Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
121 Cards in this Set
- Front
- Back
|
What does protein binding have to do with LA?
|
the more the protein binding, the longer the duration of action.
|
|
|
What property of a drug is influenced by pKa?
|
onset of action
|
|
|
What is the Max safe dose for Lido?
|
7 mg/kg
|
|
|
What is the max safe dose for procaine (novocaine)?
|
14 mg/kg
|
|
|
The max safe dose for chloroprocaine?
|
20 mg/kg
|
|
|
What is the max safe dose for tetracaine?
|
1 mg/kg
|
|
|
What is the max safe dose for mepivicaine?
|
7 mg/kg
|
|
|
What is the max safe dose for etidocaine?
|
3 mg/kg
|
|
|
The max safe dose for bupivicaine?
|
3 mg/kg
|
|
|
The max safe dose for ropivicaine?
|
3 mg/kg
|
|
|
the max safe dose for cocaine?
|
200 mg topical
|
|
|
The following are all ester LA EXCEPT:
A. Cocaine B. tetracaine C. lidocaine D. Procaine |
C
|
|
|
The following are all amide LA EXCEPT:
A. etidocaine B. bupivicaine C. Lidocaine D. Chloroprocaine |
D
|
|
|
The efficacy of the LA are all the same. T or F?
|
True
|
|
|
Which has less potential for toxicity:
A. esters B. amides |
A
|
|
|
Although allergy to any LA is very rare, which of the 2 classes have more incidence of allergic reactions?
|
esters
|
|
|
If a pt is allergic to Lidocaine, it is OK to give them bupivicaine. T or F?
|
False-all amides are out, but can receive esters
|
|
|
Name the 3 basic parts of a LA molecule
|
1. lipophilic part
2. linkage ( ester or amide) 3. hydrophilic part |
|
|
2 Chemical classes of LA are?
|
esters
amides |
|
|
Esters are metabolized by:
A. cytochrome P 450 enzymes in the liver B. hydrolyzed by cholinesterase |
B
|
|
|
Why are esters short acting?
|
metabolized by cholinesterase, so they dont need to go to liver
|
|
|
Amides are metabolized how?
A. CYP450 enzymes in the liver B. cholinesterase in plasma |
A
|
|
|
Why do we add bicarb to LA?
|
increasing the pH of the solution increases the % of the solution taht is non-ionized, (nonionized crosses into nerve) and speeds the onset.
|
|
|
What effect does hypoxia have on LAs?
|
acidosis causes % of ionization to increase, making the drug less lipid sol. So, if your LA is already inside the CNS, it cant get out-it gets trapped inside the nerve.
|
|
|
Tissue acidosis does what to lipid solubility?
|
decreases it
|
|
|
Which of the LAs is the most cardiotoxic? Why?
|
Bupivicaine-it preferentially binds to cardiac proteins.
|
|
|
The first sign of bupivicaine overdose is what?
A. circumoral numbness B. tinnitus C. seizures D. arrest |
D
|
|
|
In situations resulting in arrest from bupivicaine toxicity:
What are 2 special considerations that differ from other LAs? |
1. more difficult to resuscitate
2. treat with intralipid solution |
|
|
Mixing 2 LAs together has what effect on toxicity levels?
|
The toxicities are additive
|
|
|
What effect does pregnancy have on LA spread and depth?
|
greater in preg. Reduce dosages
|
|
|
Which of the following are unique properties of cocaine? (Choose all that apply)
A. manufactured B. topical use only C. parasympathomimetic D. blocks reuptake of NE into sympathetic nerves |
B, D
|
|
|
what is the relationship between ropivicaine and levobupivicaine?
|
Both are isomer forms of bupivicaine. They were developed to decrease the cardiotoxic effects of bupivicaine.
|
|
|
The closer the pKa is to 7.4, the _______(more or less) lipid soluble?
|
more
|
|
|
The higher the % of protein binding, the ____________(longer or shorter) the duration of action?
|
longer
|
|
|
LAs are CNS depressants-why do they cause seizures at toxic levels?
|
disinhibition ( like stage 2 of anesthesia)
|
|
|
List the following symptoms of LA toxicity in increasing order of appearance:
seizures, circumoral numbness/tingling, coma, unconsciousness, muscle twitches, visual disturbances,CVS depression, resp arrest |
circumoral numbness/tingling
visual disturbances muscular twitches seizures unconsciouness coma resp arrest CVS depression |
|
|
Why does LA toxicity tend to be self-limiting?
|
quickly redistributes
|
|
|
BZDs raise the seizure threshhold for LAs-what does this mean?
|
It will take more LA to cause seizures
|
|
|
Name 2 ways NE is broken down in body
|
1. MAO ( in cytoplasm)
2. COMT (in synapse) |
|
|
What kind of receptor is at the ganglion in the SNS?
|
nicotinic
|
|
|
What kind of receptor is at the ganglion in the PSNS?
|
nicotinic
|
|
|
what kind of receptor is at the effector organ in the SNS?
|
adrenergic
|
|
|
What kind of receptor is at the end organ in the PSNS?
|
muscarinic
|
|
|
What is the difference between presynaptic and postsynaptic alpha 2 agonists?
|
presynaptic A2 agonists stimulate the A2 receptor, that effectively decreases NE , so it has a sympatholytic effect
|
|
|
Which of the folllowing are (presynaptic) alpha 2 agonists?
A. clonidine B. isoproteronol C. dexmetedomidine D. dobutamine |
A, C
|
|
|
Where are beta 1 receptors located int eh body?
|
the heart only
|
|
|
Where are beta 2 receptors located?
|
Any place but heart
|
|
|
Interference with the synthesis of NE will have (sympatholytic or sympathomimetic) effect
|
sympatholytic
|
|
|
Blockade of NE reuptake would have an
1. symphatholytic 2. sympathomimetic effect? |
sympathomimetic
|
|
|
Three drugs that have blockade of NE reuptake?
|
cocaine
imipramine amitriptyline |
|
|
inhibition of vesicular storage of NE has
(sympathomimetic/sympatholytic) effect? |
sympatholytic
|
|
|
How do indirect acting agents work?
|
they do not go to receptor, but they cause bodies own NE to be released from vesicles
|
|
|
2 examples of indirect acting agents we use?
|
1. ketamine
2. ephedrine |
|
|
How do direct acting agents exert their effects?
|
They go directly to receptor and elicit resposne
|
|
|
Examples of direct acting agents?
|
levophed
phenylephrine isuprel |
|
|
Which of the followng are examples of indirectly acting adrenergic agents?
A. phenylephrine B. isoproteronol C. ketamine D. ephedrine |
C, D
|
|
|
How do agents that produce receptor blockade work?
|
they block the postsynaptic receptor so NE cant attach to it
|
|
|
Which of the following are examples of adrenergic receptor blockade?
A. phentolamine B. neostigmine C. edrophonium D. propranolol |
A, D
|
|
|
Sympathetic effects in the heart include:
A. decreased SVR B. increased HR C. + inotropic activity |
B, C
|
|
|
Sympathetic effects in GI system include:
A. increased tone and motility B. contraction of sphincters C. less secretions |
B, C
(" sympathetic stim=scared shitless.....) |
|
|
True or false: vasculature is controlled mainly by the PSNS?
|
False- controlled by SNS via A1 and B2 receptors
|
|
|
If a drug blocks the enzyme tyrosine hydroxylase, how does this affect the synthesis of catecholamines?
|
It reduces the production of them
|
|
|
Which of the following enzymes are involved int eh metabolism of catecholamines?
A. tyrosine hydroxylase B. COMT C. MAO D. paraglycine |
B, C
|
|
|
Interference with synthesis of a neurotransmitter would have which effect?
A. sympatholytic B. sympathomimetic |
A
|
|
|
Name an example of a drug that illustrates mechanism 2: metabolized by same pathway as the transmitters precursor. Is this sympatholytic or sympathomimetic?
|
methyldopa; sympatholytic
|
|
|
Name an example of a drug that illustrates mechanism 3: blocks transport system at nerve terminal membrane. Is this sympatholytic or sympathomimetic?
|
Cocaine or imipramine; sympathomimetic
|
|
|
Name an example of a drug that illustrates mechanism 4: blocks transport to storage vesicle. Is this sympatholytic or sympathomimetic?
|
reserpine; sympatholytic
|
|
|
Name an example of a drug that works by mechanism 5: promotion of exocytosis. Is this sympathomimetic or sympatholytic?
|
amphetamines ephedrine, sympathomimetic
|
|
|
Name an example of a drug(s) that works by mechanism 6:
preventing the release of the transmitter. Is this sympathomimetic or sympatholytic? |
clonidine, bretylium, guanadrel; sympatholytic
|
|
|
Presynaptic alpha blockers have what effect?
|
sympatholytic
|
|
|
postynaptic alpha blockers have what effect?
|
sympathomimetic
|
|
|
Name an example of a drug that works by mechanism 7: directly acting agents. Are they sympatholytic or sympathomimetic?
|
levophed, Neo, isuprel, sympathomimetic
|
|
|
Name an example of a drug that works by mechanism 8: receptor blockade, Is this sympathomimetic or sympatholytic?
|
inderal, regitine; sympatholytic
|
|
|
Name a drug taht works by mechanism 9: inhibiting the enzyme that breaks down the transmitter. Is this sympatholytic or sympathomimetic? Or is this a trick question?
|
This is a trick question: Neostigmine and edrophonium; parasympathomimetic
|
|
|
Name an example of a drug that works by mechanism 10 ( Nags own invention):
messing with the second messenger system inside the cell (by giving PDE inhibitors). Is this sympatholytic or sympathomimetic? |
milrinone; sympathomimetic
|
|
|
alpha agonist effect on eyes?
alpha blocker effect on eyes? |
mydriasis (dilation)
miosis (constriction) |
|
|
Cholinergic agonist effect on eyes?
anticholinergic effect on eyes? |
miosis (pinpoint pupils, decreased IOP)
mydriasis and cycloplegia, ^IOP |
|
|
which class of drug is contraindicated in asthmatics? Why?
|
Beta blockers-d/t bronchcocontriction
|
|
|
Alpha agonist effect on blood vessels?
Alpha blocker effect? |
vasoconstriction
vasodilation |
|
|
Lungs: which receptors?
|
Beta2
|
|
|
heart: which receptors?
|
Beta 1
|
|
|
uterus: which receptor?
|
beta 2
|
|
|
"glands": sweat, salivary
which receptor? |
Alpha 1
|
|
|
Alpha agonist effect on heart?
|
reflex bradycardia ( Neo)
|
|
|
Alpha blocker effect on heart?
|
reflex tachycardia
|
|
|
anticholinergic effect on heart?
cholinergic agonist effect on heart? |
tachycrdia ( atropine)
bradycardia |
|
|
Beta agonists have what effect on uterus?
|
relaxation (terbutaline)
|
|
|
Matching: Drug to receptor
pure alpha pure beta beta with some alpha, alpha with some beta, dopamine,beta, alpha |
pure alpha: Neo
pure beta: dobut beta with some alpha: epi alpha with some beta: levo dopa, beta, alpha: dopamine |
|
|
activation of dopaminergic receptors has what effect?
|
dilation of renal arteries
|
|
|
activation of B1 receptors by dopamine has what effect?
|
increase HR
|
|
|
activation of alpha receptors by dopamine has what effect ?
|
vasoconstriction
|
|
|
List the following receptors sensitivity to dopamine in increasing order. (which receptor is most sensitive to dopamine?)
|
1. dopamine
2. Beta 3. alpha this is why you need the highest dose for pressors, but lower dose for renal effects. |
|
|
Ephedrine is:
A. centrally acting B. Peripherally acting C. directly acting D. indirectly acting |
all are correct
|
|
|
Why is the fact that ephedrine centrl, peripherl, direct and indirect important?
|
you get 4 mechanisms with one drug
|
|
|
You have a pt with HR of 58. that you have just placed a spinal. Their BP falls to 60/40. which drug will you give: ephedrine or neo? Why?
|
ephedrine-no reflex bradycardia
|
|
|
Which part of the LA blocks the nerve: ionized or nonionized?
|
ionized blocks the nerve, nonionized gets it into the nerve-Thanks Jason!
|
|
|
What property of a drug is influenced by pKa?
|
onset
|
|
|
2 biggest reasons to add epi to LA?
|
1. less toxicity with epi because it absorbed more slowly
2. lasts longer |
|
|
Max safe dose of lido and mepivicaine are the same. What is it?
|
7 mg/kg
|
|
|
etidocaine, bupivicaine and ropivicaine are all the same safe max dose. what is it?
|
3 mg/kg
|
|
|
Why does neostigmine increase risk of PONV?
|
increases peristalsis (PSNS: rest and digest)
|
|
|
Why should you use caution when giving beta blockers to a diabetic?
|
beta blockers create hypoglycemia, but they also block one of the first signs of hypoglycemia-tachycardia
|
|
|
which class of drugs cause mydriasis and cycloplegia?
|
anticholinergics
|
|
|
which class of drugs cause mydriasis?
|
alpha agonists
|
|
|
What is the major difference between atropine and robinul?
|
Robinul is quartenary amine-cant cross BBB, so no CNS effects
|
|
|
which is better for a pregnant mom: atropine or robinul? Why?
|
robinul-can't cross placental barrier
|
|
|
Atropine or Robinul: which has sedative effect?
|
atropine: can cross BBB, so can have CNS effects
|
|
|
Which causes mydriasis and cycloplegia: atropine or robinul?
|
atropine: can cause CNS effects
|
|
|
Which is better antisialagogue: atropine or robinul?
|
robinul
|
|
|
Which demonstrates more increase in heart rate: atropine or robinul?
|
atropine
|
|
|
Which gives more smooth muscle relaxation: atropine or robinul?
|
equal
|
|
|
Which is better at preventing motion induced nausea: atropine or robinul?
|
atropine.
|
|
|
Mnemonic for atropine poisoning:
|
Red as abeet, blind as a bat, dry as a bone, mad as a hatter, hot as a hare
|
|
|
What does analeptic mean?
|
CNS stimulant effect
|
|
|
What does neuroleptic mean?
|
CNS blocking effects
|
|
|
Which of the following are effects of beta 1 stimulation?
A. decreased HR B. increased contractility C. increased automaticity D. increased HR |
B, C, D
|
|
|
Which of the following effects are seen with alpha 2 (postsynaptic) receptor stimulation?
A. hyperpolarization of CNS cells B. platelet aggregation C. increased automaticity D. Increased contractility |
A, B
|
|
|
Stimulation of Alpha 1 receptors gives which of the following?
A. vasoconstriction B. mydriasis C. relaxation of bladder sphincter D. relaxation of GI sphincters |
A, B. Actually causes contraction of both sets of sphinters
|
|
|
Stimulation of beta 2 receptors causes which of the following?
A. bronchoconstriction B. uterine relaxation C. lipolysis D. gluconeogenesis E. stress in SRNAs |
B, C, D. causes broncodilation too
|
|
|
stimulation of presynaptic alpha 2 receptors causes what?
|
inhibition of NE release
|
|
|
Someone at a bar slips something into your drink. You exhibit the following symptoms: HA, dizziness, nervousness, sweating, constipation, ^BP, ^ HR, ^ contratility. What kind of drug did they give you?
|
B1 agonist. Dumbass shouldn't have left your drink!
|
