Pharmacology Ii - 3/1510

Front 1

Asthma is a chronic, reversible inflammatory airway disease. After years of asthma however, it can become irreversible. What is sympathetic innervation to the lung like? What is the function of this innervation.

Back 1

Innervation to the tracheobroncial blood vessels and glands but not the smooth muscle. The smooth muscle does however contain the Beta 2 receptor and is influenced by Beta 2 agents.
Vasodilation is induced by the stimulation of this receptor.
Mast cell release is inhibited
Mucus clearing occurs

Front 2

What are the two sympathetic agents used in the treatment of asthma?

Back 2

The first agent was epinephrine
Albuterol is a more Beta 2 selective agent

Front 3

Describe the parasympathetic innervation of the lung.

Back 3

Acetylcholine stimulates muscarinic receptors.
The arterial and venous smooth muscle cells as well as glands are innverated causing vasoconstriction and mucus secretion.
This occurs via the vagus nerve.

Front 4

When are anti-cholinergic agents used?

Back 4

Primarily for COPD
Also for asthma if Beta 2 agonists are contraindicated for that patient.

Front 5

NANC fibers release neither norepinephrine nor acetylcholine. They are primarily under sympathetic control and show a mixed response. What is the mixed response?

Back 5

The stimulatory response induces vasoconstriction via the release of substances such as neurokinin A, calcitonin gene related peptide, substance P, bradykinin and tachykinin.
The inhibitory response involves the release of NO and vasoactive intestinal polypeptide causing vasodilation.

Front 6

NO is a marker for the severity of airway inflammation. What does a decreased NO indicate?

Back 6

Decreased NO indicates more severe airway inflammation and the dose needs to be increased.

Front 7

Stretch receptors are located in the upper and lower airways where they are innervated by myelinated and unmyelinated fibers, respectively. What are the 3 functions of these receptors? What 3 things stimulate these receptors?

Back 7

Cough, Bronchoconstriction, Mucus Secretion
Cold air, Irritants, Endogenous Inflammatory Mediators

Front 8

Vasoconstriction increases airway resistance.
What is hypersensitivity?
What is hyperreactivity?

Back 8

Hypersensitivity = Airway constriction at a lower than normal dose or stimuli possibly due to increased MLCK asthmatic BSM.

Hyperreactivity = An exaggerated response at normal to high levels. Possibly due to ASM hypertrophy.

Front 9

What are the main inflammatory mediators in acute asthma?

Back 9

Mast cells --> Histamine
CysLT and PGD2 (Slower onset)

Front 10

What are the major pathogenic cells of COPD?

Back 10

Eosinophils, Neutrophils and Macrophages
Neutrophils are resistant to corticosteroid effects and this is why steroids are not used in COPD.

Front 11

Describe the 3 major processes that take place in chronic asthma.

Back 11

(1) Cytokines and Chemokines are released to attract other inflammatory cells
(2) Tryptase (protease) induces the expression of adhesion molecules that attract eosinophils and basophils --> Hyperplasia of ASMC causing hyperreactivity
(3) Proteoglycans and Proteases cause airway remodeling which is possibly irreversible

Front 12

What 3 therapeutic agents are used to alleviate the bronchospasm initiated by mast cell spasmogens in the acute phase of asthma?

Back 12

Beta 2 antagonists
CysLT Receptor antagonists
Theophylline

Front 13

What agent is used in the late phase to alleviate airway inflammation, and airway hyperreactivity leading to bronchospasm, wheezing and coughing?

Back 13

Glucocorticoids
Other agents are also used and discussed in the next lecture.

Front 14

What are the main cells associated with COPD?

Back 14

Neutrophils and Macrophages