Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
NU 600
Exam 3 - Neuromuscular Transmission
| 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
Popular Nursing sets