Pharm: Rhinitis/cold

Front 1

Uses of H1 receptor antagonists (5):

Back 1

1) prohylactically prevent Sx of allergy. 2) sedative. 3) motion sickness. 4) common cold. 5) early Parkinson's

Front 2

Antihistamine MOAs (2)

Back 2

1) dec action of histamine on efector cells by blocking H1 receptor. 2) anticholinergic action dec parasympathetic tone of effector cells.

Front 3

When antihistamines best taken? How to choose?

Back 3

Before onset of Sx and on a regular basis. Pt wil lselect antihistamine based on cost, duration, side effects and effectiveness (no single drug best)

Front 4

First generation H1 antagonists: 1) absorption. 2) Distribution. 3) onset. 4) max effect. 5) duration. 6) metabolization

Back 4

1) good oral absorption. 2) crosses BBB and placenta. 3) onset w/in 30 min. 4) max effect at 1-2 hrs. 5) short duration of 3-6 hrs. 6) liver metabolization

Front 5

First generation H1 antagonists: Side effects (5)

Back 5

1) sedation. 2) anti-cholinergic action. 3) hypersensitivity. 4) tolerance. 5) paradoxical CNS stimulation in children.

Front 6

Which 1st gen was first? Which has less sedation? What are the other 2?

Back 6

Diphenhydramine, chloropheniramine, cyproheptadine, promethazine

Front 7

Loratadine and Fexofenadine are known as what commerically? What are they? Side effects?

Back 7

Claratin and Allegra. 2nd generation H1 antagonists. Cardiac arrhythmias at high doses or those receiving macrolide antibiotics

Front 8

2nd generation H1 antagonists have what properties in regards to 1) absorption. 2) distribution. 3) halflife. 4) sedation. 5) anticholinergic action

Back 8

1) can be altered if taken with grapefruit juice (fexofenadine). 2) little or no BBB crossing. 3) longer halflife. 4) little or no sedation. 5) little or no anticholinergic action

Front 9

Iipratropium is a what? MOA? Application? Absorption? Side effects?

Back 9

Muscarinic Cholinergic antagonist. Blocks action of ACh on muscarinic receptors on secretory cells -> reduces secretion. Topical. Poor GI absorption. Minimal side effects since so little is absorbed but can cause mild irritation.

Front 10

What are the topical Alpha Adrenergic agonists? Onset? Side effects?

Back 10

EPI and phenylephrine. Rapid onset with fw systemic side effects. Prone to rebound congestion and rhinitis medicamentosa from downregulation of receptors.

Front 11

Oral alpha adrenergic? Onset/duration? Side effects?

Back 11

Pseudoephedrine. Slower onset but longer duration. Potential for more side effects: dizziness, tremor, insomnia, irritability, palpitations, hypertension. But less potential for dependence.

Front 12

MOA of alpha adrenergic sympathomimetics?

Back 12

Mimic NE and EPI on vascular smooth mm. -> vasoconstiction which dec volume of nasal tissues

Front 13

Flunisolide and Budesonide are what? Absorption? Metabolization?

Back 13

Topical corticosteroids. Rapid local absorption due to lipid solubility. Rapid first-pass hepatic metabolization

Front 14

Topical corticosteroid side effects (2)

Back 14

1) minimal adrenal suppression. 2) high incidence of adverse effects due to vehicle? Wtf

Front 15

Topical corticosteroid effects: 1) How long for full effect? 2) inf. Cells? 3) permeability? 4) cholinergic receptors? 5) nasal Sx? 6) mediator production?

Back 15

1) 1-2 weeks. 2) dec in nasal epithelial inf. Cells. 3) dec epithelial permeability. 4) dec in secretory response from cholinergic receptors. 5) partial inhibition of immediate allergen induced nasal Sx. 6) inhibition of leukotriene and prostaglandin production

Front 16

Cromolyn solubility? Administration?

Back 16

Lipid insoluble (highly polar, hydrophilic) -> poorly absorbed by GI tract. Inhalation or insolution as eye or nose drops.

Front 17

Cromolyn delay for full effect? MOA (3)?

Back 17

Up to 1-2 weeks. 1) prevents release of histamine and other mediators from sensitized cells -> most likely by preventing IgE induced Ca influx. 2) may inhibit cAMP phosphodiesterase -> inc cAMP -> smooth mm. relaxation. 3) may inhibit IgE dependent activation of 2nd inf. cells (eosinophils and neutrophils)

Front 18

Pathophysiology of common cold?

Back 18

acute infection of upper respiratory tract, perhaps by a virus. Consequence of inf. Reaction and cholinergic activity

Front 19

Pharmacology for common cold?

Back 19

symptomatic

Front 20

How is cough coordinated?

Back 20

Within the medulla (cough center)

Front 21

Codeine is what? Property of dose?

Back 21

Opioid analgesic that dec sensitivity to cough reflux. 2) the antitussive action is at a lower dose than required for analgesia.

Front 22

Dextromethorphan is a what? How does it act?

Back 22

Opiod stereoisomer w/o analgesic effect or addiction. Acts centrally to dec sensitivty to cough center.

Front 23

Diphenhydramine is a what? How does it act? Any side effects?

Back 23

Antihistamine. Acts centrally to dec sensitivity of cough center. Probably not due to H1 receptor but rather anticholinergic activity. Sedation.

Front 24

Expectorant MOA?

Back 24

stimulates secretory activity of respiratory tract causing a reduction in the miscosity of the mucus

Front 25

Guaifenesin is a what? How does it work?

Back 25

Expectorant. Works by triggering vagal reflex (near emetic doses needed)

Front 26

Terpin Hydrate is a what? How does it work? Any side effects?

Back 26

Expectorant. Works by direct action on respiratory tract and secretory cells.

Front 27

Iodides is a what? How does it work?

Back 27

Expectorant. Works through direct action on all secretory glands. Potential for thyroid suppression and is contraindicated in those w/ hypersensitivity to iodide.

Front 28

Acetylcysteine is a what? How does it work?

Back 28

Mucolytic. Reduces sputum viscosity.

Front 29

How do demulcents (cough drops work)?

Back 29

soothes the pharynx

Front 30

How does Benzonatate (anesthetic) work?

Back 30

May act by anesthetizing the stretch or cough receptors in the respiratory tract as well as by a central mechanism (CNS + periphery)