Fichas
Ganglionic stimulant and bloackers
Fichas del conjunto (45)
- 1Nicotine and mecamylamine are stimulants and blockers, respectively, what receptors do they both act upon?Nicotinic receptors in the autonomic ganglia
- 2What do the effects of ganglionic stimulation (or blockade) depends on?the predominance of sympathetic vs parasympathetic
- 3The heart's dominant innervation at SA node is? Blockade causes?Parasympathetic (at SA node) ; tachycardia
- 4The blood vessels dominant innervation is? Blockade causes?Sympathetic; vasodilation (decrease in total peripheral resistance)
- 5The heart's dominant innervation at ventricles is? Blockade causes?Sympathetic; decrease contractility
- 6The eye's dominant innervation is? Blockade causes?Parasympathetic; Mydriasis, cycloplegia
- 7The GI tract's dominant innervation is? Blockade cause?parasympathetic; decrease tone and motility and secretion
- 8The bladder's dominant innervation is? Blockade causes?Parasympathetic; urine retention
- 9Whatis the difference between nicotine at low doses and nicotine at high doses?at low doses it is a stimulant (agonist); at high doses it is an antagonist
- 10What specific NT and receptor combo does nicotine target?Ach (NT) and nicotinic receptor
- 11At low doses, nicotine is causing depolarization but high doses what happensPersistant depolarization of membrane causes desensitation of nicotinic receptors
- 12What is a fatal dose of nicotine? Why doesn't it happen?60 mg, nicotine metabolizes quickly
- 13Nicotine acts on all subtypes of nicotine receptors including?CNS; cardiovascular and GI ganglia, and skeletal muscle
- 14What is the site of the addiction?CNS
- 15What is the initial effect of nicotine? What is it associated with?Stimulation; increased respiration
- 16Nicotine can cause vomiting by stimulating? Location?Chemoreceptor trigger zone in the medulla oblongata
- 17At higher doses, what does nicotine cause?CNS stimulation followed by depression
- 18What is the difference in cardiovascular effect at low doses of nicotine and high doses of nicotine?Low doses = increases peripheral vasoconstriction (adrenergic predominance)
High doses = decrease in BP (ganglionic blocking) - 19What is the difference in GI effects at low doses and high doses of nicotine?low doses = GI Motility
high dose = less motility - 20What is the rate of nicotine? Where is it absorbed?Fast-acting; in all routes
- 21Where is nicotine metabolized?Liver
- 22Where is nicotine excreted and as what?Kidney as cotinine
- 23What barriers can nicotine pass?Blood-brain barrier and placental barrier
- 24What are side effects of nicotine at low levels?Increased saliva, Nausea and vomiting, cramps
- 25What are the side effects of nicotine at high levels?Fainting, drop in BP, prostation (weak) collapse
- 26At low doses with stimulation GI symptoms resulting from nicotine can be controlled with?Atropine
- 27At high doses with block of neurotransmission through ganglia, what type of drug can be given?adrenergic agonist
- 28What needs to be supported with skeletal neuromuscular blockadesupport of respiration
- 29Why do patients who survive the first few hours recoverhalf-life is only 2 hours so nicotine is inactivated rapidly
- 30How do nicotine gum, patches, and inhalers wean a patient off an addiction to nicotine from smoking?gradually decrease the dosage
- 31Because nicotine therapy need to be higher enough to work what happens?side effects specifically cardiovascular like increased BP
- 32Nicotrol is inhaled nicotine for smoking cessation, what is not approved for similar therapy?Electronic cigarettes
- 33What warning do US labels of smokes have that UK disagrees with?Mixing smoking with patches may be unpredictably toxic but smoking with patches at the start has been shown to have beneficial results
- 34If a child accidentally ingests E-cig solutions, what would be used to induce vomiting?activated charcoal
- 35What is green tobacco sickness? Symptoms?Skin exposure to dissolved nicotine from wet tobacco leaves by harvesters --> N/V, weakness, dizziness, and fluctuations in BP and HR
- 36At high doses, mecamylamine was used to treat? What type of use?Severe and malignant HTN; ganglionic use
- 37Mecamylamine also has CNS uses at low doses including? Why?Tourette's syndrome & supress nicotine addiction bacuse it quiets CNS
- 38What is mecamylamine's mechanism action at ganglia?Block neurotransmission between preganglionic and postganglionic and does not affect postganglionic nerve terminals/ receptors
- 39If mecamylamine does not affect postganglia receptors, it can stillrespond to autonomic agonist like muscarinic or adrenergic receptors stimulants
- 40Which type of muscarinic receptors is affected the most by mecamylaminemuscular subtype (Mm) at skeletal muscle
- 41What are adverse reactions in BP, mouth, GI, GU, eye and CNSPostural hypotension, Dry mouth, decreased GI motility, mydriasis and sedation
- 42If a patient does into neurogenic shock due to mecamylamine blockade what is given as an antidoteNE
- 43Can mecamylamine be taken orallyyes good GI absorption
- 44Can mecamylamine cross blood-brain & placental barrieryes
- 45Hoe is mecamylamine excreted? Duration?renal excretion; 10 hours
Información
- Descripción
- El usuario ha eliminado su información de asignaturas Fichas sobre Ganglionic stimulant and bloackers, creado por Usuario eliminado el 22/10/2017.
- Creado por
- Usuario eliminado
- Visitas
- 22
- Historial
-
- Creado por Jen Orellana · 22 oct 2017
- Copiado por Jen Orellana · 22 oct 2017
- Valoración