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CPR Week 7 > 3.7.2. Pharmacology of Astma > Flashcards

3.7.2. Pharmacology of Astma Flashcards

1
Q

Adrenergic agonists stimulate what?

A

Stimulate B2-adrenoreceptors, resulting in the relaxation of bronchial smooth muscle

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2
Q

Adrenergic agonists inhibit what?

A

inhibit the release of mediators, stimulating mucociliary clearance

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3
Q

Albuterol, levalbuterol, pirbuterol, metaproterenol are what kinds of drugs?

A

B2-selective agonists: Preferred for brochoconstriction

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4
Q

With B2 selective agonists, what is their effect?

A

Enhanced B2 selectivity = Bronchodilation

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5
Q

How do we administer B2 agonists and how long does it take to activate?

A

administered by inhalation, active in 1-5 minutes

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6
Q

Long term effect of B2 agonists?

A

long-term use associated with diminished control of breathing, possibly due to down regulated B-receptors

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7
Q

Effect of B2 agonists on specific pulmonary cells?

A

Increases surfactant by Type II pneumocyte, ciliary clearence

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8
Q

B2 agonists desensitizes and downregulates a few things. What are they?

A

Desensitizes neutrophils, eosinophils, T-Cells, decreases cholinergic transmission as well as plasma exudation and mast cell releases

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9
Q

Discuss isoproterenol and what it does?

A

Isoproterenol: relatively non-selective B-receptor and potent bronchodilator

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10
Q

Discuss Epinephrine and what it acts on?

A

Epinephrine: available OTC inhalant, acts on B1, B2, and A1 receptors; onset in 5-10 min and duration 60-90 minutes

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11
Q

Salmeterol, formoterol are examples of what?

A

Long acting B2-agonists

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12
Q

Salmeterol, formoterol are administered as inhalants but with slower onset of action and longer duration. Why?

A

very lipophilic side chains that slow diffusion out of the airway (very high lipid solubility)

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13
Q

Salmeterol, formoterol, which are 50x more selective than albuterol, are used in the clinical setting primarily for what?

A

use for prophylaxis of asthma

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14
Q

Discuss the specificity of Terbutaline and it’s effect on the heart

A

moderately specific B2 agonist that is available as injection or tablet moderately cardiostimulatory

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15
Q

Side effects of Epinephrine and isoproterenol

A

Epinephrine and isoproterenol have significant B1-receptor activity and can cause increases in cardiac effects (tachycardia, arrhythmias, angina)

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16
Q

most common side-effect of B2-agonists is ____ ____.

A

most common side-effect of B2-agonists is muscle tremors (skeletal)

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17
Q

A-receptor agonists may cause _____ and _____.

A

A-receptor agonists may cause vasoconstriction and hypertension

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18
Q

What is the side effect “Tachyphlaxis” and how do we counter it?

A

Tachyphlaxis, blunted response due to prolonged use, cna be countered by switching to a different agonist or adding methylxanthine or a corticosteroid

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19
Q

Methylxanthines cause what and how?

A

broncohdilation via action on smooth muscles of the airways

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20
Q

Theophylline has _____ properties and reduces airway responsiveness to ____ and _____.

A

Theophylline has anti-inflammatory properties and reduces airway responsiveness to histamine and allergens

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21
Q

Methylxanthines does what biochemically?

A

inhibits PDE (increasing cAMP) at high doses

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22
Q

Methylxanthine pharmacologic effect (4)

A
  1. Produce rapid relaxation of smooth muscle in bronchioles 2. decrease response to histamine 3. stimulate ciliary transport of mucus 4. improve contractility of diaphragm
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23
Q

Methylxanthine has effects on other systems besides the pulmonary one. What are those effects?

A
  1. chronotropic and inotropic actions on the heart 2. pulmonary and peripheral vasodilation but cerebral vasoconstriction 3. at high doses can lead to nervousness and seizures due to medullary stimulation
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24
Q

Methylxanthine can be used for 3 things?

A
  1. as an adjunct to inhaled corticosteroids and B-agonists to improve response 2. treat COPD and emphysema 3. treat apnea in preterm infants (specifically caffeine)
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25
Q

Methylxanthine adverse effects

A
  1. Physical: arrhythmias, nervousness, vomitin, and GI bleed 2. Psych: behavioral problems in children 3. Contraindications: combined use with B2 receptors is suspected for increased asthma mortality
26
Q

Ipratrpoium and atropine are what drugs?

A

Are muscarinic antagonists

27
Q

What do muscarinic antagonists do?

A

competitive antagonists of ACh

28
Q

Muscarinic antagonists do what?

A

inhibit constriction of airways and decrease vagal-stimulated mucus secretion

29
Q

Distinguish between Ipratropium and Tiotropium

A

Ipratropium is poorly absorbed and does not cross the blood brain barrier, administered as an aerosol and therefore limits its adverse effects - short acting Tiotropium is a long-acting antagonist used to treat COPD

30
Q

Side effects of atropine

A

Atropine is readily absorbed, adverse effets include drowsiness, sedation, dry mouth, blurred vision

31
Q

How does Chromlyn Sodium work?

A

precise mechanism is unclear, inhbits release of mediators from mast cells; suppresses neutrophils, eosinophils, monocytes; inhibits cough reflexes (may be due to inhibition of chloride ion channels)

32
Q

only anti-asthmatic that inhibits early AND late phase response

A

Chromlyn Sodium

33
Q

Function of gluccocorticoids

A

produce significant increase in airway diameter, probably by attenuating PG and LT synthesis via inhibition of phosphlipase A2 reaction and general inhibition of immune response

34
Q

What does Prednisone do

A

Prednisone - Used for acute and chronic asthma exacerbations

35
Q

Zafirlukast and montelukast do what biochemically?

A

agonists of the LT receptor LT1; blocks LTC4/D4/E4

36
Q

General effect and use for Zafirlukast and montelukast

A

reduces bronchoconstrion and inflammatory cell infiltration for mild persistent asthma

37
Q

Zileuton does what?

A

inhibits 5-lipoxygenase, the rate-limiting enzyme in LT biosynthesis

38
Q

Immediate effect of Zileuton

A

immediate and sustained 15% improvement in forced expiratory volume (FEV)

39
Q

Zileuton inhibits microsomal P450’s and decreases the metabolism of ____ ____ and ____.

A

inhibits microsomal P450’s and decreases the metabolism of terfenadine, warfarin, and theophylline

40
Q

Prolastin, Aralast are what?

A

A1-proteinase inhibitors (Prolastin, Aralast)

41
Q

What do we use A1-proteinase inhibitors (Prolastin, Aralast) for and how often do we give them?

A

used to treat emphysema caused by a deficiency in a1-proteinase Weekly IV injection to treat patients homozygous for the deficiency

42
Q

Omalizumab does what?

A

Omalizumab binds to human IgE’s high-affinity Fc receptor, blocking the binding of IgE to mast cells and basophils and other cells associated with allergic response reduces early phase degranulation of mast cells and late phase release of mediators

43
Q

Omalizumab lowers serum IgE concentrations, but does not block ____________.

A

lowers serum IgE concentrations, but does not block alergen-antibody response

44
Q

Who gets Omalizumab

A

used in patients >12 yo who are refractory to inhaled gluccocorticoids and asthmatics with allergies SubQ injection every 2-4 weeks

45
Q

Increased serum levels of IgE Allergens Infections (rhinovirus, parasites, etc) Environmental exposure to all kinds of particulates and toxins Stress, Panic Medicines Food additives, Metabisulfides These are all examples of what?

A

Extrinsic Asthma triggers

46
Q

Examples of intrinsic asthma triggers

A

Normal IgE Patho disturbances Negative responses to common antigenic challenge Cold

47
Q

Asthma anatomy changes

A

Increased smooth muscle around airway Inflammation Actual trapping, which is closing of the airway

48
Q

Cells that contribute to Asthma inflammation

A

Inflammatory cells Vascular endothelial cells Epithelial cells Smooth muscle cells

49
Q

Mast cells secrete these: To cause:

A

Mast cells secrete IgE, peroxidase, chemotactic factors, cytokines, etc. This causes leaking of the endotheial barrier, SMC contraction and inflammatory cells to infiltrate the airspaces

50
Q

Bronchial gland and mast cells release histamine. This causes:

A

Bronchial gland and mast cells - histamine. This causes more recruitment of inflammatory cells, SMC contraction and increased granular secretions

51
Q

Protease production by mast cells and eosinophils do this:

A

Protease production by mast cells and eosinophils, which increases vascular permeability, further inflammatory cell infiltration, alterations to the ECM, and contributes to the permanent remodeling we see in asthma patients

52
Q

Leukotriene C4 and D4 released by leukocytes and platelets do this:

A

Leukotriene C4 and D4 released by leukocytes and platelets, which are both chemoatractants for inflammatory cells. They also cause bronchiospasm, increased mucus production, and increased vascular permeability

53
Q

Prostaglandin and chemokine release by mast cells and lung epithelial cells do this

A

Prostaglandin and chemokine release by mast cells and lung epithelial cells, further recruiting inflammatory cells

54
Q

These 3 things are late asthma events:

A

Cytokine releases (inflammatory cell recruitment including eosinophils, CD$+T lymphocytes, monocytes, neutrophils). Persistent airflow obstruction Increased airway hyperresponsiveness, SMC growth, etc.

55
Q

Airway inflammation 3 stages and what happens during them

A

Acute - Early recruitment of cells to the airway Sub-acute - Recruited and resident cells are activated to cause a more persistent pattern of inflammation Chronic - Persistent level of cell damage and repair processes

56
Q

Histologic changes we see in asthma

A
57
Q

Discuss a metered-dose inhaler

A

Metered-dose inhaler - usually contains a large volume holding channel (or “spacer”) that fits between the inhaler and the mouth. The inhaler discharges into it and the patient inhales from it

58
Q

Discuss a nebulizer

A

Nebulizer - Not as cheap or portable but doesn’t require hand/breathing coordination (therapy can be delivered by face mask)

59
Q

Discuss a dry-powder inhaler

A

Dry Powder inhaler - Developed as alternative to chlorofluorocarbon propellants

60
Q

Two concepts for treating asthma

A

Drugs that treat symptoms only - Relievers - Bronchodilatory actions, usually rapid onset

Drugs that treat underlying cause - Controllers - Antiinflammatory actions, slower acting, often prophylactic (not for emergencies)

CPR Week 7 (12 decks)

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