Uthcsa-Respiratory Pharmacology

Front 1

Name the NSAID's and describe their general MOA.

Back 1

aspirin (irreversible cox-1 & 2), salicylate (reversible cox-1 & 2), ibuprofen (reversible cox-1 & 2), indomethacin (reversible cox-1), celecoxib (reversible cox-2)

-prevent the synthesis of prostaglandins by inhibiting cox-1 and/or cox-2

Front 2

What are the medical uses of the NSAID's?

Back 2

Antipyresis- decreases PGE2 synthesis.

Analgesia- peripheral analgesia effect via decreased PG's.

Inflammation-RA, anklosing spondylitis, muscle pains.

CV disease- decreases TXA2 synthesis.

Dysmenorrhea-reduces PG's associated with painful menstruation (ibuprofen).

Inhibit early labor (indomethacin)

Closure of PDA (indomethacin)

Front 3

How does aspirin work and what is it used for?

Back 3

-irreversibly inhibits Cox-1 and Cox-2 by acetylating the active site of the enzymes.

-inhibits platelet cox-1 for the life of the platelet (9-14 d). This prevents platelets from making TXA2 (prothrombotic).
Tx: angina

Daily aspirin (80-325 mg/d) reduces MI by 50% and stroke after a TIA by 40%.

Front 4

What are the SE's of NSAID use?

Back 4

Hypersensitivity via enhanced leukotriene synthesis (nasal polyps, rhinoconjuctivitis, urticaria)

Increased BP

Increased salt/water retention via decreased renal function (decrease in PG-mediated increase in RBF and GFR).

GI ulceration/bleeding

Front 5

Name the corticosteroids and provide a general MOA

Back 5

cortisone (p.o, i.v.), hydrocortisone (p.o, i.v.) , prednisolone (p.o., i.v.), flunisolide (aerosol)

Activated gene expression to inhibit all sysnthesis of PG's and LT's.

Blocks the expression of many inflammatory mediators (Cox-2, PLA2, iNOS, cytokines)

Front 6

What are the corticosteroids used for?

Back 6

For the Tx of many diseases including allergic reactions, arthritis, asthma and nephrotic syndrome.

Front 7

What are the SE's of corticosteroid use?

Back 7

PREDNISONE (pg 170)

Also negatively feedback on the hypothlamus to decrease CRH, TRH and GnRH leading to adrenal cortex atrophy, hypothyroidism and amenorrhea, azoospermia.

Front 8

What are the drugs that interfere with leukotriene synthesis or effects?

Back 8

zileuton- inhibits lipooxygenase to decrease LT synthesis.

zafirlukast and montelukast- blocks the receptors for LTC4 and LTD4.

All for Tx of asthma.

Front 9

What are the sympathomimetic drugs that can be used to alter the tone of the bronchial smooth muscle?

Back 9

epinephrine (B2>B1>a)- 30 seconds when given s.c.

salmeterol (long t1/2), terbutaline, albuterol (B2>B1)(OUTPATIENT USE) -bronchodilations via B2 stimulation.

Inhibits the release of inflammatory mediators from mast cells. Inhibits the accumulation of eosinophils.

Front 10

What are some of the SE's of the Beta-agonists?

Back 10

Very few when given by inhalation. If p.o.--> cardiac arrythmias, hyperglycemia, hypokalemia, dizziness.

Front 11

What are some of the corticosteroids that are used in respiratory therapy and how do they work?

Back 11

beclomethasone, budesonide, flunisolide, fluticasone

Administered by aerosol but can increase Cp 4x in certain intractable situations by giving p.o. If long-term p.o., dose every other day.

Prevent immune cell recruitment and release of inflammatory mediators.

Reverses the early and late inflammatory phases.

Prevents generation of PG's and LT's.

Front 12

What are the major SE's of inhaled corticosteroid use?

Back 12

dysphonia and oral Candida

-can both be prevented by rinsing the mouth and throat with water after use.

Front 13

Ipratropium

Back 13

Inhaled muscarinic antagonist.

Bronchodilation begins in 10 min, peaks at 1-2 hrs and lasts for 4-8 hrs.

NO ANTIHISTAMINE/ANTI-INFLAMMATORY EFFECTS.

Used as a seondary therapeutic agent if B-agonists are not working. Give iprotropium to dilate airways, then use albuterol.

SE's- dry mouth and bitter taste. Use with caution in angle-closure glaucoma, GI/GU obstruction or BPH.

Front 14

Cromolyn sodium

Back 14

p.o., inhaled, nasal, eye drops.

prophylactic prevention of IgE-mediated mast cell degranulation. Prevents Ca2+ pathway that is downstream of IgE-receptor engagement.

NO MEDIATOR RELEASE

Use aerosol with care in patients with CAD of cardiac arrhythmias.

Used 10-15 min before antigenic exposure.

Reduces the incidence of bronchospasm and damage to bronchial tissue.

Front 15

Theophylline & aminophylline

Back 15

aminophylline (86% theophylline) is more water soluble than theophylline.

MOA- prevents the breakdown of cAMP downstream of B2 signaling by inhibiting phosphodiesterase.

also a specific adenosine receptor antagonist.

Lungs- dilation by relaxing smooth muscle. Increases diaphragm contraction. Increase in FEV1 and FVC.

Mast cell-prevents degranulation

CNS-causes central respiratory stimulation.

Heart-decrease in TPR with increase in HR provides increase in CO. Releases plasma epi.

Gastric-enhances gastric acid secretion.

Front 16

What are the SE's of theophylline and aminophylline?

Back 16

Careful monitoring of theophylline doses. Therapeutic window is narrow.

Contraindicated with peptic ulcer.

Use with care in CAD and recent MI.

Nausea and GI discomfort are common.

CNS restlessness, headache and tremor.

Front 17

How do you Tx Cheyne-Stokes breathing?

Back 17

aminophylline normalizes the periodic deep and shallow breathing which occurs in cycles with CS (which is associated with heart failure or CNS injury).

Front 18

How do you Tx neonatal apnea?

Back 18

aminophylline & caffeine.

Front 19

How do you Tx neonatal hypoxic respiratory failure?

Back 19

Associated with pulm hypertension.

Use inhaled Nitric Oxide.