Pharmacology Flashcards

1
Q

What does stimulation of postganglionic cholinergic fibres cause? (2) (parasymp)

A

Bronchial smooth muscle contraction

Increased mucous secretion

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2
Q

What does stimulation of postganglionic noncholinergic fibres cause? (parasymp)

A

Bronchial smooth muscle relaxation

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3
Q

In the sympathetic division, what brings about bronchial smooth muscle relaxation via β2-adrenoceptors on ASM cells?

A

Activation by adrenaline from adrenal gland

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4
Q

In the sympathetic division, what is the result of stimulated B2-adrenoreceptors? (3)

A

Bronchial smooth muscle relaxation
Decreased mucous secretion
Increased mucociliary clearance

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5
Q

In the sympathetic division, what is the result of stimulated a1-adrenoreceptors?

A

Vascular smooth muscle contraction

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6
Q

Effect of PKA on activity of MLC

A

Phosphorylates and inhibits MLCK
Phosphorylates and stimulates myosin phosphatase
–>Dephosphorylates MLC
–>Causes relaxation of bronchial smooth muscle

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7
Q

Asthma

A

A recurrent and reversible obstruction to the airways in response to stimuli that are not necessarily noxious

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8
Q

Causes of asthma attacks (4)

A

Allergens (in atopic individuals)
Exercise (cold, dry air)
Respiratory Infections (e.g.viral)
Smoke, dust, environmental pollutants

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9
Q

Intermittent attacks of bronchoconstriction can cause (4)

A

Tight chest
Wheezing
Cough
Difficult breathing

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10
Q

Chronic Asthma

A

Involves pathological changes to the bronchioles that result from long-standing inflammation

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11
Q

Pathological changes from chronic asthma (5)

A

Increased mass of smooth muscle (hypertrophy, hyperplasia)
Accumulation of interstitial fluid (oedema)
Increased secretion of mucus
Epithelial damage (exposing sensory nerve endings)
Sub-epithelial fibrosis

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12
Q

FEV1

A

Forced expiratory volume in 1 second

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13
Q

PEFR

A

Peak expiratory flow rate

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14
Q

What is bronchial hyper-responsiveness in asthma?

A

Exposed sensory nerve endings leads to increased sensitivity of the airways to bronchoconstrictor influences (hyper-reactivity and hypersensitivity)

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15
Q

Type I Hypersensitivity reaction

A

Immediate/ early phase
Bronchospasm and acute inflammation
Fall in FEV1

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16
Q

Type IV Hypersensitivity reaction

A

Late phase
Bronchospasm and delayed inflammation
More prolonged and more severe fall in FEV1 than with type 1

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17
Q

Low level TH1 response to allergen in non atopic individual

A

Phagocytosis by antigen presenting (dendritic) cell

Cell-mediated immune response involving IgG and macrophages

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18
Q

Strong TH2 response to allergen in atopic individual

A

Phagocytosis by antigen presenting (dendritic) cell

Antibody-mediated immune response involving IgE

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19
Q

Cysteinyl leukotriene (CysLTs) receptors

A

Derived from mast cells and infiltrating inflammatory cells

Cause smooth muscle contraction, mucus secretion and oedema

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20
Q

Short acting B2-adrenoceptor agonists

SABAs

A

e.g. salbutamol
Are first line treatment for mild, intermittent, asthma
Are relievers taken as needed
Act rapidly to relax bronchial smooth muscle, increase mucous clearance and decrease mediator release from mast cells and monocytes

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21
Q

Long-acting B2-adrenoceptor agonists

LABAs

A

e.g.salmeterol, formoterol
Used for treatment of nocturnal asthma
LABAs must always be co-administered with a glucocorticoid.

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22
Q

Relievers in treatment of asthma

A

Act as bronchodilators
Relief of acute bronchal spasms
SABAs and LABAs
CysLT1 receptor antagonists

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23
Q

Preventors/ Controllers in treatment of asthma

A

Act as anti-inflammatory agents that reduce airway inflammation
Reduce frequency and severity of asthma attack
Glucocorticoids
Cromoglicate
Humanises monoclonal IgE antibodies

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24
Q

CysLT1 receptor antagonists

A

e.g. montelukast, zafirlukast
Relax bronchial smooth muscle in response to cysLTs,
Effective as add on therapy against early and late bronchospasm in mild persistent asthma
Effective in combination with other medications, including inhaled corticosteriods in more severe conditions

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25
Q

Methylxanthines

A

e.g. theophylline and aminophylline
Inhibit mediator release from mast cells, increase mucus clearance
Increase diaphragmatic contractility and reduce fatigue
Are second line drugs used in combination with B2-adrenoceptor agonists and glucocorticoids
Have a very narrow therapeutic window

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26
Q

Glucocorticoids

A
E.g.hydrocortisone/cortisol
Decreases Inflammatory responses 
Decreases Immunological responses 
Increase translation of anti-inflammatory genes
Used in prevention of asthma attacks
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27
Q

Chromones

A

Second line drugs used preventatively in treatment of allergic asthma
Decrease sensitivity of irritant receptors and stabilise mast cells

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28
Q

Short acting muscarinic antagonists used for treatment of COPD

A

Ipatropium

29
Q

Long acting muscarinic antagonists used for treatment of COPD

A

Tiotropium
Glycopyrronium
Aclidinium
Umeclidinium

30
Q

Which part of muscarinic receptor antagonists’ chemical structure reduces absorption and systemic exposure?

A

Quaternary ammonium group

31
Q

M1 muscarinic receptors

A

Increase frequency of action potential resulting from nicotinic receptor stimulation

32
Q

M2 muscarinic receptors

A

Reduce release of ACh

33
Q

M3 muscarinic receptors

A

Mediate contraction to ACh

34
Q

What muscarinic antagonist is the most useful in treatment of COPD

A

M3 muscarinic receptor antagonist

35
Q

What is the drawback of using ipatropium? (SAMA)

A

Non-selective blocker of M1, M2 and M3 receptors

36
Q

How is functional selectivity of M3 receptors achieved?

A

Differences in rates of association and dissociation- Drugs act on M3 receptors longer than M1 and M2 receptors

37
Q

Short acting B2 adrenoreceptor agonists used in treatment of COPD

A

Salbutamol

38
Q

Long-acting B2 adrenoreceptor agonists used in treatment of COPD

A

Formoterol

Salmeterol

39
Q

Ultra-LABA’s used in maintenance treatment for COPD

A

Indacaterol

Olodaterol

40
Q

Rofumilast

A

Selective PDE4 inhibitor

Suppresses inflammation and emphysema in COPD

41
Q

Drawbacks of rofumilast

A

Adverse gastrointestinal effects

42
Q

Benefits/ limitations of administering glucocorticoids in combination with LABAs in COPD

A

Of benefit in patients who develop frequent and severe exacerbations when given with a LABA
Do not in themselves suppress inflammation

43
Q

Reason for glucocorticoid unresponsiveness in COPD patients

A

Oxidative/nitrative stress

Reduced HDAC2

44
Q

Drugs used in triple inhalers as one daily treatment for COPD

A

Fluticasone
Umeclidinum
Vilanterol

45
Q

Rhinitis

A

Inflammation of the nasal mucosa

46
Q

Symptoms of rhinitis

A

Rhinorrhoea
Sneezing
Itching
Nasal congestion and obstruction

47
Q

Types of rhinitis

A

Allergic
Non-allergic
Mixed

48
Q

Anti-inflammatory treatment of rhinitis

A

Glucocorticoids

49
Q

Mediator receptor blockade in treatment of rhinitis

A

CysLT1 receptor antagonist

H1 receptor antagonists

50
Q

Treatment to target nasal blood flow in rhinitis

A

Vasoconstrictors

51
Q

Anti-allergic treatment for rhinitis

A

Sodium cromoglicate

52
Q

Mechanism of glucocorticoids

A

Suppress recruitment of cytokines and mediators, eosinophils, basophils into nasal mucosa
Reduce vascular permeability

53
Q

Examples of glucocorticoids

A

beclometasone
fluticasone
prednisolone

54
Q

Mechanism of anti-histamines

A

Antagonists that block effects of histamine

55
Q

Examples of second generation anti-histamines

A

Loratidine
Fexofenadine
Cetirizine

56
Q

Mechanism of anti-cholinergic drugs

A

Antagonists which block muscarinic receptors on nasal glands that stimulate watery secretions when activated by ACh

57
Q

Possible side effects of anti-cholinergic drugs

A

Dryness of nasal membrane

58
Q

Example of anti-cholinergic drug

A

Ipatropium

59
Q

Mechanism of sodium cromoglicate

A

Mast cell stabilization

60
Q

Mechanism of cysteinyl leukotriene receptor antagonists

A

Reduce effects of CysLTs upon nasal mucosa

61
Q

Example of CysTL receptor antagonist

A

Montelukast

62
Q

Mechanism of vasoconstrictor

A

Mimic effects of noradrenaline

Act on a1-adrenoreceptors to decrease swelling in vascular mucosa

63
Q

Example of vasconstrictor

A

Oxymetazoline

64
Q

Classifications of allergic rhinitis

A

Seasonal allergic rhinitis (SAR)
Perennial allergic rhinitis (PAR)
Episodic allergic rhinitis (EAR)

65
Q

Classifications of non-allergic rhinitis

A
Infectious rhinitis
Hormonal rhinitis
Vasomotor rhinitis
Nonallergic rhinitis with eosinophila syndrome (NARES)
Drug induced rhinitis
66
Q

Types of rhinitis in which glucocorticoids are used

A

SAR
PAR
NARES
Vasomotor rhinitis

67
Q

Types of rhinitis in which anti-histamines are used

A

SAR
PAR
EAR

68
Q

Types of rhinitis in which anti-cholinergic drugs are used

A

Reduce rhinorrhoea in SAR and PAR

69
Q

Types of rhinitis in which CysTL receptor antagonists are used

A

SAR

PAR