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80 Cards in this Set
- Front
- Back
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What kind of drug is succinyl choline?
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depolarizing neuromuscular blocking
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What is the half life of succinylcholine?
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5-10 minutes
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How do you give succinylcholine?
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continuous infusion for prolonged paralysis, can be used to initiate paralysis
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How is succinylcholine inactivated?
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hydrolysis by pseduocholinesterase
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What happens if you have pseudocholinesterase deficiency and you take succinylcholine?
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half life is greatly prolonged, regain control of muscles slowly after a surgical procedure
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How do you regain control after succinylcholine administration?
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give non-depolarizing blockers, phase I: cholinesterase inhibitors facilitate it, phase II: cholinesterase inhibitors reverse it
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What patients should you not give neuromuscular blocking drugs?
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myasthenia gravis, carcinomatous neuropathy
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In what order are muscles affected by neuromuscular blockers?
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extraocular, hands/feet, head/neck, abdomen/limbs, muscles of ventilation
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What are some drug interactions of neuromuscular blockers?
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antibiotics (aminoglycosides) and inhaled anesthetics like isoflurane
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How do you administer glyceryl trinitrate?
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oral, sub-lingual, transdermal, topical spray, and IV
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What are the pharmacokinetics of Glyceryl trinitrate?
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high clearance with large inter- and intra-patient variability, 1/2 life in minutes
denitrated in vascular smooth muscle |
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How are nitrate esters metabolized?
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first pass in liver
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What kind of drug is Glyceryl Trinitrate?
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nitrate ester
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Which nitrate ester has the fastest onset?
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Nitroglycerin
sublingual or buccal tab or spray |
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Which nitrate ester lasts the longest in duration?
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Nitroglycerin transdermal patch
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What is Nitroglycerin's MOA?
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denitration to form NO, NO activates guanylyl cyclase, increases cGMP, cGMP activates cGMP dependent protein kinase
decreases cytosolic calcium, causes vascular smooth muscle relaxation (vasodilation) |
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Upon what does the bioavailability of a nitrate ester depend?
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bioavailability based on ability of muscle to denitrate the ester, not ability of the muscle to respond to NO
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What is the main effect of nitrate esters?
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dilation of veins
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How do nitrate esters affect the heart?
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reduces preload, left ventricular filling, left ventricular wall tension, leads to decreased cardiac work and myocardial oxygen consumption
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Why is dilation of veins the predominant effect of nitrate esters?
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preferential dentiration of drugs in veins
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How do nitrate esters affect teh lungs?
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reduces pulmonary congestion
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How does atherosclerosis change NO levels?
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reduces endogenous NO production (damaged endothelium and endothelial dysfunction)
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How are nitrates affected by damaged endothelium?
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they aren't
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How do nitrates affect stenotic areas?
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dilates them
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How do nitrates affect coronary arteries in vasospasm?
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dilates them
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How do nitrate esters affect arteries?
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dilates them only at high doses
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What are the non-vascular effects of nitrate esters?
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relaxation of esophagus, biliary tract, decreased platelet activity, decreased smooth muscle proliferation, decreased leukocyte adhesion
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What are some side effects of nitrate esters?
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headaches, hypotension with weakness and lightheadedness
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What should you not combine with nitrate esters?
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sildenafil and other inhibitors of cGMP phosphodiesterase Type V
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Why would you give nitrate esters?
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chronic stable angina, actue coronary syndromes, variant angina, CHF
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Why do nitrates help for CHF?
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relieve pulmonary vascular congestion in acute failure, provide afterload reduction in chronic management
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What limits the therapeutic utility of nitrates?
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tolerance
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How does the vascular tissue become unable to respond to nitrates?
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impaired nitrate ester biotransformation, scavenging of NO by superoxide, increased local vasoconstrictor production, decreased cGMP levels, desensitization of guanylyl cyclase
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What causes pseudotolerance to nitrates?
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increased intravascular volume, increased plasma renin, vasopressin, aldosterone
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How do you adjust for tolerance to nitrate esters?
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eccentric dosing to allow a period of no nitrate exposure, give as needed for precipitant of angina or during an episode
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What kind of drug is Nitroprusside?
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NO dependent vasodilator
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How does nitroprusside act?
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spontaneously converts to NO, no metabolism
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What does nitroprusside do to arteries?
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dilates them, decreases afterload
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What do nitrates do to veins?
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dilates them, decreases preload
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How do you administer nitroprusside?
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infusion only, must be protected from light
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What does nitroprusside decompose to?
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NO and cyanide
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What is included with Nitroprusside?
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Na thiosulfate (antidote to CN)
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What toxicity comes with prolonged infusion of nitroprusside?
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thiocyanate, especially with renal insufficiency
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What is the half life of nitroprusside?
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very short, rapidly acting and potent
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Why should you give nitroprusside?
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acute hypertensive crisis, perioperative hypertension control, heart failure
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What kind of drug is Hydralazine?
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direct-acting vasodilator
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How is hydralazine metabolized?
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acetylation, depends on patients
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For what would you use Hydralazine?
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hypertension, heart failure
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With what drugs do you use Hydralazine?
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beta blockers, diuretics, nitrates
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What are the side effects of Hydralazine?
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Na+ retention, myocaridal ischemia, increased myocardial mass (without beta blocker), sympathetic reflexes with reflexive tachycardia, drug-induced lupus
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How do you diagnose Hydralazine drug-induced lupus?
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positive ANA, anti-histone antibodies
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What is the primary NT of preganglionic neurons?
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ACh
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What is the primary sympathetic postganglionic NT?
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NE
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What is the NT to some sympathetic postganglionic sweat glands?
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ACh
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What is the NT to parasympathetic postganglionic fibers?
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ACh
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What is the neurotransmitter role of ATP?
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localized, released from psympathetic, parasympathetic, enteric, sensory neurons
acts at pre or postsyn sites |
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On what receptors does ATP act?
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purinergic
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What are P1 receptors sensitive to?
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adenosine
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What are P2 receptors sensitive to?
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ATP
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What synthesizes ACh?
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choline acetyltransferase
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What is the mechanism of ACh synthesis?
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choline acetyltransferase catalyzes the transfer of acetyl group from acetyl CoA to choline
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What blocks ACh release?
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botulinum toxin
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How is ACh inactivated?
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by acetylcholinesterase into choline and acetic acid
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What happens to the choline after hydrolysis of ACh?
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reutilized by presynaptic reuptake and resynthesized into ACh
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What does pseudocholinesterase do?
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non-specific cholinesterase
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What happens if you have an abnormality in pseudocholinesterase?
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deficiency, normal cholinergic nerve activity, but some drugs are poorly metabolized
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What happens if you give succinylcholine to a patient with pseduocholinesterase deficiency?
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could have prolonged muscle paralysis
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What is the rate limkiting step in NE synthesis?
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tyrosoine hydroxylase
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What inhibits tryrosine hydroxylase?
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catecholamines
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How is dopa production increased during sympathetic stimulation?
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more enzyme is synthesized, the enzyme has a higher affinity for tyrosine and reduced affinity for end products like NE
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What does tyrosine hydroxylase do?
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converts tyrosine to dopa
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What does converts DA to NE?
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Dopamine-Beta-hydroxylase
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How does droxidopa work?
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decarboxylated into NE by dopa decarboxylase, restoring NE
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How is NE released?
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ACh from preganglionic neuron acts on nicotinic receptor, induces depolarization of post-ganglionic neuron, calcium stimulates vessel excretion
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What locally reduces release of NE?
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binding of presynaptic alpha-2 receptors
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What locally increases NE release?
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binding of presynaptic beta-2 receptors
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What does angiotensin do to NE release?
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increases
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What does ACh binding to nicotinic receptor do to NE release?
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increases
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What NTs decrease NE release?
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dopamine, histamine, serotonin, adenosine, PGD2, GPE2, ACh via msucarinic receptor
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What is "uptake I"?
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reuptake of cathecholamines by norepinephrine transporter
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