Brainscape's Knowledge GenomeTM

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


See full index

PharmacologyII > Asthma/COPD > Flashcards

Asthma/COPD Flashcards

1
Q

do we have good treatments to reverse the pathology of COPD?

A

• We don’t have good treatments to reverse the pathology of COPD

  • Glucocorticoids often don’t work despite inflammation being present in COPD
  • Bronchodilators are used to provide palliative support to symptoms
  • Cessation of smoking is beneficial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the immediate and late phases of asthma?

A

Asthma consists of a immediate phase (bronchospasm) and late phase (inflammatory) of the attack

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

what are 5 AEs of Roflumilast?

A
  • GI symptoms (diarrhea, nausea, abdominal pain)
  • weight loss,
  • nausea,
  • headache
  • insomnia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how is Roflumilast usually used?

A

– Used as an adjunct to bronchodilators for patients with severe COPD

Given orally

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

how does Roflumilast work?

A

Reduces inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is Roflumilast?

A

Long-acting inhibitor of phosphodiesterase 4

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

what are AE of Inhaled Anticholinergics?

A

– Minimal side effects due to minimal systemic absorption

– Local reactions include dry mouth, nasal irritation, and nose bleeds

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

which of the two Inhaled Anticholinergics is more selective? what is it more selective for?

A

Tiotropium has greater selectivity for M3 receptors, whereas ipratropium is nonspecific for M1 – M3 receptors

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

what are two Inhaled Anticholinergics?

A
  • Ipratropium (derived from atropine)

– Tiotropium

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

what is the MOA of Inhaled Anticholinergics? and how it largely mediated?

A

–INHIBIT: Parasympathetic stimulation of muscarinic receptors on the bronchioles causes bronchoconstriction and induces bronchial secretions….. SO ALLOW FOR RELAXATION AND DECREASED SECRECTIONS

These actions are largely mediated via M3 muscarinic receptors (to a lesser extent M1)

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

how do Bronchodilators help w/ COPD?

A

– Don’t deal with the underlying inflammation but can provide useful palliation and improve symptoms

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

how do Glucocorticoids help w/ COPD?

A

Generally ineffective but may be a worthwhile treatment as asthma can coexist with COPD

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

what are some treatments of COPD?

A
  • Stop smoking – Fibrosis of small airways
  • Glucocorticoids
  • Bronchodilators
  • Inhaled Anticholinergics
  • Roflumilast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which bronchodilators are used to treat immediate phase asthma, and which are used to treat late phase asthma?

A

• Bronchodilators (β2-adrenoceptor agonists ) are used to treat the immediate phase, whereas glucocorticoids are used to treat the late phase of asthma

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

Mepolizumab/Reslizumab- what is it used to treat?

A

Used to treat eosinophilic asthma

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

• Mepolizumab/Reslizumab - what are 3 AE?

A

– Headache

– Injection site reactions

– Oropharyngeal pain

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

IL5 - what is it’s main role?

A

IL-5 is responsible for differentiation and recruitment of eosinophils

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

Mepolizumab/Reslizumab - how do they work?

A

bind to and inhibit IL-5

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

Mepolizumab/Reslizumab - what are they?

A

Are humanized monoclonal antibodies that bind to and inhibit IL-5

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

Omalizumab - what other disease is it useful for?

A

May also have utility in urticaria, allergic rhinitis, and atopic dermatitis

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

Omalizumab- how is it administered?

A

Given subcutaneously once every 2 to 4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Omalizumab- what is an AE

A

Adverse effects include anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Omalizumab- what is it used to treat?

A

Used to treat severe allergic asthma that does not respond to high doses of corticosteroids

24
Q

Omalizumab- how does it work

A

(binds to IgE and prevents their interaction with IgE receptors)

25
Q

what is Omalizumab?

A

A humanized monoclonal anti-IgE antibody

26
Q

what is asthma characterized by?

A
  • inflammation of airways
  • bronchial hyper-reactivity
  • Reversible airways obstruction
27
Q

what are 4 categories of bronchodilators?

A

– β-adrenoceptor agonists
– Theophylline/aminophylline
– Cysteinyl leukotriene receptor antagonists
– Muscarinic receptor antagonists

28
Q

what is the MOA of B2-adrenorecptor agonists?

A

Dilate the bronchi via direct action on smooth muscle cell β2-adrenoceptors

inhibit mediator release from mast cells and

inhibit TNFα release from monocytes

Increase mucus clearance by acting on cilia

29
Q

what KIND OF RECEPTOR is B2-adrenoreceptor?

A

G-protein coupled

Gs coupled - activate adenylate cyclase and increase cAMP levels (2nd messenger)

30
Q

what G subunit is B2-adrenorecptor coupled to? and how do it work to cause bronchodilation?

A

Gs

  • activate adenylate cyclase and increase cAMP…..
  • increased CAMP leads to activation of PKA (protein kinase A)
  • which phosphorylated Phospholipase C
  • which INCREASES intracellular Ca2+
  • decrease Ca2+ means decreases contraction
31
Q

1) what are some short acting B2-adrenorecptor agnosits?
2) what is the duration of action?
3) how are they used by patients?

A

1) – Salbutamol
– Terbutaline

2) Duration of action is 3-5 hrs
3) Usually taken on an ‘as needed’ basis to control symptoms and reach maximum effect within 30 min

32
Q

what are 3 AEs (adverse events) of B2-adrenorecptor agonists?

A

– Tachycardia
– Dysrhythmias
– Tremor

33
Q

what is the MOA of theophylline/aminophylline?

A

– Inhibits phosphodiesterase (PDE)
▪ Thus prevents breakdown of cAMP (increases cAMP levels)

– Inhibits adenosine receptors (competitive antagonist)

– Inhibits the release of intracellular calcium and thereby reduces smooth muscle contraction

34
Q

side effects of theophylline/aminophylline?

A

– Adverse effects include cardiovascular (dysrhythmia)and CNS toxicities (headaches & seizures)

– May also cause GI upset (nausea & vomiting) and stimulatory effects (insomnia & restlessness)

35
Q

MOA of montelukast/zafirlukast?

A

–Cysteinyl leukotriene receptor antagonists (only CysLT1 receptor)

– Antagonizing these receptors reverses several effects commonly associated with asthma listed below:

▪ Bronchoconstriction
▪ Hyperresponsive airways
▪ Mucosal edema
▪ Mucous hypersecretion

36
Q

are montelukast/zafirlukast more or less effective than B2-adrenorecptor agonists at relaxing airways?

A

less effective than β2-adrenoceptor agonists at relaxing airways

37
Q

what are the adverse effects of montelukast/zafirlukast?

A

-headache and GI disturbances (generally well tolerated)

• Zafirlukast inhibits CYP3A4 (may increase effects of warfarin)

38
Q

how are B2-adrenoceptor agnoists administered?

A

– inhalation of aerosol, powder, or nebulized solution

– In some cases can be given orally or via injection (salbutamol)

39
Q

how is theophylline/aminophylline usually administered to patients?

A

Given orally as a sustained-released preparation

40
Q

what kind of antagonist are Theophylline/aminophylline on adenosine receptors?

A

competitive antagonist

41
Q

what is Theophylline/aminophylline?

A

Methylxanthine based agent

42
Q

draw ATP to PKA, with everything involved… do the same for GTP and PKG

A

WILL ADD THE PIC LATER - HARD TO ADD- ALSO ON SLIDE 14

43
Q

how are Montelukast/zafirlukast usually taken?

A

Taken by mouth and usually in combination with an inhaled corticosteroid

44
Q

what Anti-Inflammatory Agents are used in asthma?

A

Glucocorticoids

45
Q

what are 5 Glucocorticoids given via INHALATION?

A 
beclometasone, 
budenoside,
 fluticasone, 
mometasone
 ciclesonide
46
Q

what are Glucocorticoids used for?

A

Prevent the progression of chronic asthma and are effective in acute severe asthma

47
Q

WHATS one Glucocorticoids given orally? when is this used?

A

Oral prednisolone is reserved for patients with the severest disease

48
Q

what is the general MOA for Glucocorticoids?

A

Bind intracellular receptors that then dimerize, allowing for nuclear translocation and modification of gene transcription (transcription factors)

49
Q

what are the 2 Mechanisms by Which Glucocorticoids Control Gene Expression?

A

A) Basic transactivation;
-Ligand binds to GR dimer and upregulates transcription

(B) Basic transrepression;
-Ligand binds to GR dimer, which binds a nGRE and turns off transcription

50
Q

what is the MOA of Glucocorticoids in Asthma?

A

– Inhibit proliferation of Th cells by reducing the transcription of the IL-2 gene

– This leads to reduced formation of Th2 cytokines, thereby attenuating the recruitment and activation of eosinophils

– Inhibit allergen-induced influx of eosinophils into the lung (by decreasing IL-5/IL-13)

– Reduce the production of IgE and the expression of IgE receptors

51
Q

what are AEs of Glucocorticoids? inhaled and oral?

A

– Inhaled steroids may cause (more of an issue with beclometasone and budenoside )
❑Oropharyngeal candidiasis (thrush)
❑Dysphonia (croaky voice)
❑Adrenal suppression (particularly in children)

– Oral steroids may cause
❑Increased risk of infection
❑Hyperglycemia
❑Osteoporosis

52
Q

why is there a low risk of systemic side effects of Glucocorticoids?

A

Risk of systemic side effects is uncommon due to low systemic absorption and bioavailability

53
Q

why are Glucocorticoids frequently used in combination with β2-adrenoceptor agonists for chronic asthma?

A

❑Dilation of bronchial smooth muscle will enhance delivery of glucocorticoids to the airways

54
Q

what is omalizumab used for?

A

severe allegric asthma that doesnt respond to high doses of corticosteroids.

55
Q

what are the short acting b2 agonist taken as? vs long acting?

A

taken “as needed” to control symptoms

long acting: adjunctive therapy in patients whose asthma is inadequatly controlled by glucocorticoids.

56
Q

what type of asthma is mepolizumab and reslizumab used for? what type of receptors do they target?

A

eosinophilic asthma

IL5

PharmacologyII (12 decks)

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