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Flashcards in Sweaty Pulm from a Pharm Perspective Deck (34)

What are some advantages to inhalation therapy?

1. large surface area for absorption with very little metabolism and efflux
2. more permialble to small molecules than the GI tract
3. non-invasive
4. affects seen quickly


What are some disadvantages to inhalation therapy?

1. contamination --> infections/must clean after every use
2. less efficient due to dead volume loss and size of inhalation
3. pt compliance/ability to use correctly
4. deposition of the drug in the alveoli vs. the conducting airways (think surface area)


How are lipophillic and hydrophillic drugs absorbed differently in the lung?

lipophillic are more rapidly absorbed and done so transcellularly

hydrophillic drugs are more slowly absorbed and done so through intracellular tight junctions


What determines the rate at which a drug is absorbed in the lungs?

MW and ionization: smaller, less ionized molecules are abs faster


What 4 drug types are used to treat URT diseases?
*not neosplastic

Drugs acting on CNS cough center


What 3 types of drugs are used to treat lung diseases?
*not neoplastic

bronchial tone modulators
vascular tone modulators


What autonomic receptors are used to control bronchospasm? agonist or antagonists?

B2 agonists
Muscarinic antagonsits


T or F: B2 receptors innervate bronchial smooth muscle

F: they innervate the airway SM , epithelial cells, mast cells and type II alveolar cells


Where are B2 receptors found in the lung?

airway SM , epithelial cells, mast cells and type II alveolar cells


What receptors are found in airway/bronchial smooth muscle? What effect do they have when they are active?

Sympatheic: NE or Epi binds B2 --> bronchodilation and decrease airway secreations

Parasympatheic: Ach binds M2 and M3 --> bronchoconstrict and increase airway secreations


What effect does adenosine have on bronchial smooth muscle?



What effect does Ach have on bronchial smooth muscle?



What effect does theophylline have on bronchial smooth muscle?

inhibits bronchoconstriction --> dilation


What effect does M1 receptor activation have in the lungs?

increased glandular secretions
**no effect on airway/bronchial smooth muscle!!


What effect does presynaptic M2 auto receptors have in the lung?

binds Ach and inhibits futher release of Ach --> decreases bronchoconstriction


What effect does blockage of the M2 autoreceptor have in the lungs? Why is this significant?

increases the release of endogenous Ach --> more bronchoconstriction
**it offsets any bronchodilatory drug effects


What is the selectivity of Tiotropium?

M1 and M3 receptors


What effect does M3 receptor activation have in the lungs?

increase secretions and bronchoconstriction


What drug class (and drugs) causes drying of secretions?

1st gen antihistamines + anticholinergic activity
**block M1 and M3 --> dec secretions



What drug class (and drugs) cause an increase in airway secretions?

ACh-esterase inhibitors
**inc ACh levels --> inc M1 and M3 activity --> inc secretions



What receptors control airway secretions?

M1 and M3
(activation/Ach increases secretions)


What is albuterol?
What is the major effect of it?
When is it used/what does it treat?

B2 agonist --> bronchodilation

EARLY/acute phase of asthma attack
**ineffective against the later phase bc it is an inflammation problem


What are the problems assc with high B2 agonist concentrations?

-CV stimulation/tachycardia (B1 activation --> inc HR, contractility, and CO) =
-prolong QT interval --> pro-arrhythmogenic
-hypokalemia --> pro-arrhythmogenic too!

also of note:
-widening of pulse pressure
-arterial dilation in coronary, pulmonary. and skeletal muscle
-muscle tremor (due Na/K ATPase inc activity)


How can B2 agonist use lead to hypokalemia?

stimulation of skeletal muscle Na/K ATPase causes and increase in intracell K+ and a decrease in serum K+


What are the benefits of B2 agonist therapy for the treatment of asthma?

1. bronchodilaiton opens airways
2. anti-inflam by inhibiting mast cell degranulation
3. inc mucocilliary clearance by activ goblet cells and submucosal glands and increasing beat frequency of cillia
4. dec extravasation/leakage of plasma protein --> dec edema/airway obstruction
5. dec chemotaxis, adhesion, and activation of leukocytes


What drugs should not be used at the same time as B3 agonists? Why?

1. Saquinavir: promotes hypokalemia --> arrhythmias
2. Tricyclic antidepressants (amitriptyline, desipramine): blocks re uptake of NE --> excessive bronchodilation
3. MAOIs (selegilene and rasagilene): blocks metabolism of amine --> excessive bronchodilation
4. loop and thiazide diuretics: hypokalemia --> arrhythmias
5. non-selective beta blockers (propranolol) --> opposes effects of B2 agonist


How is the issue of desensitization addressed with the use of B2 agonists?

pts receive a short course of corticosteroids that will increase the transcriptional activity and lead to an increase production of B2 receptors --> restores drug sensitivity


Describe the process of desensitization.

repeated stimulation causes phosphorylation of the C term of the BAR. B-arreston binds to the phosphorylated domain and blocks Gs binding = uncouples pathway and cAMP decreases--> signaling stops. Arrestin binds and the BAR becomes localized in a lysosome --> degradation and down-regulation


How can glucocorticosteroids treat asthma?

1. anti-inflammatory
-inhibit production of inflam cytokines
-promote production of anti-inflam cytokines
-promote apoptosis of macrophages, DC, and T cells

2. prevent desensitization of B2 receptor


What is a complication of inhaled glucocorticosteroids?

oral infections like thrush if the mouth is not rinsed after use


What role do leukotines play in asthma?

binds CysLT1 on airway smooth muscle --> bronchoconstriction, eosinophil migration, airway edema


What maintains the vascular tone in the pulmonary arteries?

balance between mediators of vasoconstriction (Ca++ and endothelin) and vasodilation mediators (PGI2 and NO --> inc cAMP or cGMP intracell)


What is the target/aim for drugs that treat PAH?

they try to restore the balance between the effects of the vasoconstrictos and the vasodilators by inhibiting intralcell Ca++ signaling and increasing intralcell cAMP and/or cGMP
**PGI2 analogs, exogenous NO, CCBs, PDE5i


What effect does adenosine have?

-induce mast cell degranulation
-inc production of cytokines
--> smooth muscle/broncho- constriction