Asthma and COPD Flashcards

1
Q

b2 agonist

A

Albuterol, Salmeterol

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2
Q

Leukotriene antagonist

A

Montelukast

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3
Q

Muscarinic antagonist

A

Ipratropium (nonselective), Tiotropium (M1, M3 but not M2 inhibitor) – quaternary amine derivatives of atropine

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4
Q

Inhaled corticosteroid

A

Fluticasone

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5
Q

Monoclonal Anti-IgE antibody

A

Omalizumab

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6
Q

Increased Raw – Obstructive Lung Disease

A
Decreased airflow	(decreased FEV1)
Airflow is limited during expiration (E)
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7
Q

decreased L-CW compliance – Restrictive Lung Disease

A

Parenchyma fibrosis

Decreased forced vital capacity (decreased FVC)

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8
Q

Asthma

A
spasmodic contraction of smooth muscle in the bronchi;
airflow obstruction (bronchospasm), bronchial hyperresponsiveness, and an underlying inflammation
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9
Q

Chronic obstructive pulmonary disease

A

Bronchitis - inflammation of the bronchi and bronchioles
Emphysema – alveolar destruction
Combination!;
Progressive decrease in lung function (clinically relevant in aged population)
↓ FEV1
Limited reversibility

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10
Q

FACTORS THAT DETERMINE AIRWAY RESISTANCE

A

Structure of the airways
Airway smooth muscle contraction
Lumen obstruction (mucus)
Elasticity of lung parenchyma

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11
Q

“Hallmark” of asthma

A

reversibility with bronchodilator

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12
Q

Positive correlation of asthma symptoms with

A

Total IgE levels

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13
Q

asthma involves

A

INFLAMMATION, REMODELING, and NERVE HYPER-REFLEXIVITY

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14
Q

what leads to decreased airflow in COPD?

A

↓ aveoli structure: ↓ elastic recoil: ↓ structural support: bronchiole collapse: ↑ Resistance: ↓ Airflow

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15
Q

asthma cell infiltration

A

Eosinophils, Mast Cells, Basophils

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16
Q

COPD cell infiltration

A

Neutrophils, Macrophages

17
Q

b-adrenoceptor agonists

A

Actively cause bronchodilation

18
Q

leukotriene and muscarinic antagonists

A

Inhibit specific inflammatory mediators

19
Q

corticosteroids

A

Reduce inflammation

20
Q

anti-IgE antibodies

A

Prevent inflammation – for asthma only

21
Q

b Adrenoceptor agonists MOA

A

Activation of β2 adrenoceptors on bronchial smooth muscle – ↑ cAMP ->relaxation -> bronchodilation
Facilitates sequestration of Ca2+
Inactivates MLCK
Inactivates MLC20

22
Q

b Adrenoceptor agonists Therapeutic Uses

A

Short-acting (e.g. albuterol)
Rescue for asthma and COPD
Long-acting (LABA) (e.g. Salmeterol)
Control for asthma and COPD

23
Q

Leukotriene Antagonist MOA

A

CysLT1 antagonist

Prevents Cys-LT-induced bronchospasm, ↓ immune cell infiltration, no ↓ AHR, very mild reversal of remodeling

24
Q

Leukotriene Antagonist Therapeutic Uses

A

Control for asthma

25
Q

Muscarinic Antagonists MOA

A

Blocks acetylcholine-induced activation of muscarinic receptors on:
Airway smooth muscle (M3) –↓ bronchospasm
Epithelial mucosal glands (M3) –↓ mucus secretion

26
Q

Muscarinic Antagonists Therapeutic Uses

A

Rescue for asthma

Control for COPD

27
Q

ACh activates neuronal M2 receptor

A

as negative feedback control of ACh release

28
Q

Inhaled Corticosteroids MOA

A

Anti-inflammatory, ↓ infiltration of eosinophils/basophils/mast cells, minor ↓ AHR, mild reversal of remodeling
↓ pro-inflammatory protein production (e.g. IL-4 and IL-5)
↑ anti-inflammatory protein production
MODULATION OF PROTEIN EXPRESSION IS SLOW-ONSET (>12 hours)

29
Q

Inhaled Corticosteroids therapeutic use

A

Control for asthma (inhalation, nasal)

Control for COPD – limited relief

30
Q

Corticosteroid: Mechanism of Action – COPD

A

Corticosteroids have little effect on neutrophilia

Corticosteroids have no effect on MORTALITY

31
Q

Anti-IgE Antibodies MOA

A

Binds to free IgE (Fc region), promotes destruction
↓ IgE from binding to FCeR1 and FCeR2
↓ expression of FCeR1 on mast cells/basophils
↓ allergen-induced IgE crosslinking on mast cells/basophils
Prevents allergen-induced bronchospasm, ↓ immune cell infiltration, ↓ exacerbations, no ↓ AHR, effect on remodeling is unclear.

32
Q

Anti-IgE Antibodies Therapeutic Uses

A

Control for severe, steroid-resistant asthma

33
Q

Anti-IgE Antibodies Rate of onset

A

Circulating IgE destroyed in hours/days

Takes more than a week for mast cell-attached IgE to reduce