pharm GRM week #11 (brief)

Week 11-Chapter 35

1. What causes the excessive mucus production in a URI?
a. inflammatory response by viral invasion

2. What causes nasal congestion in URI?
a. irritation of nasal mucosa resulting in dilated small blood vessels of the nasal sinuses

3. What 4 classes of drugs are used to treat URI?
a. antihistamines, decongestants, antitussives, and expectorants

4. What do histamine-1 receptors mediate?
a. smooth muscle contraction and dilatio of capillaries

5. What do histamine-2 receptors mediate?
a. acceleration of heart rate and gastric acid secretion

6. How does excessive histamine release cause a drop in blood pressure and edema?
a. vasodilation and increased capillary permeability, moving fluids from blood vessels into tissues

7. How do antihistamines work?
a. directly compete with histamine for specific receptor sites

8. What is the other term for antihistamines?
a. histamine antagonists or blockers

9. Which specific smooth muscle are histamine-1 antagonist particularly focused on?
a. smooth muscles surrounding blood vessels and bronchioles

10. What are the primary anticholinergic effects of antihistamines?
a. secretions of lacrimal, salivary, and respiratory mucosal glands

11. How does histamine cause pruritis?
a. stimulates nerve endings

12. What are the two main cells that release histamine?
a. basophils and mast cells

13. What do antihistamines do to smooth muscle in the bronchial tree?
a. cause extravascular muscle to contrict

14. Why is it most beneficial to give antihistamines early in a histamine-mediated reaction?
a. compete with histamine to occupy the unoccupied receptors

15. What are the consequences of histamine binding?
a. prevent consequences like vasodilation, increased secretions, and edema

16. What is the chief adverse effect of antihistamines?
a. drowsiness

17. How do the non-sedating antihistamines avoid causing drowsiness?
a. work peripherally without affecting the CNS

18. What is another name for non-sedating antihistamines?
a. peripherally acting antihistamines

19. What class of drug is loratadine (Claritin)?
a. non-sedating antihistamine

20. What class of drug is diphenhydramine?
a. antihistamine

21. Why is the use of diphenhydramine discouraged in the elderly?
a. hangover effect and increased risk of fall

22. What are the three classes of drugs used as decongestants?
a. adrenergics (sympathomimetics), anticholinergics (parasympatholytics), and corticosteroids

23. How do sympathomimetics produce decongestion?
a. constrict blood vessels to better drain nasal secretions

24. How do opioids reduce coughing?
a. suppress cough reflex

25. What are the two mechanisms of action for expectorants?
a. loosening and thinning of RT secretions and direct stimulation of secretory glands

Week 11-Chapter 36

26. Where does the oxygen-carbon dioxide exchange take place?
a. alveoli

27. What is the common feature of asthma, emphysema and chronic bronchitis?
a. obstruction of airflow through the airways

28. What is it that narrows bronchioles in asthma?
a. bronchospasm, inflammation, and edema of bronchial mucosa

29. What is the collective term for such substances as the histamines and leukotrienes?
a. inflammatory mediators

30. In asthma, what antibody sensitizes the patient to the offending allergen?
a. immunoglobulin E

31. How do bronchodilators work?
a. relax bronchial smooth muscle to dilate bronchi and bronchioles

32. What are the three classes of bronchodilators?
a. Beta-agonists, anticholinergics, and xanthine derivatives

33. How do each of the subtype beta adrenergic agonists work?
a. non-selective adrenergic drugs: stimulate alpha 1, beta 1, and beta 2 receptors
b. non-selective beta adrenergic drugs: stimulate beta 1 and beta 2 receptors
c. selective beta 2 drugs: stimulate beta 2 receptors

34. When a nonselective adrenergic agonist is given, what are the cardiovascular adverse effects?
a. increased HR, contractility, and BP

35. How are beta 2 agonists useful in treating hyperkalemia?
a. shifts potassium from blood stream to cells temporarily

36. List the adverse effects of alpha-beta agonists.
a. insomnia, restlessness, anorexia, cardiac stimulation, hyperglycemia, tremor, and vascular headache

37. How does the parasympathetic autonomic nervous system bring about bronchoconstriction? a. releases Ach which binds to bronchial trees to constrict airways

38. How do anticholinergic drugs indirectly cause airway dilation?
a. blocks Ach which causes constriction

39. What is the therapeutic range for theophylline?
a. below 20 mcg/ml

40. What do leukotrienes cause in asthmatics?
a. inflammation, bronchoconstriction, and mucus production

41. How do antileukotriene drugs work?
a. prevent leukotrienes from attaching to receptors on circulating and local immune cells

42. How are inhaled corticosteroids used?
a. control inflammatory response believed to cause bronchospastic disorders

43. How is fluticasone administered?
a. intranasally

44. Is it safe to crush a sustained-release capsule for administration?
a. no

45. What is the relationship of caffeine and beta agonist drugs?
a. increase in adverse effects like tachycardia, hypertension, headaches, nervousness, and tremors

Week 11-Chapter 40

46. Describe MTB.
a. a rod shaped bacterium thriving in highly oxygenated sites like the lungs

47. How is TB spread?
a. inhaled droplets from infected hosts to new host

48. Why is MTB more difficult to treat than most bacterial infections?
a. slow growing organism

49. Why are slow growing microorganisms difficult to kill?
a. cells are not as metabolically active compared to faster growing organisms

50. What is the most widely used antitubercular drug?
a. isoniazid (INH)

51. What it the major effect of drug therapy with antitubercular drugs?
a. reduction of cough, and therefore infectiousness