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250 Cards in this Set
- Front
- Back
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What are the 2 different kinds of local anesthetics? What are the 4 distinguishing factors.
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AMINOESTERS AND AMINOAMIDES
1. Differences in Metabolism 2. Difference in Duration 3. Allergy Potentials (MAD) |
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How are esters metabolized?
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Esters: metabolism is catalyzed by plasma and tissue CHOLINESTERASE via HYDROLYSIS- occurs RAPIDLY throughout the body.
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How are amides metabolized?
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In the LIVER by CYP1A2 & CYP3A4 (cytochrome enzymes), therefore a significant blood level may develop with rapid absorption.
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Which are shorter acting, amides or esters?
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ESTERS
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Which are longer acting, esters or amides; explain?
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AMIDES. Before they havve to be absorbed from the site of injection, taken into the bloodstream and then taken to the liver to be metabolized.
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Most likely to cause an allergic reaction: ESTERS OR AMIDES?
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ESTERS
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List the different ester local anesthetics and give their brand name along with the generic names.
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1. Cocaine (no brand name)
2. Benzocaine (no brand name) 3.Chloroprocaine (Nesacaine) 4. Procaine (Novocaine) 5. Tetracaine (Pontocaine) CBC PT |
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List the different AMIDE local anesthetics
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PR BALM
1. Prilocaine: (Citanest) 2. Ropivacaine (Naropin- think, a NARROw ROPe) 3. Bupivacaine (Sensorcaine, Marcaine) 4. Articaine (Septocaine)think doing ART in SEPTember) 5. Lidocaine (Xylocaine) 6. Mepivacaine (Carbocaine) |
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Explain allergies between esters and amides.
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Allergies to amides are extremely rare. There is NO CROSS ALLERGY among the amide class OR BTW AMIDE and ESTER agents.
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If allergic to procaine what can you use or not use.
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You can NOT use any of the other ESTER agents but you can use any of the AMIDES.
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If allergic to Lidocaine can you use any of the other amides; can you use esters?
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Yes, if allergic to Lidocaine, you can substitute any of the other AMIDE local anesthetics or use the ESTERS.
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What are the main components of the general structure of a local anesthetic molecule?
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1. An intermediate Chain (ester or amide linkage)
2. Hydrophilic End (quaternary amine) 3. Lipophilic End (Lipid soluble Portion- Benzene ring). |
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Which are more lipophilic and protein bound, esters or amides?
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AMIDES; thats why they are longer acting also.
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The longest acting ester is ...
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CHLOROPROCAINE
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The anesthetic block onset in Type A (beta, gamma and delta) fibers is---------------- and they are all lightly/heavily myelinated?
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The anesthetic block onset is Intermediate and they are all heavily myelinated.
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What nerve fiber is responsible for PREGANGLIONIC AUTONOMIC VASOMOTOR? Describe it's myelination and onset of anesthetic block.
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TYPE B NERVE FIBERS have PREGANGLIONIC AUTONOMIC VASOMOTOR FXN- they are lightly myelinated and have an early onset
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Which TYPE of nerve fibers have an early onset? what are they and what are their fxn?
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Type C fibers have an EARLY onset. They are the SYMPATHETIC (Postganglionic Vasomotor) and Dorsal Root fibers (pain, warm & cold temp, touch)
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What's the function of Type A alpha nerve fiber? onset is early, intermediate or last?
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Proprioception and Motor
Onset is LAST and it is HEAVILY MYELINATED. |
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What is the function of Type A Beta nerve fiber?
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TOUCH AND PRESSURE
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What is the fxn of TYPE A GAMMA nerve fiber?
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Muscle tone
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What is the fxn of TYPE A DELTA fiber type?
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Pain, cold temperature and touch.
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Which 3 AMIDE local anesthetics are CHIRAL Drugs and why?
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BMR
Bupivacaine; Mepivacaine and Ropivacaine: b.c they possess an asymmetric carbon atom. |
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What is the significance of the hydrophilic portion of the local anesthetics?
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It is the portion that is either going to be ionized or non-ionized.
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Explain the process of the local anesthetic's access to the sodium channels (essentially, how they work)
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When the anesthetic is injected, it reaches an equilibrium in the epineurium. The NON-IONIZED portion enters the nerve. Once inside the AXOPLASM, the drug reequilibrates and the IONIZED fraction attaches to the local anesthetic receptor on the inside of the sodium channel- and causes a block.
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Why is epinephrine added to local anesthetics...explain also, the OFFSET of the LOCALs.
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Goal of LOCAL: ACT at site of injection. When the body transports the local from that site, OFFSET occurs.
EPINEPHRINE is added to ensure MINIMAL BLOOD LOSS AND MINIMAL DRUG DISTRIBUTION through VASOCONSTRICTION of the vessels in that area. |
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Are local anesthetics ACIDIC OR BASIC DRUGS?
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BASIC DRUGS
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How does pka factor into the function/onset of local anesthetics?
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The HIGHER the pKa, the slower the onset. The LOWER the pKa (or closer to physiologic pH) the faster the onset. B/c, the closer to 7.4 the more NON-ONIZED = BETTER NERVE PENETRATION and FASTER ONSET. Remember, when pKa is closer to pH there is a 50/50 chance of non-ionized/ionized and more drug is available in the nonionized form (what you want)
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Explain relationship btw pH and pKa in Bases
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pH >pKa ; NON-IONIZED
pH = pKa; 1/2 Non & 1/2 ION pH <pKa; Ionized primarily |
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How does protein binding affect the drug's duration of action.
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The higher the drug's protein binding, the higher the drug's receptor affinity and therefore, the LONGER THE DURATION OF ACTION.
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Which local anesthetic is the fastest acting one?
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CHLOROPROCAINE
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Which LA is an analog to BUPIVACAINE?
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ROPIVACAINE
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A 1/100,000 conc of epi yields how much epi per ml.
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10mcg/ml or 0.01mg/ml
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A 1:1000ml of epi yields------ epi per ml.
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1mg of epi or 1000mcg of epi /ml
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1/200,000 of epi--------? of epi per ml
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0.005mg or 5mcg/ml
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1/10,000 conc of epi yields---- ? of epi per ml?
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100 mcg or 0.1mg of epi/ml
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What is the max epi that can be administered?
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No stronger than a 1:100,000 STRENGTH (10mcg/ml)
no more than 10mls in a 10 min period (0.1mg or 100mcg) and no more than 30mls in 1 hour or 0.3mg (300mcg) |
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On which LA agents does the addition of epinephrine have the maximum effect?
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The SHORTER-DURATION AGENTS (epi will SIGNIFICANTLY extend the duration of these agents b/c the longer the LA inherently acts, the less change/influence epi will have on it's duration b/c epi will wear off b-4 the LA does. However, with the SHORTER ACTING LA, adding EPINEPHRINE will INCREASE the duration of action.
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What conc of epi provides optimal degree of vasoconstriction when used with liedocaine for epidural or intercostal blockage?
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1:200,000 concentration.
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The addition of epinephrine with the LA decreases/increases all aspects of clinical properties except what?
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Addition of epinephrine INCREASES degree of motor or sensory blockade, duration and area of blockade. DECREASES ONSET TIME AND PEAK PLASMA CONCENTRATION (except in SPINAL anesthesia b/c adding will increase onset time in spinal anesthsia.). Think of onset as the absorption of the LA, therefore, if not being absorbed quickly b/c of vasoconstriction, then 'Onset" is decreased.
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Explain how epi decreases PEAK PLASMA CONC of LA....what does it mean.
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PPC means the liklihood of producing TOXICITY. Toxicity is secondary to high absorption of the LA; therefore, adding epinephrine which causes vasoconstriction will decrease absorption systemically and thus DECREASE the likelihoodof toxic levels of the LA.
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the most TOXIC LA is?
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TETRACAINE
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MOST CARDIOTOXIC LA is
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BUPIVACAINE
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How many mg/ml is LIDOCAINE?
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10mg/ml
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1/2 or 0.5%lidocaine is how many mg/ml
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5mg/ml
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What is the max dose of Procaine
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14mg/kg
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Max dose for chloroprocaine
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14mg/kg
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Max dose for TETRACAINE
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1mg/ml
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Max dose for Cocaine?
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3 (topical); 200mg total max
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Max dose for Lidocaine? 1 & 2 % ?
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7mg/ml for both
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Mepivacaine's max dose is
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7mg/kg
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Prilocaine's max dose is
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8.5 mg/kg
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Bupivacaine's max dose is?
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3.2 mg/kg
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Ropivacaine's max dose is?
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3.5mg/kg
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Rosenbery et al contend that doses of local anesthetics should be -------specific and ----------specific.
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BLOCK SPECIFIC
SITE SPECIFIC (spinal , epidural, cont.epi infusion) |
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What are the clinical manifestations of LAST (local anes systemin toxicity)
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Cardiac Arrest; Respiratory Arrest, Seizures, Acidosis.
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How do LA affect fetal circulation?
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Fetal pH is lower than the maternal pH (7.2- more acidotic than mom). This may result in high fetal levels of local anesthetics
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Explain the physiology of LA injected into infected wounds?
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LA are BASIC; wounds are ACIDOTIC. LA are INEFFECTIVE in infected wounds b/c the lipid solubility of local anesthetics is diminished in an acidotic environment d/t an increased concentration of the ionized, water soluble form of the drug. This prevents the loss of absorption into the nerve and thereby prevents access to the site of action. (remember- BASES IN ACIDS IONIZE)
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How does CARBONATION affect the LAs.
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Carbonation speeds the onset and intensity of action of neural blockade b/c CO2 lowers the pH within the nerve, ionizes the lipid form of the LA = increases concentration = more ionize drug to act on sodium channels. (pg 71)
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Sodium bicarb addition to LA does what?
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Increases the pH = increases conc of non-ionized form = increased lipid solubility = more rapid onset of action. (pf 71)
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Explain how ion-trapping is implicated in the complications of LA toxicity.
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LA drug overdose = pt ACIDOTIC 2ary to hypoxia and resp depression = BASIC DRUG IN ACIDIC ENVIRON equals IONIZED- therefore drug's not able to cross BBB = ENHANCED CNS TOXICITY. (pg 71)
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What are the correlates of the ff LA characteristics?
Lipid solubility Chemical Linkage Protein Binding Dissociation Constant |
Lipid Solubility =POTENCY Chemical Linkage= METABOLISM
Protein Binding: DURATION Dissociation Constant: TIME OF ONSET. |
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What are the clinical manifestations of LAST and at what concentration of LIDOCAINE do see these onset? What dose is considered therapeutic?
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Therapeutic doses are <5ug/ml (light headed, tinnitus, mouth and tongue numbness);
Toxic dose = >5ug/ml ( visual disturbance, vasciculations, Seizures, unconciousness, coma, respiratory arrest and CVS depression ie cardiac arrest. |
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The alpha phase of lidocaine is approx how long....and what does it entail?
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10 min (distribution half life); entails RAPID RATE OF DISAPPEARANCE r/t DISTRIBUTION to RAPIDLY EQUILIBRATING TISSUES
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The elimination 1/2 life aka ---------; entails what in regards to lidocaine distribution.
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Elimination 1/2 is aka as the BETA PHASE and depicts the slower rate of disappearance caused by distribution to slowly equilibrating tissues and biotransformation and excretion.
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What is the important thing to remember about LAST?
what is your intervention priority? |
LAST is SELF-LIMITING secondary to redistribution of the drug from the CNS to MUSCLE to FAT.....ENSURE
1. AIRWAY 2. BREATHING 3. CIRCULATION |
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Explain the uniqueness of bupivacaine toxicity?
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Immediate ARREST ensues...there is no other cns involvement.....the drug preferentially binds to some MYOCARDIAL PROTEINS and causes the heart to arrest (ie- MOST CARDIOTOXIC LA)
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What LA is an isomer of Bupivacaine and why was it produced?
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ROPIVACAINE is an isome of Bupivacaine. It has no cardiac binding toxicity like bupivacaine.
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What intervention is required during a bupivacaine cardiac toxicity/
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IV LIPIDS
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Of the CNS and CV signs presented during last, what are the percentages of occurrence ?
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CNS: 45%
CNS/CV : 44% CV only: 11% |
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Of the CNS effects, which is most predominant? (LOC, agitation or dizziness or seizure)
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68% with SEIZURE
7% LOC |
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The most predominant cardiovascular sign was?
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Brady/Asystole (27%)
Least was ventricular ectopy. |
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What percentage of LAST occurs in the first minute?
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50% of cases
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What percentage of LAST occurs within 5 mins
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75%
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What are the recommendations for PREVENTING LAST?
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1. Using LOWEST EFFECTIVE DOSE.
2. INCREMENTAL DOSING w/ 15-30sec pauses 3. ASPIRATE NEEDLE B4 INJECTION 4. USE OF IV MARKER like EPI (10-15ug/ml increases HR by >10beats or SBP by >15mmHg ) 5. Use ultrasound guidance. pg 79 |
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Patients who recieve potentially toxic doses of LA should be monitored closely for at least-------------------. Why?
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30minutes, b/c LAST can present >15mins after circulation time
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Goal for intervention of LAST is?
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STOP SEIZURE w/ BENZOS
like versed. if no benzo use small amts of propafol (if no cardiac depression ie brady) If Sz persists with benzo, give Succinylcholine to minimize HYPOXIA & ACIDOSIS. IF HEART ATTACK OCCURS, do ACLS. |
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During ACLS when LAST occurs, which drugs should you avoid?
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AVOID:
VASOPRESSIN CALCIUM CHANNEL BLOCKERS BETA BLOCKERS LOCAL ANESTHETICS (duh!!!) PROPAFOL (in pts w/ CV sx) |
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What percentage of Lipid Emulsion should be used? Explain how it is given.
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20% Lipid emulsion
Bolus (1.5mg/kg) over 1 min Infusion (0.25ml/kg/min)- cont for atleast 10 min after attaining circ stability Double infusion to 0.5ml/kg/min if BP stays LOW. Upper limit dose of 10ml/kg over the first 30 minutes. |
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Who do you report LAST events to?
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www.lipidrescue.org
Use of lipid during LAST is reported to www.lipidregistry.org |
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Propafol is a substitute for lipid emulsion to treat LAST. TRUE / FALSE
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FALSE
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If VENTRICULAR ARRHYTHMIA OCCURS DURING LAST, WHAT SHOULD BE USED?
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AMIODARONE
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If EPI is used in LAST what is the recommended dosage?
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10 - 100ug boluses in adults.
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The low potency and lack of specificity of available local anesthetics are due in part to?
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The weak structural constraints at their binding site on the sodium channel.
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How does pregnancy affect LA?
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Pregnancy enhances the effect of LA agents. ie- they work better in pregnant women.
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What affect does epidural anes have on uterine tone or umbilical blood flow.
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DOES NOT ADVERSELY AFFECT uterus or UBF.
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Women with preeclampsia are more prone to toxicity of LA. TRUE/FALSE
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TRUE
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RACEMIC formulations or LEVOROTARY isomer formulations - which is more cardiotoxic in pregnant women?
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RACEMIC BUPIVACAINE
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ARE LA teratogenic?
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NO, not if used correctly.
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Elimination 1/2 life is slower/faster in the fetus than adult b/c the FETUS/ADULT has a greater volume of distribution.
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Elimination 1/2 life is slower in the fetus b/c the fetus has a greater volume of distribution.
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TOXIC EFFECT IS GREATER/SMALLER OR = IN MOTHER VS BABY.
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=
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How does alkalinization affect a local anesthestic solution?
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It shortens the latency of neural blockade but INCREASES the risk of hypotension during admin of epidural anesthesia.
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Neuraxial opioid admin produces analgesia without loss of -------- or -------------.
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Sensation or Proprioception
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Combining neuraxial local anesthetic and --------- increases block density and allows for ------------------ and ------------------.
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mixing a epidural anes and an opioid increases density and allows for admin of a lower total dose of local anes and a lower incidence of side effects.
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What are examples of hydrophilic opioids?
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Morphine and hydromorphone
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What are examples of hydrophobic (lipophilic)opioids?
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fentanyl and sufentanil
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Spinal bioavailability is greater for hydrophobic or hydrophilic drugs?
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HYDROPHILIC DRUGS LIKE MORPHINE HAVE A GREATER SPINAL BIOAVAILABILITY.
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The most common side effects of neuraxial opioid administration are.....?
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Pruritis (itching) and N/V
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The most serious complications of neuraxial opioid administration are?
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Maternal RESPIRATORY DEPRESSION AND FETAL BRADYCARDIA.
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The toxicities of mixtures of short-acting agents and long acting agents should be presumed to be-------?
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ADDITIVE (WHEN USED PROPORTIONALLY)
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The effects of pregnancy on local anes potency is best explained by .....?
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Hormonal alterations, especially in Progesterone.
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What is tumescent anesthesia?
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Subcutaneous injection of large volumes of dilute LA in combination with EPI and other agents.
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What is the total dose of Lidocaine seen with tumescent therapy?
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35-55mg/kg
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Concomitant use of high LA conc and --------------can lead to death in plastic surgery cases using tumescent anes?
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SEDATIVES.
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How long after Tumescent anesthesia is performed shd practioners exercise great caution in giving additional LA?
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12-18 hours
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What is EMLA? what are the components?
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It is a topical anesthetic eutectic mixture of LIDOCAINE AND PRILOCAINE (2.5% OF EACH). It is used for IV INSERTIONS, CANNULA INSERTIONS, CIRCUMCISIONS, used on INTACT SKIN.
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What topical anesthetic is used on open cuts and what are the components?
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TAC :
Tetracaine 0.5% Epinephrine(adrenaline) 1:2000 Cocaine: 10-11.8% |
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what is the safe, max dose of TAC?
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adults : 3-4mls
kids: 0.05ml/kg |
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Which topical anes products have potential side effects....what are they?
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TAC: Seizures, cardiac arrest
EMLA: contact dermatitis and METHEMOGLOBINEMIA Topicaine: Contact Dermatitis. |
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What is ORAVERSE? What drug is it made from and what is the mech of action?
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Dental drug used to restore sensation after dental visit. Not approved for use in kids <6 or weighing <33lbs.
It is a formulation of PHENTOLAMINE MESYLATE (which is used to treat htn). It is an ALPHA -RECEPTOR BLOCKER and is used to REVERSE EPINEPHRINE and NOT reversing the LA |
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What are the unique properties of Cocaine?
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1. Naturally occuring
2. Blocks Catecholamine Reuptake (blocks epi, dopamine, norepi) 3. Sympathomimetic 4. Vasoconstrictor |
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The more protein bound the drug the shorter/longer the duration.
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THE LONGER THE DURATION.
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Of the sympathomimetic drugs, How are the ADRENERGIC AMINES divided?
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Into Catecholamines and Noncatecholamines
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List the Catecholamines.
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Think, catecholamines make your heart race, right. So, here goes DDD's are NICE (get it)?
Dobutamine (Dobutrex) Dopamine (Inotropin) Dopexamine () Norepinephrine (Levophed) Isoproterenol (Isuprel) C (for catecholamines) Epinephine (Adrenalin) |
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List the Non-Catecholamines?
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MMM PEC
Mephentermine (Wyamine) Metaraminol ((Aramine) Methoxamine (Vasoxyl) Phenylephrine (Neo-Synephrine) Ephedrine (Ephedrine) Clonidine () |
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List the NONADRENERGIC DRUGS.
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NAG DC X
Naloxone (narcan) Amrinone (Inocor) Glucagon (Glucagon) Digitalis (Lanoxin) Calcium Salts Xanthines (Aminophylline) |
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What is the enzymatic process of the biosynthesis of EPINEPHRINE? Give start to end product and state what the rate limiting enzyme is.
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Start with TYROSINE.
TYROSINE is converted to DOPA by TYROSINE HYDROXYLASE (the rate limiting enzyme); DOPA TO DOPAMINE by AROMATIC L-AMINO ACID DECARBOXYLASE. DOPAMINE converted to NOREPINEPHRINE by DOPAMINE-B-HYDROXYLASE IN THE STORAGE VESICLE. NOREPINEPHRINE IS CONVERTED TO EPINEPHRINE BY PHENYLETHANOLAMINE N METHYLTRANSFERASE |
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What are the two enzymes responsible for metabolizing catecholamines?
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MAO and COMT
MAO (MONOAMINE OXIDASE) COMT (CATECHOL-O-METHYLTRANSFERASE) |
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What kind of enzyme is MAO?
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Is is a Mitochondrial Enzyme found in nerves.
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What kind of enzymes are COMT?
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they are synaptic enzymes that brk down cathecholamines in the synapse.
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On the parasympathetic and sympathetic outflow, the preganglionic neurotransmitter is-------- and the preganglionic receptor for the neurotransmitter above is----------.
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Acetylcholine is the neurotransmitter and NICOTINIC CHOLINERGIC RECEPTOR is the preganglionic receptor
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In the parasympathetic outflow, the POST-GANGLIONIC NEUROTRANSMITTER IS? and the postsynaptic receptor is?
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Acetylcholine and the postsynaptic receptor is the MUSCARINIC CHOLINERGIC RECEPTOR
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In the sympathetic outflow, the POST-GANGLIONIC NEUROTRANSMITTER IS ------and the POST SYNAPTIC RECEPTOR ON THE EFFECTOR ORGAN IS--------------.
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NOREPINEPHRINE is the neurotransmitter and the effector organ receptor is the ADRENERGIC RECEPTOR (WHICH MAY BE ALPHA, BETA OR DOPAMINE)
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What are the properties of Muscarinic Receptors
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Increased Cognition
Gastric Acid Production BradyCardia Smooth Muscle contraction Salivary Secretions Bladder Contraction Dilation of Cerebral Arteries (Vasodilation) Dopamine Release |
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Name the ten different mechanisms by which drugs can illicit sympathomimetic or sympatholytic activity?
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1. Inteference with SYNTHESIS OF TRANSMITTER.
2. FALSE TRANSMITTERS 3. BLOCKING REUPTAKE 4. DEPLETING PROTECTIVE VESICLES 5. RELEASE OF CATECHOLAMINES 6. ALPHA-2 STIMULATION TO PREVENT RELEASE OF TRANSMITTER 7. MIMICRY OF TRANSMITTER AT POSTJUCTIONAL SITE 8. BLOCKADE OF POSTSYNAPTIC RECEPTOR 9. BLOCKING METABOLISM OF TRANSMITTER 10. INHIBITING BRK DOWN OF SECOND MESSENGER cAMP. 7. |
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What agents in the cholinergic system are involved in the interference of the synthesis of the neurotransmitter?
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Choline acetyl transferase inhibitor (minimally depletes Acetylcholine)
Alpha-Methyl tyrosine (Depletes Norepinephrine) OVERALL ACTION IS SYMPATHOLYTIC |
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What agents/ or action in the adrenergic system are involved in the interference of neurotransmitter synthesis?
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Inhibition of TYROSINE HYDROXYLASE.
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Metabolic transformation by same pathway as precusor or neurotransmitter (aka false transmitters) involves which system? and is affected by which agent. sympathomimetic or lytic?
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False transmitters involve the ADRENERGIC SYSTEM and the agent involved is METHYLDOPA. The product ALPHA METHYL DOPA displaces NE for ALPHA METHYL NOREPINEPHRINE- an alpha-2 agonist that reduces sympathetic outflow from CNS. SYMPATHOLYTIC!
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Blockage of transport system at nerve terminal (aka BLOCKING REUPTAKE OF NEUROTRANSMITTER) occurs in which system- explain the dynamics.
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Reuptake blockade occurs in CHOLINERGIC & ADRENERGIC systems.
In the CHOLINERGIC SYSTEM, there is a blockade of CHOLINE UPTAKE with consequent depletion of Acetylcholine, and ACCUMULATION OF NE AT THE RECEPTORS. Hemicholinium is the agent responsible for this process in the cholinergic system. In the ADRENERGIC system COCAINE, IMIPRAMINE, AND TRICYCLICS are involved. SYMPATHOMIMETIC |
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What agents are involved in the blockade of transport storage vesicles (aka depletion of vesicles)
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In CHOLINERGIC system is VESAMICOL and in the ADRENERGIC SYSTEM is RESERPINE.
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Explain the mechanics of the depletion of storage vesicles.
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THE OVERALL ACTION IS SYMPATHOLYTIC.
CHOLINERGIC : blockade of ACh storage. ADRENERGIC: destruction of NE by mitochondrial MAO and depletion from adrenergic terminals. |
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The promotion of exocytosis or displacement of transmitter from axonal terminal is aka
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RELEASE OF CATECHOLAMINES
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During the release of catecholamine, which system and agents are involved?
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Cholinergic: Latrotoxins (CHOLINOMIMETIC FF BY ANTICHOLINERGIC)
Adrenergic: Amphetamines, Ketamine, Tyramine (ADRENOMIMETIC) overall action is SYMPATHOMIMETIC |
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The agents involved in the PREVENTION of release of transmitter by alpha-2 stimulation are...
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Cholinergic System: BOTULINIM TOXIN
Adrenergic System: BRETYLIUM, GUANADREL, CLONIDINE, PRECEDEX . overall action is SYMPATHOLYTIC |
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MIMICRY OF TRANSMITTER AT POSTJUNCTIONAL SITES INVOLVES WHICH SYSTEM? WHAT IS THE OVERALL ACTION ? ....WITH ONE EXCEPTION BEING?
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BOTH CHOLINERGIC AND ADRENERGIC SYSTEMS ARE ACTED UPON. OVERALL ACTION IS SYPATHOMIMETIC, EXCEPT WITH CLONIDINE WHICH IS SYMPATHOLYTIC.
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Give examples of specific agents working on the ff systems and state their effect?
CHOLINERGIC MUSCARINIC NICOTINIC under adrenergic ALPHA -1 ALPHA -2 ALPHA 1&2 B1 B2 B1B2 |
CHOLINERGIC (METHACHOLINE)
MUSCARINIC (BETHANACHOL) NICOTINIC (nicotine, epibatidine) ALPHA-1 (PHNYLEPHRINE) ALPHA-2 (CLONIDINE/PRECEDEX) ALPHA1&2: OXYMETAZOLINE B1: DOBUTAMINE B2: TERBUTALINE, ALBU TEROL B1B2: ISOPROTERENOL |
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WHAT MAJOR AGENTS ARE INVOLVED IN POSTSYNAPTIC RECEPTOR BLOCKADE AND WHICH SYSTEM DO THEY AFFECT?
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ATROPINE (MUSCARINIC BLOCKADE)
ATRACURIUM (NEUROMUSCULAR BLOCKADE) TRIMETHAPHAN (GANGLIONIC BLOCKADE) or for the adrenergic system A1A2- Phenoxybenzamine- nonselective Alpha block that is IRREVERSIBLE. A1A2 - Phentolamine - nonselective alpha receptor blockade- REVERSIBLE B1B2- PROPANOLOL B1- METOPROLOL, ATENOLOL-(selective B receptor blockade) |
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THE OVERALL EFFECT OF POSTSYNAPTIC RECEPTOR BLOCKADE IS ?
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SYMPATHOLYTIC
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INHIBITION OF ENZYMATIC BREAKDOWN OF TRANSMITTER (AKA BLOCKING METABOLISM OF THE NEUROTRANSMITTER) INVOLVES WHICH SYSTEM AND OVERALL EFFECT IS ?
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OVERALL EFFECT IS SYMPATHOMIMETIC.
CHOLINERGIC SYSTEM acted upon by AChE INHIBITORS (EDROPHONIUM AND NEOSTIGMINE) ON THE ADRENERGIC SYSTEM, MAO INHIBITORS (selective and nonselective), COMT INHIBITOR (central and peripheral) used in adjunct in parkinson's disease. Overall SYMPATHOMIMETIC |
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INHIBITION OF THE BREAKDOWN OF 2ND MESSENGER (cAMP) INVOLVES WHAT AGENT. EXPLAIN THE DYNAMICS AND OVERALL EFFECT
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Interfering with the 2nd messenger system involves action on the ADRENERGIC system by PDE inhibitors like MILRINONE which causes an INOTROPIC effect. OVERALL ACTION IS SYMPATHOMIMETIC.
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The enzyme that break down cAMP is........?
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PDE- PHOSPHODIESTERASE is the enzyme responsiblie for the break down of cAMP.
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In simpler terms, give examples of agents involved in DIRECT ACTION.
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NOREPINEPHRINE
PHENYLEPHRINE ISOPROTERENOL |
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WHAT AGENT DEPLETES VESICLES?
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RESERPINE
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WHAT AGENT IS RESPONSIBLE FOR RECEPTOR BLOCKAGE
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PHENTOLAMINE
PROPANOLOL PRAZOSIN |
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WHAT AGENTS ARE INDIRECT ACTING?
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AMPHETAMINE, TYRAMINE AND EPHEDRINE
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WHICH AGENTS ARE INVOLVED IN THE BLOCKADE OF NE REUPTAKE?
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COCAINE
IMIPRAMINE AMITRIPTYLINE (Tri cyclic antidepressants) |
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THE AGENTS INVOLVED IN FALSE TRANSMITTER PROCESS ARE
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ALPHA-METHYL-DOPA
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THE AGENT INVOLVED INTHE BLOCKADE OF NE RELEASE ARE.....
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CLONIDINE
BRETYLIUM GUANETHIDINE |
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THE ONLY TYROSINE HYDROXYLASE INHIBITOR IS .....
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METYROSINE (DEMSER)
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What is the second messenger in the parasympathetic outflow?
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cGMP
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What is is second meesenger in the sympathetic outflow?
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cAMP
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Which enzymes inactivate cGMP and cAMP. Which of these enzymes are non-selective for cAMP or cGMP
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PHOSPHODIESTERASES INACTIVATE cGMP&cAMP.
1,5,6 are selective for cGMP 3,4,7 are selective for cAMP PDE2 is non-selective |
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Which drug has been recently introduced for the treatment of Parkinson's disease?How does it work.
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As an adjunct to levodopa/carbidopa therapy, TOLACPONE is a selective and reversible inhibitor of COMT.
Appears to enhance to action of L-dopa and produce less fluctuation in drug response. |
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What are the concerns with the new drug for Parkinson's disease. What is an important consideration to make when administering the drug and what physiologic parameters are affected, increased or decreased?
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TOLCAPONE (TASMAR)- concerns are that it may interact with various cardiac drugs like (DIM)- DOBUTAMINE- ISOPROTERENOL- METHYLDOPA. A reduction in the dose of these (DIM) agents shd be considered in patient on this drug.
CVP, PAP, R&L ventricular EDV are all reduced. |
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Which parts of the eyes are affected by the sympathetic NS. What are the effects?
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Radial Muscle, iris: Alpha-1 CONTRACTS it (mydriasis aka DILATION).
Ciliary Muscle :Beta-2 RELAXES it for far vision |
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What is the parasympathetic effect on the eye?
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Sphincter Muscle of the Iris is CONTRACTED (MIOSIS) by M3/M2
Ciliary Muscle CONTRACTION for near vision (ACCOMODATION) M3,M2 |
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WHAT IS THE LOSS OF ACCOMMODATION CALLED?
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CYCLOPLEGIA
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What parasympathetic receptor is found in the heart what is it's fxn.
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M2 (muscarinic receptor);
SA node: decreases HR Atria: decreases contractility AV node: dec conduction- AV block His-Purkinje (LITTLE EFFCT) Ventricle (sl. effect on contractility) THERE IS MORE OF A VAGAL EFFECT OVERALL- MORE EFFECT ON RATE!! |
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What the SYMPATHETIC EFFECTS on heart and which ADRENERGIC RECEPTOR is involved?
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BETA-1 (OVER ALL EFFECT IS
1. INCREASE IN EVERYTHING; CONDUCTION VELOCITY(ATRIA, AV, HIS, VENTRICLE), CONTRACTILITY(ATRIA, VENTRICLE); HEART RATE(SA node only), AUTOMATICITY(AV NODE, HIS, VENTRICLE) |
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What is the sympathetic effect on the ARTERIAL blood vessels and which ADRENERGIC RECEPTORS are involved
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There is VASOCONSTRICTION (ALPHA-1) & VASODILATION BETA-2.
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The blood vessels (arteries) that do not have Beta-2 effect are in the -------?
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SALIVARY GLANDS (A1/A2- constriction and reduced secretions)
SKIN/MUCOSA(A1/A2-constriction only); BRAIN- CEREBRA (A1-slight vasoconstriction) The rest are both alpha-1 and beta-2; except Renal artery which is all (A1, A2, B1, B2) |
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List the organs in which arteries are sympathetically affected.
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Coronary Arteries (A1/B2)
Skin & Mucosa (A1/A2) Skeletal Muscle (A1/B2) Cerebral (A1) Pulmonary (A1/B2) Abd Viscera (A1/B2) Salivary Glands (A1/A2)-constriction & reduced secretion) Renal Artery:(A1/A2/B1/B2) |
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The only parasympathetic effect on arterial blood vessels occurs where?
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In the SALIVARY GLANDS (M3- dilation and increased secretions)
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B1 is found strictly in the heart with few exceptions, in what organs are those?
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RENAL
GI TRACT KIDNEY (RENIN SECRTION) ADIPOCYTES to help remember: READ GI KID (read is re-nal and ad-ipocytes; gi is gi and kid is kid-ney) |
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What is the parasympathetic effect on arterial blood vessels?
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The only Parasympathetic effect on arterial blood vessels is in the SALIVARY GLANDS- M3 causes DILATION AND INCREASED SECRETIONS
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What is the parasympathetic effecto on venous blood vessels?
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NONE
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Which parts of the lungs are acted upon by the ADRENERGIC system, and which receptors are involved?
|
TRACHEAL AND BRONCHIAL SMOOTH MUSCLES -
only BETA-2 is involved in the adrenergic effect and it causes RELAXATION |
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In the Parasympathetic Effect on the LUNGS, what receptor is affected and how?
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Bronchial and Tracheal Smooth Muscles CONTRACT and the receptors involved are M2, M3
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Explain what occurs in the GI system during SYMPATHETIC response (give receptors, site of action and effect)
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GI tone & MOTILITY (DECREASES; A1, A2, B1, B2)
SPHINCTERS (CONTRACTED: A1) SECRETION(INHIBITED-A2) G.BLADDER/DUCTS (RELAXED-B2) |
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WHAT IS THE PARASYMPATHETIC EFFECT ON THE GI TRACT? WHICH RECEPTORS INVOLVED?
|
M2/M3
MOTILITY/TONE (INCREASES); SPHINCTERS (RELAX); SECRETIONS (STIMULATED); GALLBLADDER & DUCTS (RELAXED) |
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Coronary Arterial sympathetic effect?
|
constriction (ALPHA)
Dilation (BETA-2) |
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Skin and Mucosal Arterial
Sympathetic effect |
Constriction Only (ALPHA-1/2)
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Skeletal Muscles Arterial Sympathetic Effect?
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Constriction (ALPHA-1)
Dilation (BETA-2) |
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Cerebral Arterial Sympathetic Effect?
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SLIGHT CONSTRICTION (ALPHA-1)
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Pulmonary Arterial Sympathetic Effect?
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Constriction (ALPHA-1)
Dilation (BETA-2) |
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ABDOMINAL VISCERA ARTERIAL SYMPATHETIC EFFECT.
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Constriction (ALPHA-1)
Dilation (BETA-2) |
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Sympathetic Effect on arteries of SALIVARY GLANDS.
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Constriction and Decreased Secretions (ALPHA1 / 2)
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Sympathetic effect on Renal arteries.
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ALL RECEPTORS INVOLVED (a1, a2, b1, b2)
CONSTRICTION AND DILATION |
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Sympathetic effect on Veins; which receptors/ what effect?
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Constriction (ALPHA-1 & ALPHA-2) and Dilation (BETA-2)
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What is the PARASYMPATHETIC effect on the kidneys / renals?
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NONE
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What is the SYMPATHETIC effect on the Kidneys and what receptor is involved?
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RENIN SECRETION is INCREASED (BETA-1)
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In the URINARY BLADDER, is there PARASYMPATHETIC, SYPATHETIC OR BOTH?
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BOTH PARASYMPATHETIC AND SYMPATHETIC IN THE BLADDER
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What is the SYMPATHETIC EFFECT IN THE BLADDER AND WHAT STRUCTURES ARE INVOLVED?
|
Detrusor (RELAXATION- BETA2)
SPHINCTER (CONTRACTS- ALPHA1) |
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WHAT IS THE PARASYMPATHETIC RESPONSE IN THE BLADDER?
|
DETRUSOR CONTRACTION BY M3/M2
SPHINCTER RELAXATION BY M3/M2 |
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IN WHAT ORGAN SYSTEMS ARE THERE ABSOLUTELY NO PARASYMPATHETIC EFFECT?
|
U- KLAP (where c is K)
UTERUS KIDNEY LIVER ADIPOCYTES PANCREAS |
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WHICH SYSTEMS HAVE PARASYMPATHETIC RESPONSE AS COMPARED TO THE SYMPATHETIC EFFECT?
|
HEART- LUNG
HEART E-EYES LUN- LUNG UN- URINARY BLADDER(instead of uterus) G: GI TRACT |
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In the UTERUS what is the parasympathetic response and what is the sympathetic response?
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NO PARASYMPATHETIC RESPONSE IN UTERUS!!!
SYMPATHETIC RESPONSE: (CONTRACTION: IN THE PREGNANT - ALPHA1) RELAXATION (PREGNANT AND NON PREGNANT: B2) |
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PARASYMPATHETIC RESPONSE IN THE LIVER AND SYMPATHETIC RESPONSE ARE?
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NO PARASYMPATHETIC RESPONSE!!!
SYMPATHETIC EFFECT IS TO RAISE GLUCOSE LEVELS VIA GLYCOGENOLYSIS OR GLUCONEOGENESIS (ALPHA1 AND BETA2) |
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THE ONLY ORGAN SYSTEM IN WHICH B3 HAS AN EFFECT IS?
|
ADIPOCYTES
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SYMPATHETIC RESPONSE IN THE PANCREAS
|
DECREASING INSULIN SECRETION ALPHA-2
INCREASING INSULIN SECRETION BETA-2 |
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SYMPATHETIC EFFECT IN ADIPOCYTES?
|
LIPOLYSIS
(A-1; B-1; B-2; B-3) |
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What is the effect of ALPHA AGONISTS drugs on the
EYES HEART RATE HEART CONTRACTILITY HEART CONDUCTION SPD BLOOD VESSELS LUNGS GI TRACT UTERUS LIVER |
EYES: MYDRIASIS
HEARTRATE: REFLEX BRADYCARDIA HEART CONTRACTILITY AND CONDUCTION VELOCITY (NOTHING) BLOOD VESSELS (VASOCONSTRICTION) LUNGS (NOTHING) GI TRACT (DECREASED MOTILITY AND SECRETIONS) UTERUS (CONTRACTION) LIVER (INCREASED BLOOD SUGAR) |
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What is the effect of ALPHA ANTAGONIST in the:
EYES HEART RATE HEART CONTRACTILITY HEART CONDUCTION SPD BLOOD VESSELS LUNGS GI TRACT UTERUS LIVER |
ALPHA ANTAGONISTS IN THE:
EYES (MIOSIS) HEART RATE (REFLEX TACHYCARDIA) HEART CONTRACTILITY (SLIGHT REFLEX INCREASE) HEART CONDUCTION SPD(NONE) BLOOD VESSELS (VASODILATION) LUNGS (NONE) GI TRACT (NONE) UTERUS (NONE) LIVER (NONE) |
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WHAT IS THE BETA-AGONIST EFFECT ON THE EYES
HEART RATE HEART CONTRACTILITY HEART CONDUCTION SPD BLOOD VESSELS LUNGS GI TRACT UTERUS LIVER |
BETA AGONIST ON THE
EYES: NCRE HEART RATE: TACHY HEART CONTRACTILITY: INCREASED HEART CONDUCTION: INCREASED BLOOD VESSELS: VASODILATION LUNGS (BRONCHODILATION) GI TRACT (VASODILATION) UTERUS (RELAX) LIVER (INCREASE BLOOD SUGAR) |
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EFFECT OF BETA BLOCKER ON THE
EYE HEART RATE HEART CONTRACTILITY HEART CONDUCTION BLOOD VESSELS LUNGS GI TRACT UTERUS LIVER |
BETA BLOCKER EFFECTS ON THE
EYE: DECREASES INTRAOCULAR PRESSUE HEART RATE: BRADY HEART CONTRACTILITY: DECREASED HEART CONDUCTION SPD: DECREASED BLOOD VESSELS: VASOCONTRICTION LUNGS: BRONCHONSTRICTION GI TRACT (NCRE) UTERUS (NCRE) LIVER (HYPOGLYCEMIA) |
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WHAT IS THE CHOLINERGIC EFFECT ON
EYES HEART RATE HEART CONTRACTILITY HEART CONDUCTION BLOOD VESSELS LUNGS GI TRACT UTERUS LIVER |
CHOLINERGIC EFFECT ON
EYES: MIOSIS (DECREASED IOP) HEART RATE: BRADY HEART CONTRACTILITY: SL. DECREASE HEART CONDUCTION: DECREASED BLOOD VESSELS: NCRE LUNGS: BRONCHOCONSTRICTION GI TRACT: INCREASED MOTILITY AND SECRETIONS UTERUS & LIVER : NCRE |
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|
WHAT'S THE EFFECT OF THE ANTI-CHOLINERGIC SYSTEM ON
EYES HEART RATE HEART CONTRACTILITY HEART CONDUCTION BLOOD VESSELS LUNGS GI UTERUS LIVER |
ANTI-CHOLINERGIC EFFECTS ON THE
EYES: MYDRIASIS (INCREASED IOP), CYCLOPLEGIA HEART RATE: TACHY HEART CONTRACTILITY (INCREASED SLIGHTLY) HEART CONDUCTION (INCREASED) BLOOD VESSELS: NCRE LUNGS: SLIGHT BRONCHODILATION GI: DECREASED MOTILITY AND SECRETIONS UTERUS AND LIVER: NCRE |
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BETA AGONISTS AND ANTICHOLINERGICS ARE SIMILARLY ACTING IN WHAT SYSTEMS?
|
HEART
LUNG GI |
|
|
WHAT IS PHENYLEPHRINE?
WHAT'S THE RESPONSE ON SYS, DIASTOLIC, HR AND SVR |
PURE ALPHA
SYSTOLIC : MAJOR INC DIASTOLIC: MAJOR INC HR: REFLEX BRADY (MIN) SVR: MAJOR INCREASE |
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|
WHAT IS THE OTHER NAME FOR LEVOPHED?
WHAT KIND OF DRUG IS IT AND WHAT ARE THE EFFECTS ON S/D BP, HR AND SVR |
NOREPINEPHRINE
(MOSTLY ALPHA/ SOME BETA); SYS: MAJOR INCREASE DIA: MODERATE INCREASE HR:MINIMUM INCREASE SVR: MAJOR INCREASE |
|
|
WHAT IS THE OTHER NAME FOR EPINEPHRINE AND WHAT KIND OF DRUG IS IT? WHAT'S ITS EFFECT ON SYS/DIA BP, HR & SVR
|
AKA ADRENALIN
EPI IS MOSTLY BETA, SOME ALPHA SYS BP: MOD INCREASE DIA BP: MOD DECREASE HR: MAJOR INCREASE SVR: MIN DECREASE |
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|
WHAT IS THE OTHER NAME FOR ISOPROTERENOL AND WHAT KIND OF DRUG IS IT? WHAT'S THE EFFECT ON SYS/DIA BP, HR, AND SVR?
|
ISUPREL
PURE BETA SYS: MOD. INCREASE DIA: MAJOR DECREASE HR: MAJOR INCREASE SVR: MAJOR DECREASE |
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|
WHAT KIND OF DRUG IS DOPAMINE AND WHAT ARE IT'S EFFECT ON BP, HR AND SVR
|
DOPAMINE IS DOPAMINE, BETA AND ALPHA.
IN LOW DOSES (DOPAMINE EFFECT) IN MEDIUM DOSES (DOPA AND ALPHA EFFECTS) HIGH DOSES (DOPA, ALPHA AND BETA EFFECTS) SYS: MIN INCREASE DIA: MOD DECREASE HR: MIN INCREASE SVR: MOD DECREASE |
|
|
HOW DOES THE DIASTOLIC RESPONSE RELATE TO THE SVR IN INOTROPIC DRUG EFFECTS?
|
DIASTOLIC BP = SVR
Diastolic BP is essentially your vascular resistance b.c its what's in your vessels when the heart is relaxing. |
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|
WHAT IS THE OTHER NAME FOR DOBUTREX AND WHAT KIND OF DRUG IS IT? EFFECT ON BP/HR/SVR
|
DOBUTAMINE
PURE BETA DRUG SYS BP (MOD INCREASE) DIA BP (MAJOR DEC) HR (MINIMUM INCREASE) SVR (MOD DECREASE) |
|
|
WHAT ARE THE FOUR THINGS SEEN WITH INOTROPIC PRIMARY ALPHA DRUGS
|
VASOCONSTRICTION
REFLEX BRADYCARDIA INCREASED SYSTOLIC INCREASED DIASTOLIC |
|
|
WHAT ARE THE FOUR RESPONSES SEEN WITH THE PRIMARY BETA IONOTROPIC DRUGS
|
VASODILATION
+ INOTROPY/CHRONO AND DROMOTROPE INCREASED SYSTOLIC BP DECREASED DIASTOLIC BP. |
|
|
WHAT IS THE EFFECT OF CATHECHOLAMINES ON ALPHA-1 ADRENOCEPTOR
|
Postsynaptic: VASOCONSTRICTION
|
|
|
WHAT ARE THE EFFECTS OF CATHECHOLAMINES ON ALPHA-2 ADRENOCEPTORS?
|
CNS: Sedation, Decreased Sympathetic Outflow
Presynaptic: Decreased NE release Postsynaptic: Vasoconstriction |
|
|
What are the effects of cathecholamines on the Beta-1 receptors?
|
CARDIAC EFFECTS include Chronotropy and Inotropy
|
|
|
What are the effects of cathecholamines on the Beta-2 receptors?
|
Cardia effects also : inotropy and chronotropy.
Smooth Muscle Relaxation in Bronchial and Vascular |
|
|
WHAT IS THE ORDER OF THE CATHECHOLAMINES FROM PURE ALPHA TO PURE BETA
|
P - NEED- I
PHENYLEPHRINE NOREPINEPHRINE EPINEPHRINE EPHEDRINE DOPAMINE DOBUTAMINE ISOPROTERENOL. |
|
|
OUTSIDE OF THE BRAIN, WHAT ARE THE OTHER MAJOR SITES OF DOPAMINE RECEPTORS?
|
BRAIN
KIDNEY AND MESENTERY |
|
|
In general, what are the 3 major goals in treating pts in shock as it relates to the heart, and vessels?
|
You want the heart to:
1. BEAT STRONGER (+ inotrope) 2. BEAT SLOWER (slower heart rate) 3. want VASODILATION |
|
|
EXPLAIN THE DIFFERENT DOSES FOR DOPAMINE ADMINISTRATION.
|
2-5ug/kg/min =(primarily dopamine receptor) inc'd renal and mesenteric blood flow.
5-10ug/kg/miin (B1 agonist) >10ug/kg/min (B1 and Alpha1 with ALPHA1 PREDOMINATING) |
|
|
WHAT ARE DIFFERENT ROUTES THAT CLONIDINE CAN BE GIVEN THROUGH?
|
ORAL
IM IV EPIDURAL INTRATHECAL |
|
|
WHAT IS THE ORAL BOLUS DOSE FOR CLONIDINE?
|
150ug. 4-5ug/kg
|
|
|
BOLUS IM DOSE FOR CLONIDINE IS?
|
2ug/kg
|
|
|
Bolus dose and IV infusion dose for clonidine are?
|
BOLUS:150ug or 4-8ug/kg
IV infusion :2ug/kg/hr |
|
|
Bolus dose for epidural clonidine is?
Infusion dose for clonidine given intrathecally is? |
150ug or 6-8ug/kg
infusion dose for epidural admin of clonidine is 12.5-70 ug/kg/hour or 1-2ug/kg/hr |
|
|
Intrathecal bolus and infusion doses of clonidine are?
|
30-225ug bolus dose
infusion intrathecally is 8-400ug/d |
|
|
Name the natural cathecholamines.I IS THEIR MOA DIRECT OR INDIRECT
|
EPINEPHRINE
NOREPINEPHRINE DOPAMINE DIRECT ACTING |
|
|
WHAT ARE THE SYNTHETIC CATECHOLAMINES?
|
ISOPROTERENOL AND DOBUTAMINE
|
|
|
OF THE SYNTHETIC NONCATECHOLAMINES, WHICH ONES ARE INDIRECT ACTING?
|
EPHEDRINE
AMPHETAMINES |
|
|
OF THE SYNTHETIC NONCATECHOLAMINES, WHICH ARE DIRECT ACTING?
|
PHENYLEPHRINE.
EPHEDRINE IS BOTH INDIRECT AND DIRECT |
|
|
THE TWO NONCATECHOLAMINE DRUGS NOT USED IN IV INFUSIONS ARE?
|
EPHEDRINE AND AMPHETAMINES)
|
|
|
OF THE CATECHOLAMINES AND NONCATECHOLAMINES, WHICH HAVE CNS EFFECT?
|
EPINEPHRINE
ISOPROTERENOL EPHEDRINE AMPHETAMINE |
|
|
WHAT IS THE SINGLE IV DOSE FOR EPHEDRINE?
|
10-25 MG
|
|
|
WHAT IS THE SINGLE IV DOSE FOR PHENYLEPHRINE?
INFUSION DOSE |
0.5 - 10 MG
20-50 |
|
|
WHAT IS THE SINGLE IV DOSE FOR EPI?
WHAT IS INFUSION DOSE RANGE FOR EPI? |
SINGLE DOSE EPI: 2-8ug
INFUSION (1-20ug/min) |
|
|
OF THE NATURAL CATECHOLAMINES, WHICH ARE NOT USED IN SINGLE IV DOSING?
|
NOREPINEPHRINE AND DOPAMINE ARE NOT USED IN SINGLE IV DOSING
|
|
|
WHAT IS THE CONT INFUSION DOSE FOR DOPAMINE
|
2-20ug/kg/min
|
|
|
What are the single and infusion doses for Isoproterenol?
|
1-4ug single dose iv
1-5ug/min |
|
|
Of the 3 anticholinergic drugs discussed, atropine, scopolamine and glycopyrolate, which of these is NOT LIPID SOLUBLE? WHAT IS THE SIGNIFICANCE OF THIS?
|
ROBINUL or GLYCOPYROLATE;
Significance is that it does not have CNS effects b/c it does not cross the BBB. Therefore no sedation, no mydriasis or cycloplegia and no reduction in nausea induced motion sickness. |
|
|
which drugs have analeptic effects? what are the manifestations
|
AMPHETAMINES
(CNS STIMULATION) Wakefulness, alertness, decreased fatigue, increased initiative, self confidence, increased concentration, elation, euphoria, anorexia increased speech and motor activity |
|
|
what are neuroleptic effects?
|
blocking the stimulation of the CNS. You see the opposite of the analeptic effect.
|
|
|
what is the mneumonic for atropine poisoning?
|
RED AS A BEET, BLIND AS A BAT, DRY AS A BONE, MAD AS A HATTER, HOT AS A HARE.
|
|
|
WHICH ANTICHOLINERGIC OF THE 3 DRUGS ATROPINE, SCOPOLAMINE AND GLYCOPYROLATE HAVE THE GREATEST INFLUENCE ON DECREASING GASTRIC HYDROGEN ION SECRETION?
|
THEY ALL HAVE THE SAME EFFECT ON DECREASING GASTRIC SECRETIONS
|
|
|
WHICH DRUG HAS THE HIGHEST SEDATION EFFECT/ LOWEST SEDATION EFFECT?
|
SCOPOLAMINE- HIGH
ATROPINE- LOW |
|
|
ANTISIALOGOGUE (NO SPIT) EFFECT (LIST DRUGS FROM HIGHEST TO LOWEST
|
SCOPOLAMINE +++
GLYCOPYROLATE ++ ATROPINE + |
|
|
ANTIMUSCARINIC DRUG THAT INCREASES HEARTRATE (FROM HIGHEST TO LOWEST)
|
ATROPINE
GLYCOPYROLATE SCOPOLAMINE |
|
|
ANTIMUSCARINIC DRUG THAT RELAXES SMOOTH MUSCLE. (FROM HIGHEST TO LOWEST)
|
ATROPINE = GLYCOPYROLATE (BOTH EQUAL)
SCOPOLAMINE (+) |
|
|
THE ONLY ADVANTAGE ATROPINE HAS OVER GLYCOPYROLATE IS ?
|
INCREASING HEART RATE
AND SMOOTH MUSCLE RELAXATION |
|
|
THE ONLY ADVANTAGE THAT GLYCOPYROLATE HAS OVER ATROPINE IS?
|
IN DRYING SECRETIONS.
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GLYCOPYROLATE AND ATROPINE HAVE WHICH EFFECTS IN COMMON?
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DECREASING GI ACID
RELAXING SMOOTH MUSCLE. |
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RANK THE EFFECT OF ANTIMUSCARINICS IN MYDRIASIS AND CYCLOPLEGIA
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SCOPOLAMINE (+++)
ATROPINE (+) GLYCOPYROLATE HAS NO EFFECT ON CNS. |
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AT WHAT DOSE OF ATROPINE ARE THE PARASYMPATHETIC NERVES COMPLETELY BLOCKED.
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2MG
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AT 0.5MG OF ATROPINE YIELDS WHAT EFFECT?
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SLIGHT BRADYCARDIA
ANHYDROSIS (SWEAT INHIBITION) SOME DRYNESS OF MOUTH |
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1 MG OF ATROPINE YIELDS WHAT EFFECTS?
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DRY MOUTH
TACHY THIRSTY PUPIL DILATION (MILD) |
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AT 5MG OF ATROPINE
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CAN'T SEE
CAN'T PEE CAN'T SHIT CAN'T SPIT HOT, HEADACHE, RESTLESS AND FATIGUE |
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AT 10 MG OF ATROPINE, WHAT ARE THE MANIFESTATIONS?
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RAPID/WEAK PULSE
IRIS OBLITERATED-CANT SEE RESTLESSNESS EXCITEMENT HALLUCINATIONS DELIRIUM COMA SKIN FLUSHED ATAXIA |
