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pharm test 2 resp

Antihistamines, decongestants, antitussives, bla bla bla lilk8tob

Most common colds result from a : viral infection (rhinovirus or influenza virus)
Functions of histamine: dilation of capillaries & increased permeability -> lower BP, contraction of smooth muscles, acceleration of HR
H1 receptors mediate smooth muscle contraction & dilation of capillaries
H2 receptors mediate the acceleration of the HR and gastric acid secretion
Antihistamines: compete w/ histamine for unoccupied receptors- can't knock histamine off receptors, so it is best to take med early in histamine-mediated rxn
adverse consequences of histamine binding: vasodilation, increased cap. permeability w/ resultant edema
Antihistamines- therapeutic uses anticholinergic effects- reduce nasal, salivary, and lacrimal gland hypersecretion; in skin: reduce cap. permeablilty, and itching
nonsedating vs sedating- nonsedating work peripherally to block the actions of histamine & therefore do not have CNS effect (don't cross BBB)
Loratidine (Claritin) drug class: antihistamines
Cetirzine (Zyrtec) drug class: antihistamines
diphenhydramine (Benadryl) drug class antihistamines
Loratidine (Claritin) sedating? nonsedating, take 1x/day, for seasonal allergic rhinitis
Cetirzine (Zyrtec) sedating? nonsedating (unless at high doses), take 1x/day, for seasonal allergic rhinitis
diphenhydramine (Benadryl) sedating? is sedating, works peripherally and centrally; potent anticholinergic effects
Diphenhydramine (Benadryl) uses: hives, motion sickness, PD, sleep aid
Which group of nasal decongestants is rarely used? anti-cholinergic because you get systemic absorption- urinary retention, dry mouth..
advantage of oral nasal decongestants prolonged effects, no rebound congestion; BUT: delayed onset & effects less potent
Pro/Con topical nasal decongestants prompt onset, BUT: rebound congestion after prolonged use
inhaled intranasal steroids & anticholinergic nasal decongestants not much rebound congestion, often used prophylactically
MOA: decongestants (adrenergic) shrink engorged nasal mucous membranes by constricting the small arterioles that supply the structures of the upp. resp tract
SNS stimulation produces: increased HR, vasoconstriction, low GI/GU, bronchodilation
Decongestant SE nervousness, insomnia, palpitations, tremor
Antitussives- purpose suppress cough
Antitussives- opiates & dextromethorphan work by: suppressing the cough reflex through a direct action on the cough center (medulla)
Nonopioid antitussives work by: suppressing cough reflex by anesthetizing (numbing) the stretch receptor cells in the respiratory tract
Dextromethorphan (Vicks formula 44, Delysm) drug class: antitussives
Dextromethorphan (Vicks) info: nonopioid, nonaddicting, no CNS depression, works directly on medulla cough center
Expectorants - purpose aid in coughing up & spitting out mucus (yummy)
Guaifenesin (Robitussin, Humabid) drug class: expectorants
Guaifenesin (Robitussin, Humabid) drug facts: thins difficult to cough up mucus in the resp. tract. 1/2life=1 hour, SE: N/V, GI irritation
When on expectorants, you should: drink more fluid to loosen and liquefy secretions
H1 blockers: review prevent harmful effects of histamine & are used to treat seasonal allergic rhinitis, anaphylaxis, reaction to insect bites...
H2 blockers: review used to treat gastric acid disorders
Nonsedating antihistamines cause: dry mouth
define chronic bronchitis continuous inflammation of the bronchi
define emphysema air spaces enlarge as a result of the destruction of the alveolar walls (surface where O2 and CO2 exchange takes place is reduced)
The two classes of bronchodilators: xanthine derivatives, beta-agonists
xanthine derivatives- used for prevention of asthmatic symptoms (have slow onset of action, so not used for acute attack)
xanthine derivatives- drug effects cause bronchodilation by increasing CAMP levels
xanthine derivatives- "trophic effects" positive inotrope and positive chronotrope - increases blood flow to the kidneys -> diuretic effect
SE of xanthines N/V, GE reflux during sleep, sinus tachycardia, palpitations, dysrhythmias, increased urinatino, hyperglycemia
Therapeutic ranges of xanthines - where metabolized? 10 to 20 mcg/ml - liver
Theophylline (Theo-Dur, Slo-Bid) drug class xanthines
Theophylline (Theo-Dur, Slo-Bid) used for; treatment of chronic resp. disorders
Beta-2 adrenergic agonists- used when? during the acute phase of an asthma attack
when a beta-2 adrenergic receptor is stimulated, _______ (enzyme needed to make cAMP) is activated adenylate cyclase
Increased levels of cAMP made available by beta-2 adrenergics cause: bronchial smooth muscles to relax, which results in increased airflow
beta-2 specific drug effects: dilating effect on the peripheral vasculature- decreases BP, temporary decrease in serum K+
beta-1 receptor stimulation causes: increased HR & force of contraction
When on Beta-2 adrenergics, do not also take: MAOI's or other sympathomimetics
Albuterol (Proventil, Ventolin) drug class: beta-adrenergic; beta2 specific
Albuterol used most for: treatment of acute attacks of asthma, can also be used to prevent attacks
Albuterol side effects: Nausea, anxiety, palpitations, increased HR, tremors
Epinephrine (Adrenaline) drug class: beta-adrenergic (alpha-beta agonist)
Epinephrine's beta2 stimulating effect: bronchodilation
Epinephrine (adrenaline)'s alpha 1 effect constriction of mucous membranes = nasal decongestant
Ipratropium bromide - drug class: anticholinergics
ipratropium bromide- uses actions slow & prolonged, so not for acute asthma, but for COPD
ipratropium bromide SE: dry mouth, GI distress, headache, coughing, anxiety
What are leukotrienes (LTs) produced in response to an allergen- in asthma, cause inflammation, bronchoconstriction, and mucus production
What do antileukotriene agents do? Prevent LT's from attaching to receptors located on circulating cells & cells w/in lungs (blocks inflammation)
antileukotriene drug effects prevent smooth muscle contraction of the bronchial airways, decrease mucus
antileukotriene therapeutic uses prophylaxis & chronic treatment of asthma (not for acute attacks)
antileukotriene agents- improvement in: 1 week
antileukotriene SE: HA, nausea, dizziness, insomnia, diarrhea
antileukotriene- should monitor what? liver enzymes
Montelukast (Singulair) drug class: antileukotrienes
Corticosteroids- used for antiinflammatory effects, which lead to decreased airway obstruction
advantage of inhaled corticosteroids action is limited to the topical site of action- lungs; prevents systemic effects
Mechanism of action- corticosteroids reduce inflammation, enhance activity of beta-agonists
Corticosteroids- SE: pharyngeal irritation, coughing, dry mouth, oral fungal infections
Beclomethasone diproprionate (Beclovent, Vanceril) drug class: Corticosteroids
Beclomethasone dipropionate (Beclovent, Vanceril) drug facts: oral inhalation, long term control, topical activity
Mast cell stabilizers are used: as adjuncts to the overall management of patients w/ asthma- for prophylaxis only
Mast cell stabilizers are ____acting because indirect- prevent the release of the intracellular chem. mediators that cause bronchospasm (don't block receptors)
Do mast cell stabilizers have bronchodilator activity? Nope, so are only used prophylactically
Mast cell stabilizers are more effective in preventing asthma caused by: extrinsic factors such as allergens
Mast cell stabilizers SE: coughing, sore throat, rhinitis, bronchospasm, taste change, HA
Long or short term control: anticholinergics (ipratropium bromide) Long term
Long or short term control: antileukotriene (Montelukast- Singulair) long term
Long or short term control: corticosteroids (Beclovent) long term
Long or short term control: Mast cell stabilizers long term
Long or short term control: systemic steroids quick relief
beta2 adrenergic (Albuterol) quick relief
Created by: lilk8tob



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