Pharm Exam 4: Histamines, Vasodilators, Asthma Meds

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choward04
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Pharm Exam 4: Histamines, Vasodilators, Asthma Meds
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2013-03-14 18:27:11
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  1. Cell-to-cell communication occurs via what compounds?
    Peptides
  2. Name 3 examples of Kinins (vasodilator).
    • 1. Bradykinins
    • 2. Natriuretic peptides
    • 3. Vasoactive
  3. Name 4 examples of Intestinal Peptides (Vasodilators).
    • 1. Substance P
    • 2. Neurotensin
    • 3. Calcitonin gene related peptide
    • 4. Adrenomedullin
  4. Name 5 vasoconstricting peptides.
    • 1. Angio II
    • 2. Vasopressin
    • 3. Endothelins
    • 4. Neuropeptides Y
    • 5. Urotensin
  5. T or F.  The activation of renin is usually caused by vasoconstriction of the blood vessels.
    FALSE (renin is stimulated by vasodilation and then causes vasoconstriction)
  6. What is an example of renin release inhibitor?
    Angio II (negative feedback cycle)
  7. What are 4 stimulators of renin?
    • 1. Decrease Na+ delivery
    • 2. Decrease renal arteriole pressure
    • 3. Sympathetic Nerve stimulation (B1)
    • 4. cAMP
  8. Where is vasopressin produced?
    Vasopressin--> produced in hypothalamus & supraoptic nucleus
  9. What stimulates vasopressin production?
    Reductions in plasma volume
  10. What is the main result of vasopressin simulation?
    -Increase WATER reabsorption
  11. T or F.  Vasopressin is an arterial vasoconstrictor in times of physiologic stress, like shock.
    True (improves BP)
  12. What are the 3 types of functions of vasopressin?
    • 1. V1a--> mediates vasoconstriction
    • 2. V1b--> potentiates release of adrenocorticotropic hormones
    • 3. V2 --> mediate ADH hormones
  13. Vasopressin is a V1 & V2 agonist or antagonist?
    Vasopressin is a V1/V2 agonist
  14. What are 3 examples of synthetic vasopressin and the name of a brand drug?
    • -Terlipressin, relcovaptan, Conivaptan
    • -BRAND- Pitressin
  15. What are 2 adverse effects of vasopressin?
    • 1. Severe vasoconstriction
    • 2. Water intoxication
  16. What are the 3 forms of endothelin and where do they come from?
    • ET-1--> MAIN ONE, vascular endothelium
    • ET-2--> kidneys & intestine
    • ET-3--> brain, GI, kidneys
  17. Are ET-1 dose-dependent or time-dependent?
    ET-1--> dose dependent
  18. What are some physiologic action T-1? (5)
    • 1. rapid ⇓ in BP (nitric oxide) followed by prolonged ⇑
    • 2. ⇑ BP as result of vascular smooth muscle contraction
    • 3. Positive inotropic/chronotropic actions on the heart
    • 4. Renal vasoconstriction (⇓ GFR,⇓ excretion)
    • 5. Proliferation of vasc. smooth m, cardiac cells, glomerular cells
  19. Where are ETa receptors located?
    smooth muscle cells (affinity for ET1&3)
  20. Where is ETb receptors located?
    Vascular endothelial cells (affinity for ET1&3)
  21. What is an example of a nonselective endothelin receptor blocker and what is it's physiological result?
    Bosentan--> causes vasodilation & decrease arterial pressure
  22. Kinins are a vasoconstrictor or vasodilator?
    Vasodilator
  23. What are 2 significant roles of kinins?
    In inflammation & pain
  24. What is the MOA of kinins?
    -Vasodilation of vasculature in heart, skeletal muscle, & liver
  25. What is the respiratory effect of kinins?
    Bronchoconstriction--> contraction of smooth muscles
  26. What is bradykinin found in the body?
    Plasma
  27. Describe the 2 active roles of bradykinin?
    • -Symptoms of inflammation
    • - Eliciting pain in nociceptive afferents of skin & viscera
  28. What HTN medication can also stop circulation of bradykinin?
    ACE-Inhibitor
  29. What does natriuretic mean?
    Excretion of sodium into the urine
  30. What stimulates ANP production?
    • Stretch of the aorta
    • --> like in CHF, renal failure, SIADH
  31. What is the major effect of ANP?
    Vasodilation and decrease arterial blood flow
  32. Where are BNP mainly synthesized?
    HEART (released in response to atrial blood volumes)
  33. What is an adverse effect of BNP?
    fatal renal failure (avoid BNP synthetics in patients with comorbidities_
  34. Where are C-type peptides mainly located?
    CNS
  35. Which of the natriuretic peptides is a potent vasodilator?
    C-type natriuretic peptide
  36. T or F.  Histatmines are inflammation modulators
    True (stored as basophils/mast cells)
  37. Quick review of the immunologic release.
    • -IgE binds w/ mast cell on membrane
    • -Cell degranulates--> release histamines
    • -Cause immediate Type I rxn
    • -Negative feedback loop mediated by H2 receptor
  38. What are 5 effects of H1 stimulation?
    • 1. Increased venular permeability
    • 2. Increased bronchial/intestinal smooth m contraction
    • 3. Increase nasal mucous production
    • 4. Widened pulse pressure
    • 5. Increased HR/CO
  39. What are 3 responses to H2 stimulation? (GI)
    • 1. Increased venular permeability
    • 2. Increased gastric acid secretion & airway mucous
    • 3. Inhibition of neutrophil/eosinophil influx
  40. What are the 2 effects of histamine of the nervous system (H1 receptor)
    • 1. Pain
    • 2. Pruritis
  41. What are the 4 effects of histamine of the Cardio system
    • 1. Decreased BP (vasodilation of arterioles
    • 2. Reflex tachy
    • 3. Flushing, H/A (vasodilation)
    • 4. Edema--> leading to urticaria
  42. What is the bronchial smooth muscle effect of histamine?
    Bronchoconstriction
  43. What is the GI effect of histamine?
    contraction of intestinal smooth muscle
  44. Which H receptor plays the major role in stimulating gastric acid secretion?
    H2 receptor
  45. What is the "triple response" of histamines?
    • 1. erythema at site
    • 2. Edema
    • 3. Pruritis
    • (4. flare)
    • ***Primarily H2 effects
  46. Which anti-histamine generation has anti-cholinergic side effects?
    First generation (very sedating too)
  47. Which histamine generation is used most for allergic rhinitis?
    2nd generation
  48. Which Anti-histamine generation are mostly metabolized by CYP3A4 therefore having more drug interactions?
    2nd generation
  49. T or F.  2nd generation have little or no sedation effects
    True
  50. Which anti-H1 generation is useful in preventing nausea, motion sickness.
    1st generation
  51. What are 6 pharmacodynamics of anti-histamines (mostly 1st).
    • 1. Sedation
    • 2. Anti-nausea/anti-emetic
    • 3. Anti-parkinson effects (treat dystonia)
    • 4. anticholinergic actions (dry secretions, blurred vision, constipation)
    • 5. alpha blocking actions (orthostatic hypotension)
    • 6. Local anesthesia
  52. What are 3 side effects of Anti-H 1st generation.
    • 1. CNS depression
    • 2. Urinary retention
    • 3. Difficulty urinating
  53. What body functions does serotonin have an impact (4)?
    • 1. mood
    • 2. sleep
    • 3. appetite
    • 4. temperature regulation
  54. T or F.  The effects of serotonin are similar to Histamines.
    True (stimulant of pain/itch & role in symptoms from insect/plant stings)
  55. T or F.  Serotonin can can tachycardia and hypertension.
    True (activates chemoreceptor reflex)
  56. What the effects of serotonin on the respiratory system?
    • -Bronchoconstriction (with cancer patients)
    • -Hyperventilation during chemoreceptor reflex
  57. What are some effects of serotonin on the cardio system?
    • -Contraction of vascular smooth m
    • -Constricts veins
    • -causes platelet aggregation
  58. What are the effects of serotonin on the GI tract?
    • -promotes peristalsis
    • -Cisapride--> enhances motility at 5-HT4 receptors
  59. What are the 2 serotonin receptors in the brain that are responsible for migraines?
    • - 5HT1D
    • -THT1B

    **activation causes vasoconstriction and pain diminishes
  60. Which drugs are 5HT1D/1B agonists?
    Triptans
  61. What is the peak concentration time and half life of Triptans?
    peak in 15min, half-life 2-4hrs
  62. What are some adverse effects of Triptans (4)?
    • 1. altered sensation (warm/tingly)
    • 2. muscle weakness
    • 3. dizziness,
    • 4. coronary vasospasm
  63. What patients should NOT receive Imitrex (triptan)?
    -Patients w/ known CAD, uncontrolled HTN, or PVD because can cause coronary vasospasm
  64. What are 3 adverse reactions of Sumatriptan (imitrex)?
    • 1. Dizziness/hot sensation
    • 2. burning, heaviness, flushing
    • 3. N/V
  65. What type of meds should not be taken concurrently with a sumatriptan?
    SSRIs--> can cause serotonin syndrome
  66. What are common symptoms associated with asthma?
    • History--> wheezing (esp at night), chest tightness, difficulty breathing
    • **symptoms at night are key
  67. When mast cells degranulate, what mediators are released?
    • 1. Histamine
    • 2. Tryptase
    • 3. Leukotrienes
  68. What PFT level is usually diagnostic for asthma?
    FEV1 <80% based on age/height
  69. What are the 5 pathways that drugs work on to treat asthma?
    • 1.  Reduce amt of IgE bound to mast cells
    • 2. Prevent mast cell degranulation
    • 3. block actions of mediators (histamine/leukotrienes)
    • 4. Inhibit effects of Ach
    • 5. Directly relax smooth muscle
  70. What 2 drugs are acute relief meds for asthmas?
    • 1. short acting beta agonists
    • 2. short acting corticosteriods (usually PO)
  71. What 3 drugs help "control" asthma?
    • 1. Long acting corticosteroids (ICS)
    • 2. Long acting beta agonist (LABA)
    • 3. Leukotriene pathway inhibitors
  72. Where are alpha 1 receptors primarily found?
    • Smooth muscles of arterioles, eye, gut, skin, veins
    • **so stim usually cause contraction of smooth muscle cells
  73. What are 3 effects of stimulation of Beta2?
    • 1. Decrease GI motility
    • 2. Bronchodilation
    • 3. Vasodilation in skeletal/cardiac muscles
  74. Sympathomimetics delivered by inhalation have a direct effect on:
    Pulmonary smooth muscle
  75. T or F. Epi stimulates which receptors?
    alpha 1 & beta 1
  76. Name 4 drugs that are B2 selective drugs, short acting.
    • 1. albuterol
    • 2. terbutaline
    • 3. metaproterenol
    • 4. pibuterol
  77. Which B2 selective drugs can be given PO?
    • 1. Albuterol
    • 2. terbutaline
  78. What 2 drugs are Long-acting beta agonists?
    1. Salmeterol & formoterol
  79. Why are LABAs not used as monotherapy?
    -Have no anti-inflammatory effects and can make it worse by itself because it opens airways but has no effects on increase mucous
  80. T or F. LABAs should NOT be initiated in patients with significantly worsening/acutely deteriorating asthma
    True
  81. When would Theophylline (a methylxanthine) be used for treatment?
    Resistant COPD (a phosphodiesterase inhibitor--> ⇑cAMP--> smooth muscle relax, decreaes inflammation, stimulate cardio fxn)
  82. What are 4 side effects of methylxanthines?
    • 1. Nervousness, insominia
    • 2. tachy (increased CO)
    • 3. Stimulates gastric acid and digestive enzymes
    • 4. weak diuretic
  83. What is the therapeutic level of methylxanthines? What level does cardiac arrythmias occur?
    • Therapeutic--> 5-20
    • Arrhythmias--> >40
  84. What are the effects of Anti-muscarinic agents and when are the normally used in respiratory cases?
    • 1. Inhibit Ach--> blocks contraction of airway smooth muscle and increases the secretion of mucous (not good?)
    • 2. Frequently used for COPD, occassionally for acute asthma
  85. T or F.  Anti-muscarinic agents may be used in combo with albuterol for enhancement effects.
    True
  86. What 5 things are Inhaled corticosteriods shown to improve?
    • 1. severity of symptoms
    • 2. Airway size
    • 3. Airway reactivity
    • 4. frequency of exacerbations
    • 5. Quality of life
  87. What asthma med is the "cornerstone" of long term asthma therapy?
    ICS
  88. What are 4 side effects of ICS with long-term use?
    • 1. cataracts
    • 2. osteoporosis
    • 3. thrush
    • 4. reduction in bone marrow density (flovent)
  89. What hygiene teaching should be given to patients taking ICS?
    Rinse mouth out after use--> can cause thrush
  90. T or F. ICS can take weeks to achieve maximal effect.
    True
  91. After how many days of use should oral corticosteroids be tapered off of?
    if used > 5days to avoid adrenal insufficiency
  92. What are the effects of Leukotrienes in the airway?
    • 1. Bronchoconstriction
    • 2. increases reactivity
    • 3. mucosal edema
    • 4. mucus hypersecretion
    • 5. hypersensitivity to histamine
  93. Which leukotriene inhibitor prevents SYNTHESIS of leukotrienes?
    Zileuton (Zyflo)
  94. Which leukotriene inhibitors prevent leukotriene BINDING to cell receptors?
    • 1. Zafirlukast (Accolate)
    • 2. Montelukast (SIngulair)
  95. What are the effects of Leukotriene Pathway Inhibitors (3)?
    • 1. Increase airway size
    • 2. Decrease airway reactivity
    • 3. Decrease airway inflammation

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