| Drug |
Info |
| 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 |
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