Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Drug Treatment of COPD and Rhinitis > Flashcards

Drug Treatment of COPD and Rhinitis Flashcards

1
Q

COPD causes?

A

Smoking

Air pollution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Characteristics of COPD?

A

Airflow reduction that is, in some patients, partially reversible
Progressively worsens by symptom exacerbation inc. cough and mucous production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Two main disease processes in COPD?

A

Emphysema

Bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Specific pathway of COPD development from harmful agent?

A

Smoking (air pollution)
Stimulates resident alveolar macrophages
Cytokine production
Activates neutrophils, CD8 T cells, increased macrophage numbers
Release of matrix metalloproteins (like elastase, decreased elastic recoil) and free radicals causes chronic bronchitis and emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does chronic bronchitis involve?

A 
Inflammation of bronchi and bronchioles
Cough
Clear mucous sputum
Infections with purulent sputum
Increasing breathlessness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does emphysema involve?

A

Distension and damage to alveoli
Destruction of acinial pouching in alveolar sacs
Impairs gas exchange and elastic recoil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of muscarinic ACh receptors in humans?

A

M1, M2 and M3, at different locations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Function of M1 ganglia?

A

Facilitate fast neurotransmission mediated by ACh acting on NICOTINIC receptors (nAChR)

Mediate a SLOW excitatory post-synaptic potential, increasing action potential frequency resulting from nicotinic receptor stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Function of M2 ganglia?

A

Postganglionic neurone terminals - act as INHIBITORY AUTORECEPTORS, reducing ACh release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Function of M3 ganglia?

A

Smooth muscle neuroeffector junction

Mediate contraction to ACh (also present on mucous-secreting cells and increase secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Desirable receptors for blocking to relieve COPD symptoms?

A

Block M1 and M3 receptors to reduce smooth muscle contraction
Do not block M2 as, when stimulated, it decreased ACh transmission; blocking increases ACh transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cornerstone of COPD treatment? Describe what the drugs do

A

Reducing parasympathetic activity with muscarinic receptor antagonists - PHARMACOLOGICAL antagonists of bronchoconstriction caused by smooth muscle M3 receptor activation in response to ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mechanism of muscarinic ACh receptor antagonists in COPD?

A

M3 muscarinic receptor stimulates Gq/11 which activates phospholipase C, breaking PIP2 down to IP3
Stimulates Ca2+ release from SR
Leading to contraction

Drugs block M3 receptor so ACh does not bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Licensed competitive muscarinic receptor antagonists?

A

Short-acting muscarinic antagonists (SAMAs) - Ipratropium and oxitropium

Long-acting muscarininc antagonists (LAMAs) - tiotropium and aclidinium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Administration of SAMAs and LAMAs?

A

Inhalational route

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Difference atropine and more recent muscarinic receptor antagonists?

A

Atropine has a tertiary amine
Ipratropium and tiotropium have a quaternary ammonium group
Reduces absorption and systemic exposure, avoiding multiple adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Relieving effects of muscarinic ACh receptors?

A

Effect is mainly PALLIATIVE and have little effect on COPD development
Relax bronchospasm
Basal block ACh mediated basal tone
Decrease mucous secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Preferred muscarinic receptor antagonists and why?

A

Ipratropium is a non-selective blocker of M1, M2 and M3 and there are more selective agent like tiotropium now

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is tiotropium more selective than ipratropium?

A

Greatly longer half-life at M3 muscarinic receptor; aclidinium is also selective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

β-adrenoceptors used in COPD treatment?

A

Via inhalation
Salbutamol (SABA)
Salmeterol and formoterol (LABA)
(no effect on inflammation)_

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ultra-LABA examples?

A

Indacaterol - rapid onset of action

Once daily dosing is effective

22
Q

Recommendation for moderate COPD treatment?

A

Combination of a LABA and a LAMA is superior to either drug alone in increasing FEV1

LABA/LAMA combination most effective when both drugs are deposited in same location in airways (some drugs are being developed with both LABA and LAMA)

23
Q

LABA and LAMA combination use logic?

A

Drugs work via complementary mechanisms to cause smooth muscle contraction

24
Q

Other drugs used in COPD treatment?

A

PDE4 (phosphodiesterase-4) expressed in neutrophils, T cells and macrophages - inhibition may have inhibitory effect on inflammatory and immune cells

Rofumilast - selective PDE4 inhibitor, suppresses inflammation and emphysema in animal COPD (approved as oral drug for severe COPD accompanied by chronic bronchitis ) - limiting adverse GI effects

25
Q

Combination inhalers in COPD treatment?

A

β-adrenoceptor agonists co-administered with glucocorticoids

26
Q

When are glucocorticoids not useful in COPD?

A

Glucocorticoid unresponsiveness in COPD may be due to due to oxidative/nitrative stress (chronic inhalation of tobacco smoke) - HDAC2 reduced in COPD

27
Q

What is rhinitis? characteristics?

A

Involves acute, or chronic, inflammation of nasal mucosa characterised by:
Rhinorrohea (runny nose - watery mucus accumulation in nasal cavity)
Sneezing
Itching
Nasal congestion & obstruction (swelling of nasal mucosa due to dilated blood vessel)

28
Q

Types of rhinitis?

A

Allergic (seasonal - SAR - perennial - PAR - and episodic have similarities to allergic asthma)
Non-allergic
Mixed

29
Q

Steps in allergic rhinitis?

A

Inhaled allergen increases specific IgE levels
IgE binds to receptors on mast cells and basophils
Re-exposure causes mast cell and basophil degranulation
Mediator release, like histamine, CysLTs, tryptase, prostaglandins - cause rhinitis symptoms
DELAYED response due to recruitment of lymphocytes and eosinophils to nasal mucosa contributes to congestion and obstruction

30
Q

Define non-allergic rhinitis

A

Any rhinitis, acute/chronic, that does not involve IgE - dependent events

31
Q

Causes of non-allergic rhinitis

A 
Infectious rhinitis - largely viral
Hormonal rhinitis - pregnancy
Vasomotor rhinitis (disturbances that are idiopathic - unknown causes)
NAR with eosinophilia syndrome (NARES)
Drug/medication induced rhinits
32
Q

Define mixed rhinitis

A

Allergic and non-allergic components

Occupation rhinitis

33
Q

What do rhinitis and rhinnorhea both involve?

A

Increased mucosal blood flow, increased blood vessel permeability, or both
All increase volume of nasal mucosa and cause difficulty breathing in

34
Q

Overview of targets in rhinitis and rhinorrhea treatment and drugs used for targeting?

A

Anti-inflammatory - glucocorticoids
Mediator receptor blockade - H1 receptor antagonists (anti-histamines) , CysLT1 receptor antagonists
Nasal blood flow - vasoconstrictors
Anti-allergic - sodium cromoglicate

35
Q

Glucocorticoid mechanisms in treatment on rhinitis and rhinnorhea?

A

Reduce vascular permeability, recruitment & activity of inflammatory cells and release of cytokines & mediators
Reduce all rhinitis symptoms, including nasal congestion, over several weeks

36
Q

Use of glucocorticoids in rhinitis and rhinnorhea treatment?

A

Mainstay of SAR and PAR therapy; are of value in NARES and vasomotor rhinitis
Effective as monotherapy
Frequently applied TOPICALLy as a spray to nasal mucosa (intranasal once daily usually)
May be given orally short-term in severe cases

Can be combines with anti-histamines in moderate-to-severe rhinitis

37
Q

Examples of glucocorticoids?

A

Beclometasone
Fluticasone
Prednisolone (oral)

38
Q

Mechanisms of anti-histamines/H1 receptor antagonists in rhinitis treatment?

A

Competitive antagonist of H1 receptors and reduce effects of mast cell derived histamine inc:
Vasodilation and increased capillary permeability
Activation of sensory nerves
Mucous secretion from submucosal glands

39
Q

Uses of anti-histamines?

A

Effective in SAR, PAR, and episodic, AR but less so for non-allergic rhinitis
Effective as monotherapy
Administered orally or as intranasal spray (azelastine)

Less effect upon congestion that on other symptoms

40
Q

Types of anti-histamines?

A

First and second generation agents
Second generation is preferred due to reduced sedation (do not cross blood-brain barrier) and lack of anti-cholinergic effects
First generations ability to suppress rhinorrhea may arise from anti-cholinergic activity

41
Q

Examples of second generation anti-histamines?

A

Loratidine
Fexofenadine
Cetirizine (mild anti-inflammatory action as well)

42
Q

Mechanisms of anti-cholinergic drugs/muscarinic receptor antagonists in rhinitis treatment?

A

ACh released from post-ganglionic parasympathetic fibres activates nasal gland muscarinic receptors , causing watery secretion contributing to rhinnorhea - blocked by mby muscarinic antagonists

43
Q

Uses of mucarinic antagonists in rhinitis treatment?

A

Effective in reducing rhinnorhea in PAR and SAR but no influence on itching, sneezing and congestion

Administered via nasal route but may cause dryness of nasal membranes (no other adverse effects)

44
Q

Muscarinic receptor antagonists used in treatment of rhinitis?

A

Ipratropium

45
Q

Mechanism of sodium cromoglicate treatment of rhinitis and uses?

A

Purportedly mast cell stabilisation but uncertain
Used as maintenance treatment of allergic rhinitis with onset of action (4-7 days but may be weeks for full effect

Nasal administration - less effective than nasal corticosteroids

46
Q

Mechanisms of CysLT receptor antagonists in rhinitis treatment?

A

Reduce effects of CysLTs upon nasal mucosa

47
Q

Uses of CysLT receptor antagonists in rhinitis treatment?

A

Equi-effective with anti-histamines in treating PAR and SAR - may be additive effect

Administer via oral route and should be particularly considered for patients with AR and asthma

48
Q

Examples of CysLT receptor antagonists used in rhinitis treatment?

A

Montelukast

49
Q

Mechanisms of vasoconstrictors in rhinitis treatment?

A

Act as direct/indirect sympathomimetics to mimic effect of noradrenaline - produce vasoconstriction via α-adrenoceptor activation; decreases swelling in vascular mucosa

50
Q

Examples of vasoconstrictors in rhinitis treatment?

A

Oxymetazoline - selective α1-adrenoceptor agonist (giving intranasally) and is effective, short-term, in reducing congestion in allergic rhinitis

51
Q

Cautions with oxymetazoline use?

A

Nasal administration for > few days not recommended due to development of rebound increase in nasal congestion upon discontinuation (RHINITIS MEDICAMENTOSA) - due to receptor desensitisation and downregulation

Pharmacology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions