Pharm: Asthma/copd

Front 1

What does the upper and lower respiratory tract have that the other doesn’t?

Back 1

Upper: venous sinuses. Lower: smooth muscle

Front 2

FEV1 / FVC for Normal? Obstructive? Restrictive?

Back 2

1) 80% 2) decreased. 3) increased or normal

Front 3

List 3 ways to obtain obstructive lung disease.

Back 3

1) secretion of mucus. 2) constriction of smooth muscle. 3) dynamic compression of airways.

Front 4

blood flow, ventilation, and V/Q are greatest where in the lung?

Back 4

bottom, bottom, top of the lung

Front 5

Asthma early response: What initiates? What is the outcome? What inhibits? What doesn't?

Back 5

1) mast cell mediators (histamine, leukotriene, etc). 2) smooth mm. contraction, mucus secretion, vascular leakage, flushing. 3) bronchodilators. 4) anti-inf.

Front 6

Asthma late response: What induces what? What cell shows up at 2-8 hrs and what pathology is seen in addition to early response? At 1-2 days? What is the late response assoc w/? What alleviates, what doesn't?

Back 6

inc mediators induce vasospasm. Eosinophils, fibrin deposition. Macrophages and fibroblasts, tissue destruction. Late response is associated with hyperresponsivity both to allergic and nonallergic stimuli. Corticosteroids alleviate, bronchodilators do not.

Front 7

3 Neurogenic components to asthma?

Back 7

1) sensitization of afferent nerve endings in airway. 2) release of inf. Neuropeptides. 3) stimulation of bronchoconstriction through efferent cholinergic pathways

Front 8

long-term control of asthma: Useful for? Not useful for? Characterized by? Examples (6)

Back 8

1) managing Sx. 2) preventing asthma attack. 3) anti-inf. Actions. 4) corticosteroids, cromones, long acting beta2 agonists, theophyline, leukotriene modifiers, anti-IgE Ab

Front 9

Quick relief medications for asthma typically do what two things? Examples (3)

Back 9

1) relieve bronchoconstriction by relaxing smooth mm. and/or interfere with NT/autocoid/cytokine release. 2) systemic corticosteroids, short beta2 agonists, ipratropium

Front 10

5 things to consider to help improve the TI of asthma drugs?

Back 10

1) deliver locally. 2) modulate immune response. 3) receptor selective/duration. 4) avoid GI tract absorption. 5) if absorbed systemically -> rapidly metabolize

Front 11

2 ways to Tx status asthmaticus?

Back 11

1) beta agonists. And/or 2) systemic corticosteroids

Front 12

List 4 corticosteroids

Back 12

beclomethasone, budesonide, ciclesonide, methylprednisolone

Front 13

List 3 routes of administration for corticosteroids.

Back 13

1) inhalation for long term control. 2) systemically for acute exacerbations. 3) topically for long term rhinitis control.

Front 14

corticosteroids: 1) inflammatory mediators? 2) adrenergic bronchodilators? 3) mucus? 4) immune reponse?

Back 14

1) inhibits synthesis of mediators. 2) restores reponse -> inc # of beta2 receptors and inc responsiveness. 3) dec mucus production. 4) inhibits immune response

Front 15

corticosteroid systemic metabolism? Lipid solubility? How long to see reponse?

Back 15

rapid metabolism. High lipid solubility. Days to weeks to see full effect.

Front 16

4 side effects of corticosteroids.

Back 16

1) suppression of HPA axis in children w/ systemic use. 2) promotion of oropharyngeal candidiasis. 3) dysphonia. 4) bone loss

Front 17

What is unique about beclomethasone?

Back 17

first one, locally active; readily metabolized

Front 18

What is unique about budesonide?

Back 18

approved for young children; nebulizer

Front 19

What is unique about ciclesonide?

Back 19

prodrug that is activated in the lung

Front 20

What is unique about Methylprednisolone?

Back 20

IV soluble form -> parenterally

Front 21

Name 2 cromones. How are they administered? Solubility property?

Back 21

cromolyn and nedocromil. Inhalation. Poorly absorbed (not lipid soluble)

Front 22

Cromolyn: List 2 effects. 3 uses.

Back 22

1) inhibits early response, late response, and bronchial hyperreactivity. 2) inhibits Ag, cold induced, and exercise induced asthma. 3) long term control but requires 4-8 weeks to see if pt will respond. 4) prophylatically for exercise or exposure. 5) nasal spray/eye soln for allergic rhinitis

Front 23

Cromolyn: 2 MOAs

Back 23

1) prevents Ca influx that is provoked by IgE Ab-Ag interaction of mast cell. 2) prevents mast cell release of anaphylaxis mediators

Front 24

Nedocromil uses (2). Spectrum compared to comolyn?

Back 24

1) long term control since it is only useful after 3-4 days. 2) prophylactically before exercise or exposure. Broader spectrum than cromolyn

Front 25

Nedocromil has what 2 MOAs?

Back 25

1) inhibits activation of resident mast cells, epithelial cells, and alveolar macrophates by immunologic and nonimmunologic means. 2) inhibits attraction and activation of circulating inf. Cells

Front 26

Zileuton is a what? Use? Administered? Duration? Metabolized?

Back 26

1) anti-leukotriene - 5-lipoygenase inhibitor. 2) long-term control. 3) oral. 4) short. 5) by the liver

Front 27

Zileuton MOA (3)

Back 27

1) inhibits conversion of arachadonic acid -> leukotriene A4. 2) attenuates bronchospasm by allergen/nonallergen. 3) attenuates inf. Response by allergen

Front 28

Zileuton: 2 side effects and contraindictation

Back 28

1) elevates liver enzymes. 2) interferes w/ metabolism of warfarin, theophyline, propranolol. 3) contraindicated for liver disease

Front 29

What is Montelukast? Use? Administration? Duration? Metabolization?

Back 29

1) (Singular) Anti-leukotriene - leukotriene receptor antagonist. 2) Long-term control. 3) orally. 4) long duration. 5) by liver and excreted in bile

Front 30

Montelukast MOA (2)

Back 30

1) attenuates bronchospasm by allergen/nonallergen. 2) attenuates inf. Response produced by allergen.

Front 31

ipratropium is a what? 3 Uses?

Back 31

Muscarinic cholinergic antagoinist. 1) quick relief. 2) long-term control if pt. intolerant to Beta-agonists. 3) prevention of exercise induced asthma

Front 32

ipratropium MOA (2):

Back 32

1) promotes bronchodilation -> blocks ACh at cholinergic receptors on airway smooth mm. 2) reduces secretion -> blocks action of ACh on secretory cells

Front 33

Ipratropium application? Side effect? Onset? Duration?

Back 33

1) locally. 2) local irritation. 3) slow. 4) long

Front 34

Beta adrenergic agonists: Uses (2)

Back 34

1) quick relief to stop acute Sx. 2) taken chronically for long-term relief by reducing responsiveness of smooth mm. to histamine and leukotrienes

Front 35

Beta adrenergic agonists: MOA (3)

Back 35

increases adrenyl cylase activity to: 1)relax smooth mm. 2) inhibit mast cell mediator release. 3) increase mucociliary clearance

Front 36

Beta adrenergic agonists: Side effects (3)

Back 36

1) Receptor based -> vasoconstriction, cardiac stimulation, skeletal mm. tremor. 2) refractoriness, but may be counteracted by corticosteroid. 3) may mask disease progression

Front 37

Beta agonists with immediate onset and short duration?

Back 37

epinephrine and isoproterenol

Front 38

Beta agonists with rapid onset and intermediate duration?

Back 38

Terbutaline and Pributerol

Front 39

Beta agonists with intermediate onset and prolonged duration?

Back 39

Albuterol, Lev-albuterol

Front 40

Beta agonists with slow onset but very prolonged action?

Back 40

Salmeterol and Formoterol

Front 41

The beta agonists show higher selectivity for which? Which 2 don't follow this?

Back 41

1) Greater selectivity for B2 > B1. 2) EPI acts at all alpha and beta and Isoproterenol acts at all beta

Front 42

Advantage of Lev-albuterol over albuterol?

Back 42

More active biologically with fewer CV side effects

Front 43

2 side effects of Salmeterol?

Back 43

1) get down regulation of receptors after prolonged exposure -> need inc dose of other short term drugs. 2) NOT to be given alone -> risk of CV death

Front 44

Name 4 methylxanthines

Back 44

Theophyllin, theobromine, aminophyline, caffeine

Front 45

methylxanthines: 3 Uses

Back 45

1) Bronchodilator for acute asthma when beta agonist is inadequate. 2) long term control. 3) Tx of recurrent apnea of prematurity

Front 46

methylxanthines: 3 MOAs

Back 46

1) Block adenosine receptors…..then 10x the amt to….2) inhibit cAMP phosphodiesterase -> inc cAMP -> mm. relaxation. 3) alter translocation of intracellular Ca

Front 47

methylxanthines effect on 1) smooth mm. 2) mucociliary. 3) mast cells. 4) diaphragm. 5) respiratory. 6) heart. 7) blood vessels

Back 47

1) relaxation of airway smooth mm. 2) inc mucociliary clearance. 3) inhibit Ag induced release of mast cell mediators. 4) Strengthen diaphragmatic contractions and inc resistance to fatigue. 5) stimulation of medullary respiratory centers. 6) positive ionotropic and chronotropic effect on heart. 7) vasodilation of systemic (except cerebral) and pulmonary vessels.

Front 48

methylxanthines have what property that causes what recommendation?. List of side effects.

Back 48

Very narrow TI so regular determinations of [plasma]. HA, N/V, insomnia, anxiety, heartburn, uclers, tremor, convulsions, arrythmia

Front 49

methylxanthines: 1) Bioavailability? 2) Distribution? 3) noteworthy of dosage?

Back 49

1) good oral bioavailability. 2) widely distributed -> crosses BBB and placenta. 3) dosage MUST be INDIVIDUALIZED and check that plasma level regularly

Front 50

methylxanthines: Property of halflife? 2) what inc? 3) what dec?

Back 50

1) wide variation in halflife. 2) hepatic disease, COPD, cimetidine, macrolide antibioltics, oral contraceptives, acute alcohol. 3) smoking, chronic phenobarbital, phenytoin, chronic alcohol

Front 51

What is Omalizumab? MOA? Administered? Limitation?

Back 51

1) anti-IgE Ab. 2) it binds circulating IgE -> reduces releases of mast cell and basophil release of mediators to allergens. 3) administered SQ at 2-4wk intervals. 4) some pt do no respond.

Front 52

Antihistimines? Herbals?

Back 52

H3 receptor antagonists. ASHMI

Front 53

3 pharmalogical interventions for chronic bronchitis?

Back 53

1) beta-adrenergic sympathmimetrics. 2) methylxanthines. 3) muscarinic cholinergic antagonists

Front 54

Emphysema is what? What are 2 mechanisms causes?

Back 54

destruction of alveolar septa, enlargement of distal air spaces, and loss of lung elasticity. 1) neutrophil elastase destorys CT of lung parenchyma. 2) pts may lack alpha 1 antitrypsin

Front 55

What do you use to Tx emphysema (4)?

Back 55

In general the same drugs you use to Tx asthma. 1) Theophylline. 2) alpha1 proteinase inhibitor -> b/c of elastase. 3) DNAse to break up mucus plugs. 4) Muscarinic cholinergic antagonists (tiotropium)