monitored due to drug interaction

A

Oral theophyline

59
Q

Anti-inflammatory that can trigger bronchospasm in sensitive individuals

A

Oral ibruprofen

60
Q

A CysLT-1 receptor antagonist, used as an add-on therapy in asthma

A

Oral montelukast

61
Q

Monoclonal antibody against IgE that reduces IgE receptor expression

A

Subcutaneous omalizumab

62
Q

SABA used to relieve bronchospasm in mild to moderate asthma

A

inhaled salbutamol

63
Q

Add on B-2 agonist that responds poorly to initial management

A

Inhaled salmeterol

64
Q

B2 agonists end in

65
Q

B2 agonist examples

A

Salbutamol

Salmeratol

66
Q

Inhaled corticosteroids

A

Beclomethasone

Fluticasone

67
Q

Inhaled corticosteroids end in

68
Q

CysLT-1 examples

A

Montelukast

Zafirlukast

69
Q

CysLT-1 end in

70
Q

Methylxanthines

A

Theophyline

71
Q

Asthma immune response

A
  1. IgE antibody attaches to mast cells
  2. Degranulation occurs
  3. Inflammatory mediators released causing bronchospasm, mucosal oedema and mucous formation
72
Q

Pathophysiology of COPD

A

Inhalation of noxious gases/particles leads to inflammation, mucocilliary dysfunction and tissue damage

73
Q

Cigarette smoking with COPD

A
  1. Activates macrophages
  2. Activates neutrophils
  3. Proteases released causing alveolar wall dysfunction (emphysema) and mucous hypersecretion (bronchiectasis)
74
Q

COPD Treatment

A
  1. SABA
  2. LAMA
  3. LABA
  4. LAMA/LABA combination inhaler
  5. LABA/ICS combination inhaler
  6. LABA/LAMA/ICS combination inhaler
75
Q

LAMA

A

Long acting muscarinic receptor agonists
Reduce bronchospasm caused by irritant
Decrease mucous secretion

76
Q

Treat acute exacerbation of asthma

A 
Oxygen
Salbutamol
Hydrocortisone
Ipratropium
Theophylline
Magnesium sulfate
ANaethetist
77
Q

Treat acute exacerbation of COPD

A 
ipratropium 
Salbutamol
Oxygen
Amoxicillin
Prednisolone
78
Q

Aetiology of restrictive thoracic disease

A

Impaired alveolar gas exchange
Fluid in alveolar spaces
Consolidation of alveolar air spaces
Inflammatory infiltrate of alveolar walls

79
Q

LAMA example

A

Ipratropium

80
Q

PDE4 inhibitors

A

COPD only
Roflumilast
Anti-inflammatory

81
Q

Mucolytics

A

COPD only
Oral carbocisteine
Reduce sputum

82
Q

D dimers

A

Fibrin degradation product

Increased = thrombosis, inflammation, malignancy, heart failure

83
Q

COPD

A

Airflow reduction, partially reversible, progressively worsens

84
Q

2 types of COPD

A

Chronic Bronchitis

Emphysema

85
Q

Chronic Bronchitis

A

Inflammation of bronchi and bronchioles
Cough
Clear sputum
Increasing breathlessness

86
Q

Emphysema

A

Distension and damage to alveoli
Destruction of acinal pouching in alveolar sacs
Loss of elastic recoik

87
Q

LAMA’s end in

88
Q

Fexofenadine

A

Competitive H1 receptor antagonist used to treat allergic rhinitis

89
Q

Ipratropium

A

A short acting drug that blocks acetylcholine non-selectively,

90
Q

Rofumilast

A

PED4 inhibitor, given orally for COPD

91
Q

Sodium cromoglicate

A

Mast cell stabiliser used in asthma

92
Q

Rhinitis

A

Inflammation of nasal mucosa

May be allergic, non-allergic or mixed

93
Q

Allergic Rhinitis

A

Seasonal
Perennial
Episodic

94
Q

Non-allergic Rhinitis

A 
Doesn't involve IgE
Infection
Hormonal Imbalance 
Vasomotor disturbances
Medications
95
Q

Anti-inflammatory treatment

A

Glucocorticoids

96
Q

Mediator receptor blockade treatment

A

H1 receptor antagonist

CysLT receptor antagonist

97
Q

Nasal blood flow treatment

A

Vasconstrictors

98
Q

Anti-allergic

A

Sodium cromoglicate

Phoebe's Resp (23 decks)

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