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First Year med - dundee > 70R. Pharmacology in COPD > Flashcards

70R. Pharmacology in COPD Flashcards

1
Q

what is COPD

A

Chronic obstructive pulmonary disorder

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2
Q

what is COPD in tad more detail

A

Progressive airflow obstruction and lung hyperinflation that is, in some patients, partially reversible

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3
Q

what are symptoms of COPD

A

dyspnoea, chesty cough, mucus, wheezy, chest

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4
Q

how is COPD diagnosed and what is the FEV1/FVC ratio

A

through spirometry - Post bronchodilator FEV1/FVC ratio 0.7

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5
Q

what are some of the Systemic manifestations in COPD

A

deconditioning and muscle weakness

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6
Q

who does copd mainly effect

A

middle aged/older adults who are smokers and around air pollution

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7
Q

what are the 2 types of COPD

A

Chronic Bronchitis and Emphysema

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8
Q

what is chronic bronchitis

A

inflammation of bronchi and bronchioles

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9
Q

what are some symptoms of chronic bronchitis

A

Cough
Clear mucoid sputum
Infections with purulent sputum
Increasing breathlessness

**Purulent means containing pus, a thick, yellowish liquid that comes from an infection in the body.

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10
Q

what happens in emphysema

A

distension and damage to the alveoli

destruction of acinial pouching in alveolar sacs

loss of elastic recoil

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11
Q

When someone smokes or is exposed to air pollution, what is stimulated?

A

Alveolar Macrophages in the lungs

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12
Q

alveolar macrophages that have been stimulated by smoke/air pollution produce what?

A

Cytokines

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13
Q

activated alveolar macrophages release cytokines which activate what?

A

neutrophils , CD8 T cells, and more macrophages

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14
Q

after smoking you end up with all these cells: neutrophils , CD8 T cells, and more macrophages. what do they release

A

matrix metalloproteinases and free radicals

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15
Q

can you give me an examples of a matrix metalloproteinase

A

elastase

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16
Q

There is an increased resistance to Air Flow During …………….in COPD

A

expiration

**exhalation phase fails - breathing out is hard work with copd

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17
Q

describe the inhalation of a severe copd patient

A

near normal

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18
Q

what are the 3 Muscarinic Acetylcholine Receptors in the Airways

A

M1, M2 and M3

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19
Q

where are M1 receptors found

A

ganglia (nerve clusters in the airways)

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20
Q

what is M1’s function

A

helps speed up nerve signals (fast neurotransmission) By making a slow signal that makes the nerve cells fire more often. In summary, nAChRs initiate the fast response, and M1 receptors sustain and amplify this response, ensuring efficient communication in the ganglia

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21
Q

where can you find M2’s

A

Found on postganglionic neuron terminals.

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22
Q

what are M2’s function

A

Act as inhibitory autoreceptors.
M2 receptors reduce the release of ACh.
When M2 receptors are blocked, the inhibition is lifted, leading to an increase in ACh release

aka
They act like brakes to reduce the release of ACh.
How: When these receptors are blocked, the brakes are off, and more ACh is released.

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23
Q

when M2’s are blocked what happens to ACh

A

there is an increase in release

24
Q

where can you find M3’s

A

On airway smooth muscles and mucus-secreting cells.

25
Q

what are M3’s function

A

Cause muscles to contract and increase mucus production.

When ACh binds to M3 receptors, the muscles contract.
Mucus cells: When ACh binds to M3 receptors, more mucus is produced.

26
Q

so out of M1-M3 which one is the most important in treatment with patients with copd and why

A

M3
well if you are reducing M3 which when bound to by ACh causes smooth muscle of the airway to contract and have lots of mucus production then you are not constricting the airway as much which helps people with copd

explained further -
ACh Release: ACh is released from postganglionic parasympathetic fibers and epithelial cells in the airways.

M3 Receptor Activation: ACh binds to M3 receptors on airway smooth muscle (ASM), causing the muscles to contract, leading to bronchoconstriction.

Antagonist Action: Muscarinic receptor antagonists bind to M3 receptors, preventing ACh from binding.

Result: This blockade prevents the contraction of airway smooth muscle, thereby reducing bronchoconstriction and helping to keep the airways open

27
Q

so these muscarinic receptor antagonists do what? (in summary)

A
  • reduces bronchospasm
  • blocks ACh from increasing basal tone
  • decreases mucus secretion
28
Q

are muscarinic receptor antagonists curing the copd

A

No, they have a palliative effect: These medications mainly provide symptomatic relief and have little effect on the progression of COPD.

29
Q

what are the 2 types of muscarinic antagonists

A

SAMA and LAMAs
short acting muscarinic antagonist
long acting muscarinic antagonists

30
Q

name a SAMA

A

Ipratropium

31
Q

name 4 LAMAs

A

§ Tiotropium
§ Glycopyrronium
§ Aclidinium
§ Umeclidinium

32
Q

how are SAMA/LAMAs administered

A

inhalation

33
Q

which out of theses LAMAs § Tiotropium
§ Glycopyrronium
§ Aclidinium
§ Umeclidinium
are black triangle drugs and need MHRA surveillance

A

Glyc, aclid and umec

34
Q

what does atropine and ipratropium and tiotropium have on there chemical structure to avoid adverse effects

A

quaternary ammonium group

35
Q

is ipratropium selective or non selective

A

non selective blocker of M1,2 and 3

36
Q

why are M3 Selective Blockers Superior to Ipratropium?

A

Because with ipratropium you block M1,2 and 3. Blocking M3 and M1 is desirable but blocking M2 is not. This is because release of Ach from parasympathetic postganglionic neurons is increased by auto receptor antagonism

and remember you don’t want to block M2 because M2 Receptors: Act as inhibitory autoreceptors that reduce ACh release. Blocking M2 receptors can increase ACh release, potentially worsening bronchoconstriction.

37
Q

what are the 3 types of beta-adrenoreceptor agonists administered by inhalation

A

SABA- salbutamol
LABA - salmeterol and formoterol
UltraLABA - indacaterol and olodaterol

38
Q

so which should you use for copd patients? Muscarinic antagonists or beta adrenoreceptor agonists?

A

both combined

39
Q

what do A combination of a β2 agonist and a muscarinic antagonist do/increase

A

increase FEV1 (forced expiratory volume)

40
Q

what are the benefits of having combination inhalers

A

easy to use
dont allow adjustment of the dosage

41
Q

why is it a good idea to take a LABA and a LAMA

A

LAMA - blocks activation of ACh so prevents bronchoconstriction
LABA - agonist on B2 causes relaxation

42
Q

what are MABAs

A

muscarinic antagonist and Beta2 agonist. Basically a single drug that is both of these combined

43
Q

what other drugs are used to treat copd

A

glucocorticoids

44
Q

B-adrenoceptor agonists and/or muscarinic receptor antagonists can be co-administered with …………………. in combination inhalers.

A

glucocorticoids

45
Q

what do glucocorticoids increase risk of in COPD patients

A

Pneumonia

46
Q

what do triple inhalers contain

A

LABA, LAMA and glucocorticoid

47
Q

what is a benefit of glucocorticoid steroids

A

when given with a LABA they are helpful to patients with severe exacerbations

48
Q

what are some downsides to glucocorticoids

A
  • increased pneumonia risk
  • do not alone suppress inflammation
    -might not work if patient smokes
49
Q

apart from LAMAs, LABAs and glucocorticoids, what other drugs are used in COPD (name 2)

A

Phosphodiesterase-4 (PDE4)
Rofumilast

50
Q

Explain Phosphodiesterase-4 (PDE4) mode of action

A

PDE4 is an enzyme expressed in inflammatory cells like neutrophils, T cells, and macrophages.

Blocking PDE4 can reduce inflammation and immune cells

51
Q

Explain rofumilast mode of action

A

Roflumilast is a selective PDE4 inhibitor that suppresses inflammation and emphysema in animal models of COPD.

It is approved for oral treatment of severe COPD, particularly in patients with chronic bronchitis and a history of exacerbations

52
Q

what are some side effects of rofumilast

A

gastrointestinal effects

53
Q

what are some comorbidities associated with COPD

A

Osteoperosis
GI diseases
Metabolic Syndromes
Resp disease
CardioVas Diseases
Depression and anxiety

54
Q

what approach should you take when treating COPD

A

personalized patient centered approach - precision medicine

55
Q

personalized patient centered approach - precision medicine in COPD should include….

A

Frequent Exacerbations: Monitor and manage based on exacerbation frequency.

ICS(inhaled corticosteroids) History: Review exacerbation history before starting or continuing ICS.

Side Effects: Regularly assess the risk of pneumonia and other side effects from ICS.

Patient Preferences: Engage patients in treatment decisions to enhance adherence and outcomes.

First Year med - dundee (67 decks)

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