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Pharm Stack 1
Pharm lecture 1
| Question | Answer |
|---|---|
| what are autocoids | chemicals that act very locally but have wide effects |
| what amino acid is histamine synthesized from | histidine |
| what cells are histamine chiefly stored in with low turnover | mast cells and basophils in bronchial and intestinal mucosa |
| what cells are histamine chiefly stored in with high turnover | non-mast cells in gastric mucosa and CNS |
| what is anaphylaxis | sudden, severe, potentially fatal, systemic allergic rxn that can involve various areas of the body and commonly caused by food, insect stings, medicines and latex |
| what triggers the release of histamine | antigens (inhalants, food, drugs), anaphylatoxins from complement activation, cholinergic agents (Ach), non immunologic H releasers, physical stimuli (heat, cold, vibrations), prostaglandins and Beta Adrenergic agents (EPI, ISO), |
| when histamine receptors are activated what occurs intracellularly | levels of ATP and GTP increase cAMP levels and trigger exocytosis and degranulation of Histamine |
| what type of receptor is H1 coupled to | Gq protein |
| what type of receptor is H2 coupled to | Gs protein |
| what type of receptor is H3 coupled to | Gi protein |
| what type of receptor is H4 coupled to | Gi protein |
| H1 receptors populate which type of cells | blood vessels, smooth muscle, heart, CNS |
| H2 receptors populate which type of cells | Gastric mucosa, heart, uterus, CNS |
| what effect do H1 receptors induce upon activation | increased: vascular permeability, airway SMC, VD and flushing, mucos secretion, pruritis, NT in CNS |
| what effect do H2 receptors induce upon activation | increased: gastric acid secretion, nasal airways resistance, respiratory mucus secretion, SM- relaxation in lower airways |
| where are H3 receptors located and what effect do they induce upon activation | airways, GI tract and CNS mainly and induce decreased histamine synthesis and release form nerve cells and decreased NT release |
| where are H4 receptors located and what effect do they induce upon activation | bone marrow, peripheral blood leukocytes, spleen, thymus, colon and effect is unknown |
| increased permeability of post capillary venules by H1 activation produce what | contraction of endothelial cells |
| dilation of small blood vessels is caused by | contraction, leading to an increase in permeability |
| which histamine receptor has a higher affinity, more rapid onset and decline | H1 receptors |
| which histamine receptor has a more slower onset and sustained effect when effecting the CVS | H2 receptors |
| what effects does histamine have in the CVS | adhesion molecules and leukocyte recruitment, edema |
| what effect does histamine have on neural system | sensory nerve ending stimulant via H1 mediating paina nd itch |
| what effects does histamine have on inflammation after an intradermal injection | triple response (red spot, wheal, and flare) which can be induced after am intradermal injection |
| what can stimulate a parietal cell | ACh (muscarinic type receptor), Gastrin and Histamine (H2 receptor, released from ECL cells) |
| what do parietal cells secrete | HCl acid |
| in the gut, histamine is released from which cells | enterochromaffin like cells (ECL) |
| excessive HCl can lead to | gastritis, gastric ulcers, peptic acid disease |
| what is histamines role in the immune response | histamine is loaded in granules in IgE sensitized mast cells and upon Antigen binding, the the intracellular [Ca++] increases and causes exocytosis of granules as well as other factors like cytokines and prostaglandins to illicit an immune response |
| first generation antihistamines- general duration of action | from 6- 12 hours duration of action, therefore must be taken several times a day |
| second generation antihistamines- general duration of action | 12- 24 hours duration of action, therefore can be taken only once or twice a day |
| first generation antihistamines- sedative effects | medium to high sedative effects, cant drive! |
| second generation antihistamines- sedative effects | very low to low sedative effects, can drive! |
| intranasal antihistamines- duration of action and sedative effects | 12 hoursduration of action, low sedative effects |
| antihistamines get metabolized by what | hepatic metabolism by p450 |
| what is the selectivity ad mechanism of action of 1st generation drugs | select for H1 receptors and work via a competitive, reversible antagonism |
| H1 antihistamines have what effect | incomplete block of H1 induced VD of respiratory and GI smooth muscle, triple response blocked |
| what are some H1 antagonists adverse effects on CNS | depressive: sedation and impaired ability |
| what are some H1 antagonists adverse effects on behavior | confusion, apathy |
| what are some H1 antagonists adverse effects on stimulatory systems and GI | muscle spams, appetite stimulation, GI discomfort |
| what are some H1 antagonists adverse effects on Ach activities | Histamine receptors are very similar to Ach Muscarinic receptors so these too will be blocked and anticholinergic effects like dry mouth and urinary retention occur |
| what are some serious side effects of antihistamines | cardiotoxicity because of QT prolongation which may precipitate ventricular tachycardias |
| what is given upon first generation antihistamine overdose | because anticholinergic activity is the main effect, we give physostigmine, an ach-esterase inhibitor to counteract the OD (will cross BBB) |
| at high doses of antihistamines what effects are seen | CNS (seizures, hallucinations, psychosis) are the adverse effects |
| what are some uses of H1 antagonists | allergies, especially immediate or early phase rxns such as urticaria and rhinitis (would be less useful in late phase rxns like asthma and anaphylaxis) b/c H1 is fast acting, motion sickness, emesis reduction |
| what is the mechanism of helicobacer pylori infection | infects the lower stomach (antrum) and causes inflammation of the gastric mucosa until an ulcer is created causing bleeding into stomach, the body tries to kill bacteria by increasing acid levels which makes cycle worse |
| what disease does helicobacer pylori infection cause | peptic ulcer disease |
| what are the drugs used to tx peptic ulcer disease | antacids, PPIs, H2 antagonists and antibiotics + bismuth are used to tx this disease |
| what is the mechanism of H2 anatagonists | inhibit acid secretion production by reversibly competing with histamine for binding to H2 receptors on the basolateral membrane of parietal cells, no significant effect on GI motility |
| what are the adverse effects of H2 anatagonists | generally well tolerated except cimetidine which has a weak anti-androgenic activity in elderly causing gynecomastia, also inhibits p450 and can therefore have drug-drug interactions |
| what is Zollinger- Ellison Syndrome | this causes one or more tumors in the duodenum or in the pancreas known as gastrinomas which secrete the hormone gastrin in large amounts. this hormones leads to extreme production of acid in the stomach causing peptic ulcers |
| what is the drug of choice for treating Zollinger- Ellison Syndrome | PPIs are the drug of choice for this disease |
Created by:
ama2114
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