1What are nonlipidic autacoids?
Histamine, serotonin, and endogenous peptides.
2What are lipidic autacoids?
Prostaglandins, leukotrienes, and cytokines.
3What are histamine and serotonin (5-HT)?
Biologically active amines that function as neurotransmitters.
4What is histamine's role in allergic reactions?
It mediates immediate allergic and inflammatory reactions.
5What is histamine's role in the stomach?
It stimulates gastric acid secretion.
6What are histamine's neurological functions?
It functions as a neurotransmitter and neuromodulator.
7What is histamine's role in inflammation?
It contributes to chemotaxis of white blood cells toward inflamed tissue.
8From which amino acid is histamine formed?
Histidine.
9Which cells are responsible for histamine release?
Mast cells and eosinophils;
10What triggers histamine release from sensitized mast cells?
Antigens contacting cells associated with IgE antibodies.
11What does mast-cell degranulation require?
Calcium and energy.
12What is another source of histamine release?
Damaged tissues.
13What vascular effects does histamine cause?
Vasodilation and increased capillary leakage.
14What percentage of the population is sensitive to environmental allergies according to the lecture?
10–20%.
15Which histamine-mediated disorders are listed in the lecture?
Allergic rhinitis, anaphylaxis, angioneurotic edema, drug fevers, insect-bite reactions, and urticaria.
16What are the four histamine receptor types?
H1, H2, H3, and H4.
17Where are H1 receptors found?
Smooth muscle and endothelium.
18Where are H2 receptors found?
Gastric mucosa.
19Where are H3 receptors found according to the lecture?
Nerves in the gut responsible for peristalsis.
20Where are H4 receptors found?
White blood cells; they are associated with chemotaxis.chemotactic factor
21What is histamine's neural action?
It strongly stimulates sensory nerve endings, especially those mediating pain and itching.
22What is histamine's vascular action?
Vasodilation and a decrease in blood pressure.
23What is histamine's effect on bronchioles?
Bronchoconstriction due to contraction of bronchial smooth muscle.
24Why are people with asthma especially sensitive to histamine?
Histamine can cause bronchoconstriction.
25What is histamine's effect on intestinal smooth muscle?
It causes contraction.
26What clinical use of histamine is mentioned in the lecture?
As a provocative test in pulmonary function testing.
27What is the physiological antagonist of histamine?
Epinephrine.
28What are histamine receptor antagonists also called?
Histamine blockers.
29How do H1 antagonists produce anti-allergy effects?
By antagonizing histamine at H1 receptors.
30What are the two generations of H1 antagonists?
First-generation and second-generation agents.
31Which class of first-generation H1 antagonists includes diphenhydramine?
Ethanolamines.
32Which first-generation ethanolamines are listed in the lecture?
Carbinoxamine, clemastine, diphenhydramine, and dimenhydrinate.
33Which first-generation ethylenediamines are listed?
Pyrilamine, tripelennamine, and PPA.
34Which first-generation alkylamines are listed?
Chlorpheniramine and brompheniramine.
35Which second-generation H1 antagonist is an alkylamine?
Acrivastine.
36Which second-generation H1 antagonist is a piperazine?
Cetirizine.
37Which second-generation piperidines are listed?
Astemizole, levocabastine, loratadine, terfenadine, and fexofenadine.
38Which additional receptors may first-generation H1 antagonists affect?
Muscarinic, dopamine, α1-adrenergic, and serotonergic receptors, depending on the drug.
39Which receptors does diphenhydramine also interact with?
Muscarinic receptors.
40Which receptors does promethazine also interact with?
Dopamine, muscarinic, and α1-adrenergic receptors.
41Which receptors does cyproheptadine also interact with?
Serotonergic receptors.
42What are the key characteristics of second-generation H1 antagonists?
High H1 selectivity, limited blood-brain barrier penetration, less sedation, and long half-lives.
43What is the primary indication for second-generation H1 antagonists in the lecture?
Allergic rhinitis.
44What are the three major effects of antihistamines listed in the lecture?
Antihistaminic, anticholinergic, and sedative effects.
45Are antihistamines curative for the common cold?
No. They provide palliative symptom relief.
46Which common-cold symptoms can antihistamines relieve?
Sneezing and runny nose.
47What characterizes traditional antihistamines?
They are older drugs that act peripherally and centrally and have anticholinergic effects.
48Name two traditional antihistamines and their brand names.
Diphenhydramine (Benadryl) and chlorpheniramine (Chlor-Trimeton).
49Why were nonsedating antihistamines developed?
To reduce unwanted adverse effects, especially sedation.
50How do nonsedating antihistamines act?
They act mainly peripherally to block histamine, causing fewer CNS effects.
51What is an advantage of nonsedating antihistamines?
Longer duration of action, which can improve compliance.
52Give two examples of nonsedating antihistamines.
Fexofenadine (Allegra) and loratadine (Claritin).
53Which H1 antagonists are used for allergic rhinitis?
Chlorpheniramine and loratadine.
54Which H1 antagonists are used for motion sickness?
Meclizine and chlorcyclizine.
55Which H1 antagonists are used as hypnotic agents?
Doxylamine and diphenhydramine.
56Which H1 antagonist is used for pruritus?
Hydroxyzine.
57Which H1 antagonist is listed for serum sickness?
Promethazine.
58Which H1 antagonist is listed as an antiemetic?
Promethazine.
59Which H1 antagonist is listed as an antitussive?
Diphenhydramine HCl.
60Which H1 antagonist is listed for carcinoid tumors?
Cyproheptadine.
61Which H1 antagonist is listed for allergic conjunctivitis?
Levocabastine.
62What additional effects can H1 antagonists produce?
Sedation, anxiolysis, anti-nausea and motion-sickness effects, antiparkinsonian effects, and anticholinergic effects.
63What are the listed uses of diphenhydramine?
Anti-allergy, antiparkinsonian, and sedative effects.
64What are the listed uses of hydroxyzine?
Antipruritic and anxiolytic effects.
65What are the listed uses of meclizine?
Motion sickness and vertigo.
66What are the actions of cyproheptadine described in the lecture?
H1 antagonism, prevention of serotonin production, allergy treatment, serotonin syndrome treatment, and increased appetite.
67Which drugs are listed as second-generation H1 blockers?
Fexofenadine, loratadine, and cetirizine.
68What is the purpose of H2 receptor blockers?
To reduce excess gastric acid secretion, including in peptic acid disorders.
69Which H2 blockers are listed in the lecture?
Cimetidine, famotidine, nizatidine, and ranitidine.
70Which H2 blocker is associated with CYP450 inhibition?
Cimetidine.
71Which drugs may accumulate when cimetidine inhibits CYP450?
Warfarin, phenytoin, theophylline, propranolol, diazepam, and phenobarbital.
72How is ranitidine described in the lecture's H2 blocker section?
As a weak inhibitor; the lecture also states it was withdrawn due to carcinogenic effects.
73What is histamine's effect on small blood vessels?
It causes vasodilation and increased permeability, allowing substances to leak into tissues.
74What is the antihistamine effect on small blood vessels?
It prevents vasodilation and increased permeability.
75Which secretions does histamine stimulate according to the lecture?
Salivary, gastric, lacrimal, and bronchial secretions.
76What is the antihistamine effect on these secretions?
It prevents salivary, gastric, lacrimal, and bronchial secretions.
77How do antihistamines affect allergic immune responses?
They bind histamine receptors and prevent histamine from causing a response.
78What skin effects do antihistamines produce?
They block capillary permeability, wheal-and-flare formation, and itching.
79What is the anticholinergic drying effect of antihistamines?
Reduced nasal, salivary, and lacrimal gland secretions.
80What symptoms may improve because of the anticholinergic drying effect?
Runny nose, tearing, and itchy eyes.
81What are common anticholinergic adverse effects of antihistamines?
Dry mouth, difficulty urinating, constipation, and changes in vision.
82What sedative adverse effect can antihistamines cause?
Drowsiness ranging from mild sleepiness to deep sleep.
83What should nurses assess before antihistamine treatment?
The condition or allergic reaction requiring treatment and any drug allergies.
84When are antihistamines contraindicated according to the lecture?
During acute asthma attacks and in lower respiratory diseases.
85In which conditions should antihistamines be used cautiously?
Increased intraocular pressure, cardiac or renal disease, hypertension, asthma, COPD, and pregnancy.
86Which symptoms should patients report during antihistamine treatment?
Excessive sedation, confusion, or hypotension.
87What activities should patients avoid while taking sedating antihistamines?
Driving and operating heavy machinery.
88Which substances should patients avoid combining with antihistamines?
Alcohol and other CNS depressants.
89What should patients check before combining antihistamines with other medications?
They should consult the prescriber before taking other prescription or OTC medicines.
90When are antihistamines best tolerated according to the lecture?
When taken with meals, to reduce gastrointestinal upset.
91How can patients manage dry mouth from antihistamines?
Frequent mouth care, chewing gum, or sucking sugarless hard candy.
92What should nurses monitor during antihistamine treatment?
The intended therapeutic effects.
93What enzyme converts histidine into histamine?
L-histidine decarboxylase.
94Which enzymes metabolize histamine in the lecture's diagram?
N-methyltransferase and diamine oxidase.
95What is the first product in the N-methyltransferase pathway?
N-methylhistamine.
96Which enzyme acts on N-methylhistamine in the diagram?
Monoamine oxidase.
97What products are shown in histamine's metabolism diagram?
N-methylhistamine, N-methyl imidazole acetic acid, imidazole acetic acid, and imidazole acetic acid riboside.