Term
| What is the difference between phase 1 and phase 2 reactions |
|
Definition
phase 1: HYDROLYZE, OXIDIZE, AND / OR REDUCE. Usually via P 450 system.
Phase 2: conjugation of the parent compound to make it more poloar |
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Term
| What is the difference between zero order elminiation and first order elminiation |
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Definition
| first order eliminiation is most specific to what we see in aneshtesia. Here a set fraction is eliminatied per unit of time. While in zero order elminiation removal ofa constatn amount of drug per unitof time. |
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Term
| do lipid soluble drugs or hydrophilic drugs have large volumes of distribution..why |
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Definition
| lipophillic drugs have large volume of distribution due to the fact taht when you add lots of the drug it tends to leave the blood for those lipid loving tissues. as a result you end up with less circulating in the body therefore the VOD is large. (amt given / conc in blood) |
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Term
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Definition
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|
Term
| each half life represents a ~~~ % reduction in plasma concentration of a drug |
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Definition
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Term
| at how many half lives does it take until a drug lacks clinical activity |
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Definition
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|
Term
| vessel rich group includes what five organs |
|
Definition
1. heart
2. kidneys
3. liver
4. brain
5. lungs |
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Term
| an inverse agonist does what when it binds to a recepot |
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Definition
| it binds, acts as an agonistm, except its activation of the receptor causes an response that is opposite of the natural endogenous molecule. |
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Term
| structurally, why are some drugs able to be non competiive antagonist of a ligand |
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Definition
| usually due to strong covalen bonding |
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Term
| local anesthetics often bind to what protein |
|
Definition
| alpha 1 acid glycoprotein |
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|
Term
| what cranial nerves contain parasympathetic nerves |
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Definition
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|
Term
| thiopental broken down b y |
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Definition
|
|
Term
| example of zero order elimination is the elminiation of |
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Definition
| alcohol.. only this much can be broken down in time. So constant amount like 1 beer an hour. or 2 beers an hour. |
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Term
| describe the therapeutic index of a drug |
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Definition
| LD50 / ED50 equals therapeutic index. So if drug has therapuetic index of 100/1 thats preetty safe it takes 100 x the effective dose to kill the person . but if it is 2/1 that is very dangerous. Neostigmine is like this. So close to lethal dose. lethal dose equals LD. |
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Term
| What type of Muscarinic receptors are found in the cardiac tissue |
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Definition
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|
Term
| What is COMT and where does it come from |
|
Definition
| It is made in the liver and breaks down NE via methylation |
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Term
| what are the Alpha and beta if any effects of isoproterenol |
|
Definition
Alpha 1,2
Beta 1,2
and ionotropic |
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|
Term
| name two beta 2 agonist which are also effective tocolytics |
|
Definition
1. terbutaline
2. ritodrine |
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|
Term
| side effects of beta 2 agonism are |
|
Definition
| hypokalemia, and hyperglcyemia |
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Term
| name two alpha antagonist and which is competitive and which is non-competitive. |
|
Definition
Phenoxybenzamine: Irreversible, NONCOMPETITIVE. Does its own shit and does not care about anything else
Phentolamine: is compettive |
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Term
| Which type and name of a drug is used to treat pressor infiltration into someones arm |
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Definition
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Term
|
Definition
|
|
Term
| what receptor do you block to blunt reflex tachycardia |
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Definition
| BLOCK ALPHA 1 receptor. (SELECTIVELY) |
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Term
| prazocin, terazocin, tamsulosin all act on what receptor |
|
Definition
| alpha 1 selective antagonist |
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Term
|
Definition
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|
Term
| why is esmolol so fast acting |
|
Definition
| its metabolized by hydrolysis via red cell esteras |
|
|
Term
| whats the ratio of Alpha to beta blockade of labetolol |
|
Definition
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|
Term
| name two drugs that are beta blockers and have some alpha properties |
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Definition
|
|
Term
| where is nitroprusside broken down |
|
Definition
| in RBCs and result in accumulation of cyanide. |
|
|
Term
| Name three Sx of cyanide toxcity |
|
Definition
1. tachyphylaxis
2. metabolic acidosis
3. increased PvO2 |
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|
Term
| how is cyanide metabolized |
|
Definition
| cyanide is converted to thiocyanate in the liver by rhodanase through transsulfuration |
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|
Term
| Does nitroprusside or nitroglycerine available fastest and why |
|
Definition
| Nitroprusside immediately donates NO while nitroglycerine requires active reduction to release NO |
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|
Term
| how does hydralazine work |
|
Definition
| promotes influx of potassium into vascular smooth muscle resulting in hyperpolarization of the cell membrane and relaxation of the smooth muscle |
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|
Term
| which phospodiestersase inhibitor causes platelet inhibtion |
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Definition
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|
Term
| most common side effect of ACE inhibitor is |
|
Definition
|
|
Term
| how does angiotensin receptor blockers work |
|
Definition
| block angiotensin II from receptor site |
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|
Term
| difference between angiotensin receptor blocker and ACE I is? |
|
Definition
| ACE-I has side effects like cough and blocks ANGT 1 to 2 while ARB blocks A II from binding to Angiontensin receptor and does not have cough s/e |
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|
Term
| what percentage of AcH actually reach their receptors..the remainder go where |
|
Definition
| 50% of AcH reach receptors while the rest either are hydrolzyed or diffuse away |
|
|
Term
| prejunctional AcH are positive or negative feedback |
|
Definition
|
|
Term
| The effect of sux is mitigated by breakdown or diffusion out of the junction |
|
Definition
| DIFFUSION. Sux cannot be broken down in the junction needs to diffuse based on conc gradiet out into the plasma where it can be broken down |
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|
Term
| This Sx indicates a patietn who has just received sux has a 20% chance for also having MH |
|
Definition
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|
Term
| name benzylisoquinolinium compounds |
|
Definition
| atracurium and cis-atracurium |
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|
Term
| Name how cisatricurium is eliminated and what the major route is |
|
Definition
| Ester hydrolysis, renal and hoffman's elminiation. 70% elminated via hoffman's elimination. 15% via renal. |
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|
Term
| The two categories of non depolarizers are |
|
Definition
1. benzylquinolinium
2. steroidal compounds |
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|
Term
| the half life of atracurium and cisatricum is |
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Definition
|
|
Term
| half life of pancuronium is |
|
Definition
|
|
Term
| the majority of pancuronium is elminated via |
|
Definition
|
|
Term
| Does pancuroium have active metabolites |
|
Definition
| YES. 3-OH. Which retains 1/2 the neuromuscular blocking activity of pancuronium |
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|
Term
| primary elminiation of rocuronium is via |
|
Definition
|
|
Term
| which muscle blockers have active metabolites and what are they called |
|
Definition
Sux:
1.
2.
Pancorunium:
1. 3-OH Pancuronium (1/2 potency)
Vecuonium
1. 3-OH |
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|
Term
| Even with four twitches during recovery there can still be a blockade of the neuromuscular junction of ___ % |
|
Definition
|
|
Term
| For intermediate NMBD the time from apost tetanic coun of 1 indicates how long until reappeearance of a normal twitch |
|
Definition
| 15-30 minutes. So patient is deep and TOF will not work again for that long. The only reason you got a twitch during this test was because you flooded the junction with tons of AcH from a long tetanus of 5 seconds. Then immediately applied a single or TOF and only got 1/4. |
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|
Term
| Where does neostigmine act on |
|
Definition
| causes a covalent bond the estereratic site of the enzyme |
|
|
Term
| where does pyridostigmine work on the enyzme |
|
Definition
| by forming a covalent bond on the esteraertic site |
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|
Term
| How does edrophonium work on AcHase enzyme |
|
Definition
| COMPETITIVE binding to the anionic site. |
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|
Term
| Why is edrophonium fast acting..explain its physiology |
|
Definition
| it forms a bond to the anionic site of the AcHase enzyme that is not covalent thereofre it rapidly binds but also rapidly leaves the enzyme |
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|
Term
| physostigmine is what kind of chemical compound |
|
Definition
| tertiary amine which allows it to cross the BBB |
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|
Term
| GABA: explain its chemical structure |
|
Definition
| a pentameric transmembrane protein |
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|
Term
| explain the three effects of barbiturates on the brain and how this helps in brain injury patients |
|
Definition
1. decrease CMRO2 by 50%
2. Decrease in CBF
3. Decrease in ICP |
|
|
Term
| can barbiturates cause ventilatory depression |
|
Definition
|
|
Term
| what do barbiturates do to our cardiovascular system |
|
Definition
1. decrease CO
2. Decrease Preload |
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|
Term
| Whats the clinical issue with thiopental as far as receovery goes |
|
Definition
| Its elimination half life is 6-24 hours!!! So pts are groogy for ever. |
|
|
Term
| what is the issue with methohexital? Why is it better in regards to recovery than thiopental |
|
Definition
| Methohexital has an elminiation half life of only 2 hours but it may induce EEG seizure activity. |
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|
Term
| What part of GABA do benzos work on |
|
Definition
|
|
Term
| Name the five properties of benzos |
|
Definition
1. anxiolytic
2. sedative
3. hypnotic amnestic
4. central muscle relaxant
5. anticonvulsant properties. |
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|
Term
| What is the relationship of benzos to other drugs and ventilatory depression |
|
Definition
| Minimal ventilatory depression on its own but if used with other drugs especially opioids it causes profound ventilatory depression synergestic effect |
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|
Term
| what benzos are formulated in propylene glycol which causes pain with injection |
|
Definition
|
|
Term
| Why does midazolam linger if given as an infusion. |
|
Definition
| it has an ACTIVE metaoblite known as 1-OH midazolam |
|
|
Term
| whats the reversal for benzo overdose |
|
Definition
|
|
Term
| whats the dangerous side effect of flumazenil if given to fully reverse a chronic benzo user |
|
Definition
| can cause seizures if pts on long term benzos |
|
|
Term
| etomidate is formulated as a ____ enatiomer (R or S.. + or -) |
|
Definition
|
|
Term
| where is etomidate metabolized |
|
Definition
| in liver by ester hydrolysis |
|
|
Term
| two big side effects of etomidate you should anticipate |
|
Definition
1. myoclonus
2. adrenal supression |
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|
Term
| where is propofol metabolized |
|
Definition
| in the liver by conjugation to inactive metabolites |
|
|
Term
| elmination half life of propofol is |
|
Definition
|
|
Term
| what additives are in propofol solutions to inhbiit bacterial growth |
|
Definition
1. metabisulfite
or
2. EDTA |
|
|
Term
| What properties of propofol make it nice for brain injuried patients |
|
Definition
1. decrease CBF
2. Decrease CRMO2
3. Decrease ICP |
|
|
Term
| Name signs and sx of propfolol infusion syndrome |
|
Definition
1. rhabodmyolysis
2. metabolic acidosis
3. renal failure |
|
|
Term
| ketamine works central or spinal |
|
Definition
|
|
Term
| What does ketamine do to patients lungs |
|
Definition
| POTENT BRONCHODILATOR..since it is a central SNS stimulator. Think of it as EPI FOR SEDATION! |
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|
Term
| the key difference in effects of opioids lies in what property difference between each drug |
|
Definition
| difference in each drug lipid solubility |
|
|
Term
| The principle CLEARANCE mechanism of all opioids is via |
|
Definition
|
|
Term
| Opioids cause the CO2 response curve to switch to the left or right |
|
Definition
|
|
Term
| This drug is 10x as powerful as morphine while this drug is 1/10 as powerful as morphin |
|
Definition
10x > stronger than moprhipn = dilauidd
1/10 as strong as morphine = demerol |
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|
Term
| fentanyl is ___ x more powerful than morphine |
|
Definition
|
|
Term
| fentanyl context sensitive half life chart says that for bolus of... |
|
Definition
1-5 mcg/kg: 1/2 Contex = 8-30 min
6-10 mcg/kg: 1/2 context = 60-90 min
>10 mcg/kg: 1/2 context = 16 hours. |
|
|
Term
| the most powerful opioid is? It is ___ x more powerful than morphine |
|
Definition
| sufentenil which is 1000x more powerful than morphin |
|
|
Term
| Why does alfentanil have such a rapid onset |
|
Definition
| due to low pKA therefore 90% exists in the non-ionized form |
|
|
Term
| nubain doses are equal, less or greater tha nmorphine and by how much |
|
Definition
|
|
Term
| this drug is similar to nubaine with antago at mu and agonist at kappa |
|
Definition
|
|
Term
| major side effects of narcan given to opioid addicted patients |
|
Definition
1. HTN
2. Tachy
3. pulmonary Edema
4. dysrhythmias (VT, VF) |
|
|
Term
| which ABX inhibit an enzyme that clears benzos and narctoics and therefore should be used with caution? Which enzyme do they inhibit |
|
Definition
| Macrolides like erythromycin inhbiit p 450 which is what helps clear benzos and narcotics |
|
|
Term
| Max infusion rate for vanco to avoid red man's syndrome |
|
Definition
|
|
Term
| Which ABX group has high risk of prolonging QT syndrome |
|
Definition
| Quinolones such as ciprofloxacin |
|
|
Term
|
Definition
|
|
Term
| whats the clinical concern with patients on ritonavir |
|
Definition
| an antiviral for HIV, protease inhibitor but also inhibits CYP3A4. So you may have prolong effects of drugs like versed, fent, demerol ect. |
|
|
Term
|
Definition
|
|
Term
| nitrous has profound effects on what part of respirator system |
|
Definition
| PROFOUND depression of ventilatory response to arterial hypoxemia |
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|
