NU 600 Word Scramble
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Question | Answer |
What is the dose, onset, and duration of succinylcholine? | Dose=1-1.5mg/kg up to 150mg; Onset=30-90sec; Duration=8-15min |
Succinycholine is metabolized by what metabolic process? | hydrolysis |
Succinycholine increases pressures in what three areas of the body? | cranial, ocular, abdominal |
Succinylcholine attaches to ______ subunits. | alpha |
How much of a rise in potassium is seen with succinylcholine? | +0.5meq/L |
A depolarizing neuromuscular blockade is also referred to as a ___________. | Phase I blockade |
What is the manifestation of a Phase I Block? | Fasciculations follows by flaccid paralysis |
What medications potentiate and antagonize the action of succinylcholine? | Potentiate=anticholinesterases; Antagonize=NDMR |
What are the characteristics of a Phase I block seen on a PNS? | a)decr. contraction in response to single twitch stim b)decr. amplitude but sustained response to cont. stim c)TOF ratio >0.7 d)absence of posttetanic facilitation e)augmentation of NMB with anticholinesterase |
When will a Phase I block develop into a Phase II block? | Repeat doses of sch (>2mg/kg) or w/sch infusion |
Repeated doses of sch will lead to a Phase II block, describe this process. | Postjxn membrane does not respond normally to ach even when postjxn membrane repolarizes |
The duration of a Phase II block mimics the duration of action of a _______________. | Nondepolarizing neuromuscular blocking drug |
Alterations of what two electrolytes can augment the effects of NDNMBDs? | High Mg, Low K |
Administering an anticholinesterase drug in Phase I will ________ the blockade, while giving the same medication in Phase II will ________ the blockade. | Enhance; antagonize |
What anticholinesterase could be used to test the current level of blockade and what is the dose? | Edrophonium; 0.1-0.2mg/kg |
Define tachyphylaxis. | Sudden and abrupt decreased response to a drug |
Transition from a Phase I to Phase II block occurs at what dose of sch? | 2-4mg/kg |
vWhat type of drug can be used to antagonize a Phase II block? | anticholinesterase |
Where is plasma cholinesterase synthesized? | liver |
What are 3 causes of prolonged activity of sch? | Decreased hepatic production of plasmacholinesterase, atypical plasmacholinesterase, severe and prolonged hepatic dz |
Why does SCh have a brief duration of action? | Rapid hydrolysis in plasma (before the NMJ) |
Patients being treated with what 3 disease may be taking drugs that decrease plasma cholinesterase activity? | Glaucoma (echothiophate), myasthenia gravis (neo-, pyrido- stigmine), cancer (nitrogen mustard, cyclophosphamide) |
High levels of what hormone is associated with decreased plasmacholinesterase activity? What patient population is this effect seen in? | estrogen; parturients at term |
Give examples of two insecticides that decrease plasma cholinesterase activity? | carbamate, organophosphates |
How does Reglan influence plasma cholinesterase? | Reduces its activity |
What lab test can determine inherent activity of plasma cholinesterase? | Dibucaine test |
_____% inhibition of plasma cholinesterase activity after giving Dibucaine is considered a normal response. | 80 |
What type of drug is Dibucaine? | local anesthetic |
What does the the Dibucaine test reflect and what is the normal value? | The % of inhibited plasma cholinesterase; 80% |
What is the Dibucaine %, incidence, and duration of action of NMB for the homozygous patient with decreased plasma cholinesterase activity? | 20-40%; 1:3000; 4+ hours |
What is the Dibucaine %, incidence, and duration of action of NMB for the heterozygous patient with decreased plasma cholinesterase activity? | 60%; 1:500; up to 60min |
What are the adverse effects of SCh? | Dysrhythmias, hyperK, myalgia, myoglobinuria, incr. intragastric press., increased intraocular press., increased ICP, sustained skeletal muscle spasm |
What are 3 cardiac dysrhythmias that could be seen with SCh? | Bradycardia, junctional rhythm, sinus arrest |
MH is an inherited disorder of what body system? | skeletal muscleWhat |
What is the trigger for MH? | VAA and SCh |
What role does calcium have in MH? | Dysfunction in Ca reuptake mechanisms leads to 500 fold increase in intracellular calcium levels |
What are the effects of intracellular flooding of calcium? | sustained muscle contraction, severe hypoxia, lactic acidosis, membrane instability, rhabdomyolysis, ARF |
The clinical features of MH are all features of a ____________ state. | Hypermetabolic |
What are the clinical features of MH? | Masseter spasm, muscle rigidity, tachypnea, tachycardia, HTN, cardiac arrhythmias, myoglobinuria, increased creatinin phosphokinase |
What are the steps to initiate in the treatment of MH? | Administer Dantrolene, call for help, stop the VAA, 100% O2, manually hyperventilate, use a clean breathing system, abort surgery, cooling measures |
What is the dose for dantrolene? | 1mg/kg then 1-2.5mg/kg q10min until MH is controlled |
What is the maximum dose for MH? | 10mg/kg |
What is dantrolene's method of action? | Impairs calcium dependent muscle activity by decreasing intracellular calcium concentration |
How is dantrolene prepared? | 20mg dantrolene with 3gm mannitol mixed in 60ml water |
Who first discovered the ACh neurotransmitter? | Otto Loewi |
What are the 2 different types of receptors that ACh acts upon? | Nicotinic (ion-gated peptid) and muscarinic (G-protein coupled) |
Which subunit of the nicotinic receptor does ACh bind? | alpha subunit |
Identify the different subunits on a nicotinic receptor? | delta, beta, 2 alpha, gamma |
What are two functions of G-protein coupled receptors? | Help extracellular molecules travel to intracellular environment; signal transduction |
What are the different subunits of G-protein coupled receptors? | alpha, beta, gamma |
Skeletal muscle is innervated by the ______. | Motor neuron (motor nerve) |
Where does the motor neuron arise from? | ventral horn of spinal grey matter |
What and from what is ACh manufactured? | Manufactured in nerve terminal from acetate and choline |
Where are acetate and choline derived from? | acetate=acetyl-coA (mitochondria); choline=dietary intake and liver |
What enzyme combines acetate and choline to form ACh? | acetyl transferase |
Where is ACh stored? | Nerve terminal in quanta |
Nicotinic cholinergic receptors are located on the __________ and contained within _________. | Motor end plate; folds or gyri |
What causes ACh release from the nerve terminal of the motor neuron? | Influx of calcium into the nerve terminal, causing ACh vesicle to fuse with the nerve membrane and release ACh into the synaptic cleft |
Each vesicle of ACh contains _________ molecules of ACh. | 5,000-10,000 |
How many vesicles of ACh are released with each depolarization? | 200-400 |
SCh is broken down by _________, ACh is broken down by __________. | Plasma cholinesterase; acetylcholinesterase |
What electrolyte is required for the release of ACh? | Calcium |
Created by:
philip.truong
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