Respiratory (Pharmacology Of Obstructive Lung Disease)

Front 1

The parasympathetic system CONSTRICTS/DILATES the bronchial system.

Back 1

constricts (via stim of vagus nerve that releases ACh, which binds to M3 in smooth muscle cells within bronchial walls

Front 2

how does the sympathetic system dilate bronchi?

Back 2

catecholamines from adrenal glands binding to beta-2 receptors

Front 3

what are NANC?

Back 3

they cause both bronchoconstriction (by releasing neurokinin A, calcitonin gene-related peptide, etc) or bronchodilation (by releasing nitric oxide and VIP)

Front 4

review the pathophysiology of COPD

Back 4

Smoke/irritants draw in alvelar macrophages and neutrophils to release proteinases (ie. elastases). This, along with Cd8 T cells, will cause 2 things: alveolar wall destruction (emphysema) and/or mucus hypersecretion (chronic bronchitis)

Front 5

review the pathophysiology of asthma:

remember to mention what type of inflammatory cell types are resp for early and late phase asthma...

Back 5

it's basically an allergic response

- allergen causes mast cell to degranulate and release of mediators (like histamine, leukotriences) leading to early bronchoconstriction
- later, they also cause influx of inflammatory cells (esp eosinophils)...leading to airway edema and more airflow obstruction

Exposure to allergen causes synthesis of IgE, which binds to mast cells in the airway mucosa. On reexposure to allergen, antigen-antibody interaction on mast cell surfaces triggers release of mediators of anaphylaxis: histamine, tryptase, prostaglandin D2 (PGD2), leukotriene C4, and platelet-activating factor (PAF). These agents provoke contraction of airway smooth muscle, causing the immediate fall in FEV1. Reexposure to allergen also causes the synthesis and release of a variety of cytokines: interleukins 4 and 5, granulocyte-macrophage colony stimulating factor (GM-CSF), tumor necrosis factor (TNF), and tissue growth factor (TGF) from T cells and mast cells. These cytokines in turn attract and activate eosinophils and neutrophils, whose products include eosinophil cationic protein (ECP), major basic protein (MBP), proteases, and platelet-activating factor. These mediators cause the edema, mucus hypersecretion, smooth muscle contraction, and increase in bronchial reactivity associated with the late asthmatic response, indicated by a fall in FEV1 2-8 hours after the exposure.

Front 6

what is the best drug delivery mechanism (for bronchodilation) for infants and small children?

what about in ERs?

Back 6

nebulizers for both!!

Front 7

tell me about the mechanisms of the following in causing bronchodilation:
-beta agonists
-PDE inhibitors
-muscarinic antagonists

Back 7

Beta agonists --> increase rate of cAMP synthesis by AC (causes relaxation of smooth muscle)

PDE inhibitors (theophylline) --> decrease rate of cAMP degradation

Muscarinic antagonists --> inhibit bronchoconstriction (at the receptor itself)

Front 8

put these in order of shortest to longest acting beta-agonist:

albuterol, salmeterol, epinephrine

Back 8

epinephrine < albuterol < salmeterol

Front 9

can you give only albuterol for asthmatic patients? why or why not?

Back 9

no, bc it only relaxes airway smooth muscles, but have no effect on chronic inflammation, which is what is needed for asthmatic patients

Front 10

what is the most commonly used "rescue" inhaler?

Back 10

albuterol

Front 11

what are the long acting beta-2 agonists?

Back 11

salmeterol and formoterol

Front 12

T or F. You should never use LABA as sole therapy for asthmatic patients or any patietns undergoing acute exacerbation of asthma.

Back 12

T.

Front 13

what are the side effects of long-acting beta-2 agonists

Back 13

muscle tremor, tachycardia and palpitation, hyperglycemia/hypokalemia, V/Q mismatch, tachyphylaxis (resistance to drug)

Front 14

do beta-2 agonists alone help for asthmatic patients?

Back 14

no, they relieve sx's but don't control underlying inflammation

Front 15

what is the 1st line tx in COPD?

Back 15

anticholinergics

Front 16

name a short-acting and long-acting anticholinergic.

Back 16

short-acting = ipratropium (usually used with albuterol)

long-acting = tiotropium

Front 17

how do anticholinergics work in COPD?

Back 17

- Block vagal pathways-decreases vagal tone
- Blocks reflex bronchoconstriction caused by inhaled irritants

Front 18

name the common methylxanthine and its mechanism

Back 18

theophylline (causes the same effects as caffeine)... probably via phosphodiesterase inhibition

- problem is that it has a very narrow therapeutic window

Front 19

Relate how Theophylline metabolism is affected by different medications and disorders.

Back 19

if pt has conditions like liver dz, CHF, older age, viral conditions, febrile; or taking drugs like macrolide antibiotics, cimetidine, quinolone, propanolol, allopurinol (for gout) --> theophylline have decreased metabolism and increased levels

if you smoke, younger age, hyperthyroidism, use barbiturates/phenytoin, theophylline increases in metabolism and you have less levels in your body

Front 20

what are the toxicities of theophylline

Back 20

GI symptoms most common (irritation, burning and nausea); CNS stimulation; tachycardia

Front 21

What are the various anti-inflammatory medications?

Back 21

-Corticosteroids (most commonly used for asthma)
-Leukotriene Modifiers
-Mast-cell stabilizers (cromolyn sodium/Nedocromil - useful in children only)
-Anti Ig-E therapy

Front 22

what is the first line tx in acute asthma?

Back 22

systemic or oral corticosteroids (most effective anti-inflammatory med's)

though oral is not really used bc of so many SEs, except for exacerbations of asthma

Front 23

what is the first line tx in daily asthma management?

Back 23

inhaled corticosteroids

Front 24

when should anti-IgE be used?

Back 24

for extremely, severe asthma pts who are not controlled by other drugs (bc of their SEs...flu-like sx's, anaphylaxis

Front 25

what are the medications you can use for smoking cessation?

Back 25

bupriopion (antidepressant that undermines the reuptake of dopamine and norepinephrine; produce more dopamine, which is supposed to help lower the cravings)

varenicline (chantix) - partial agonist of nAchR

Front 26

what are the benefits of using nicotine patch for smoking cessation?

Back 26

there's no nicotine withdrawal syndrome that accompanies its usage

Front 27

what is the best combination for smoking cessation success?

Back 27

nicotine patch + buproprion + counseling

Front 28

what are the criteria for oxygen therapy?

Back 28

only in very severe cases of COPD (with chronic respiratory failure)

Front 29

how do leukotriene modifiers work?

Back 29

When a person has asthma, the inside walls of the airways can become swollen and covered with a layer of mucus, partially blocking the flow of air into and out of the lungs.

Leukotrienes are among the chemicals released by the body that contribute to this process.

Leukotriene Modifiers are new medications that reduce and prevent the swelling inside the airways before it starts, stop the mucus from forming and lessen the muscle tightening around the airways. Leukotriene Modifiers work to prevent an episode from starting. They are not used to treat symptoms.

Front 30

what are the different leukotriene modifiers?

Back 30

1) zileuton
2) zafirlukast and monteleukast

Front 31

how big do the particles have to be for good effect of metered dose inhalers

Back 31

2-5 micrometers

Inhalation therapy deposits asthma medications directly, but not exclusively, in the lungs. Distribution of inhaled drug between lungs and esophagus depends on particle size and efficiency of delivery to lungs. Most material, approximately 90%, will be swallowed and absorbed, entering the systemic circulation. Some drug also will be absorbed from the lungs. Optimal particle size for deposition in small airways is 1 to 5 mm (so small).