Dr. Todorov
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| What is Histamines effect on VSM? | Vasodilation and edema
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| What is Histamines effect on non-VSM? | Contraction of bronchial and other NVSM
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| What is Histamines other effects? | Itching; increase in gastric acid secretion
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| What is Serotonins effects on VSM? | Vasoconstriction in most vascular beds
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| What is Serotonins effect on NVSM? | Contraction of gatrointestional and other NVSM
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| What is Serotonins other effects? | Central nervous system neurotransmission; stimulation of platelet aggregation
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| What are the Eicosanoids? | -Leukotrienes -Prostaglandin E, F, & I-Thromboxane A2
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| What effects do Leukotrienes have on VSM? | Vasoconstrition or Vasodilation
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| What effects do Leukotrienes have on NVSM? | Contraction of bronchial and other NVSM
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| What other effects do Leukotrienes have? | Inflammatory effects; Increase in vascular permeability
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| What effets do Prostaglandin E have on VSM? | Vasodilation
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| What effects do Prostaglandin E have on NVSM? | Relaxation of bronchial muscle and contraction of uterine muscle
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| What other effects do Prostaglandin E have? | Inhibition of gastric acid secretion
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| What effects do Prostaglandin F have on VSM? | Vasoconstriction in most vascular beds
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| What effects do Prostaglandin F have on NVSM? | Contraction of bronchial and uterine muscle
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| What other effects do Prostaglandin F have? | Increase in aqueous humor outflow
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| What effects do Prostaglandin I have on VSM? | Vasodilation
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| What effects do Prostaglandin I have on NVSM? | Contraction
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| What other effects do Prostaglandin I have? | Inhibition of platelet aggregation
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| What effect do Thromboxane A2 have on VSM? | Vasoconstriction
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| What effect do Thromboxane A2 have on NVSM? | Contraction
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| Whatother effects do Thromboxane A2 have? | Stimulation of platelet aggregation
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| What effects are mediated by H1 histamine receptors? | Histamine receptor antagonist;Used in the treatment of allergic reactions
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| What effects are mediated by H2 histamine receptors? | Histamine receptor antagonist; Used to control gastric acid secretion
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| Where is serotonin released? | From mast cells, enterochromaffin cells, and platelets;Released from the neurons
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| Where are the Autocoids site of action? | The autocoids are local hormones;Therefore they have a Paracrine effects restricted to the tissues in which they are released.
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| What are the effects of the autocoids? | mediatied via specific G-protein coupled receptors (GPCR)
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| What are the side effects of the first and second generation antihistamines? | First Generation:Sedation (paradoxical excitement in childrenAnticholinergic: Dry Mouth, Blurred vision, tachycardia, urinary retentionSecond Generation:No SedationIncreased ECG QT interval: arrhythmia
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| What is a first-generation antihistamine? | Diphenhydramine (Benadryl)
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| What is a second-generation antihistamine? | Fexofenadine (Allegra)
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| Is serotonin an autocoid or neurotransmitter? | Both;serotonin is an autocoid (released from mast cells, Enterochromaffin cells, and platelets) and a neurotransmitter (released from neurons)
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| What effects do Serotonin do? | -Promotes GI motility -Component of platelet clotting process-Contraction of vascular and nonvascular smooth muscle-Maybe precusor to Migraines-Mediator of the symptoms of Carcinoid Syndrome: ( carcinoid tumor, a neoplasm of enterochromaffin cells
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| What are some serotonin agonists? | -Buspirone (Buspar)-Sumatriptan (Imitrex)-Tegaserod (Zelnorm)
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| What are some serotonin antagonists? | -Clozapin (Clozaril)-Cyproheptadine (Periactin)-Methysergide (Sansert)-Ondansetron (Zofran)
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| What is the clinical use of Buspirone (Buspar)? | Serotonin AgonistAnxiety; Depression
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| What is the clinical use of Tegaserod (Zelnorm)? | Serotonin AgonistIrritable bowel syndrome. Taken off the market b/c of heart attacks, stroke, and worsening chest pain.
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| What is the clinical use of Sumatriptan? | Serotonin AgonistMigraine Headaches
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| What is the clinical use of Clozapine (Clozaril)? | Serotonin AntagonistSchizophrenia
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| What is the clinical use of Cyproheptadine (Periactin)? | Serotonin AntagonistCarcinoid syndrome; pruritus; urticaria
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| What is the clincal use of Methysergide (Sansert)? | Serotonin AntagonistCarcinoid syndrome; migraine headaches
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| What is the clinical use of Ondansetron (Zofran)? | Serotonin AntagonistNausea and vomiting
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| Where do Eicosanoids originate from? | They are autocoids that are derived from arachidonic acid and other 20-carbon fatty acids.
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| What is formed via the 5-lipoxygenase pathway? | Leukotrienes
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| What is formed via the cyclo-oxygenase pathway? | Prostaglandins, Thromboxane, Prostacyclin(non-steroidal anti-inflammatories)
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| What substances are thromboxanes derived from? | Prostaglandins
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| What is corticosteroids mechanism of action? | Eicosanoid Synthesis Inhibitors;Block synthesis of all eicosanoids by promoting the synthesis of inhibitory proteins called Annexins or Lipocortins.They inhibit phospholipase A2 and block release of arachidonic acid
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| What are Corticosteroids effects? | Eicosanoid Synthesis Inhibitor;-Anti-Inflammatory, -Antinocieptive (reducing sensitivity to painful stimuli)-Antiallergic-Antineoplastic
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| What are Nonsteroid anti-inflammatory drugs mechanism of action? | Eicosanoid Synthesis Inhibitor;Block both prostaglandin and thromboxane fornation by reversible (ibuprofen, indomethacin) or irreversible (aspirin) inhibition of COX activity.
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| What are the NSAIDs effects? | Eicosanoid Synthesis Inhibitor;-Anti-inflammatory-Antinocieptve (alleviate pain)
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| What are Leukotriene Inhibitors mechanism of action? | Inhibitors of 5-lipoxygenase-Antagonist of leukotriene receptors
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| What substances are thromboxanes derived from? | Prostaglandins
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| What is corticosteroids mechanism of action? | Eicosanoid Synthesis Inhibitors;-Block synthesis of all eicosanoids by promoting the synthesis of inhibitory proteins called Annexins or Lipocortins.They inhibit phospholipase A2 and block release of arachidonic acid
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| What are Corticosteroids effects? | Eicosanoid Synthesis Inhibitor;-Anti-Inflammatory, -Antinocieptive (reducing sensitivity to painful stimuli)-Antiallergic-Antineoplastic
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| What are Nonsteroid anti-inflammatory drugs mechanism of action? | Eicosanoid Synthesis Inhibitor;-Block both prostaglandin and thromboxane fornation by reversible (ibuprofen, indomethacin) or irreversible (aspirin) inhibition of COX activity.
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| What are the NSAIDs effects? | Eicosanoid Synthesis Inhibitor;-Anti-inflammatory-Antinocieptve (alleviate pain)
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| What are Leukotriene Inhibitors mechanism of action? | Eicosanoid Synthesis Inhibitor;-Inhibitors of 5-lipoxygenase-Antagonist of leukotriene receptors
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| What is the Clinical use of Leukotriene Inhibitors? | Asthma management
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| What are the major effects of endotheli-1? | Endothelin-1 Antagonist;-Peptide release from vascular endothelial cells --Vasoconstrictor opposing the effects of NO-Elevated in Pulmonary Arterial Hypertension (PAH)
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| What is a Endothelin-1 Antagonist that is used for Pulmonary Arterial Hypertension (PAH) and what is a side effect of that drug? | Endothelin-1 Antagonist;-Bosentan (Tracleer)-Possible teratogenic effects
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| What does Alprostadil (caverject) do and what is it used for? | PGE1; VasoDilation;Used to treat erectile dysfunction
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| What histamine receptor is responsible for increased gastric secretions? | H2
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| What histamine receptor is responsible for inhibition of nerutransmitter release? | H3
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| What inhibits the synthesis of prostaglandins? | Aspirin
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| Where is serotonin released from? | Serotonin is an autocoid that is released from mast cells, enterochromaffin cells, and platelets. Serotonin is also a neurotransmitter that is released from neurons.
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| What is Clozapine and how is it used? | Clozapine is a serotonin antagonist and it is used as an antipsychotic.
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| What is corticosteroids mechanism of action? | Block synthesis of all eicosanoids by promoting the synthesis of inhibitory proteins called ANNEXINS and LIPOCORTINS. they inhibit phospholipase A2 activity and thus prevent the release of arachidonic acid.
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| What are Eicosanoid Synthesis Inhibitor? | Corticosteroids & NSAIDs
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| What are NSAIDs mechanism of action? | Block both prostaglandin and thromboxane formation by irreversible or reversible inhibition of COX activity
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