Term
what is the diameter of
1. A-delta fibers
2. C Fibers |
|
Definition
1. A delta fibers: 1-4 um
2. C fibers: 0.4-1.2 um |
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Term
| On what lamina does A delta fibers innervate? |
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Definition
|
|
Term
| On what lamina does C fibers innervate? |
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Definition
|
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Term
| What type of interneuron is at the substanstia gelatinosa that inhibits pain |
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Definition
|
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Term
| Lamina II where pain fibers synapse is also called the |
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Definition
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Term
| Enkephalin attaches to receptors on what nerve class? It works by inhibiting release of? |
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Definition
| Enkephalin will be released and attaches to nerve terminals on C fibers. By attaching here it inhibits release OF SUBSTANCE P |
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Term
| Describe the pain pathway starting from brain to spinal cord |
|
Definition
| 1. Periventricular nuclei found in periadqueductal gray will send signal via enkephalin neurons to raphe magnus nucleus in the pons --> Then that sends a signal via the serotonergic neurons to enkephalin neurons in the rexed's lamina II. Those then release enkephalin into the synapse to inhibit the release of substance P on the C fibers. |
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Term
| Spinal analgesia is mostly mediated by what Mu receptors? While supraspinal analgesia primarily mediated by what Mu receptors? |
|
Definition
Spinal analgesia via Mu 2
Supraspinal analgesia via Mu 1 |
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|
Term
| Supraspinal analgesia occurs mostly in what parts of the brain |
|
Definition
1. limbic system
2. hypothalamus
3. thalamus |
|
|
Term
| what mu receptor is responsible for miosis |
|
Definition
|
|
Term
| what opioid receptor is responsible for euphoria while this one is responsible for dysphoria |
|
Definition
mu 1 - euphoria
kappa - dysphoria |
|
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Term
| what opioid receptor is responsible for bradycardia |
|
Definition
|
|
Term
| what opioid receptor is responsible for physical dependence |
|
Definition
| Mu 2 PRIMARY and also Delta |
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Term
| what opioid receptor is responsible for respiratory depression |
|
Definition
|
|
Term
| what opioid receptor is responsible for constipation |
|
Definition
|
|
Term
| what opioid receptor is responsible for diuresis |
|
Definition
|
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Term
| what opioid receptors are responsible for dependence and which are low risk for dependence |
|
Definition
Depedence: MU2 and Delta
Low risk for dependence: Mu1 and Kappa |
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Term
| Morphine: describe characteristics |
|
Definition
Peak: 15-30 minutes
* Rapid conjugation with glucuronic acid in liver and in kidneys
* Accumulates rapidly in kidneys, liver and skeletal muscle
* Active metabolite = Morphine-6-glucoronide
* Patients: Ok for liver sick pts, Extreme caution in renal pts due to inability to excrete in urine the active metabolites. |
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|
Term
| How do opioids cause bradycardia |
|
Definition
| due to stimulation of the vagal nuclei in the medulla. Causes a direct depresant effect on SA node and slows conduction in AV node |
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|
Term
| Do opoiods always decrease CBF and ICP? |
|
Definition
| No NOT ALWAYS. IF the patient is hypoventilating the opioids will not produce decrease CBF and decrease ICP |
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|
Term
| When would you most likely see muscle rigidity related to opioids? |
|
Definition
| during rapid, LARGE, doses |
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|
Term
| The two most common drugs that can cause muscle rigidity from large dose administration are |
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Definition
|
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Term
| Is sleep or sedation an indication of appropriate analgesia? |
|
Definition
| NOOOOOOOOOOOOOOOOOOOOOO. Sedation precedes analgesia. |
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Term
| If you have a patient with suspected MI related angina but come up wiht a differential diagnosis of biliary colic from this class of meds __________ what can you administer to differentiate? |
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Definition
| Opioids can cause biliary colic. To differentiate this angina from an MI compared to biliary colic induced by opioids; you can give narcan. If pain goes away then it is biliary colic from the opioids |
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Term
| if you suspect spasm of the sphincter of oddi you will see what on xray |
|
Definition
| constriction of the common bile duct |
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|
Term
| sphincter of oddi spasm can be reversed with what medications |
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Definition
|
|
Term
| How do opioids cause nausea |
|
Definition
| by direct innervation to the chemoreceptor trigger zone |
|
|
Term
| which opioid is the most potent |
|
Definition
|
|
Term
| Which opioid has the fastest elimination |
|
Definition
|
|
Term
| which opioid has a contect sensitive 1/2 life that increases with duration of use |
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Definition
|
|
Term
| the elimination 1/2 life of alfentanil is |
|
Definition
|
|
Term
| which opioids have histamine release |
|
Definition
|
|
Term
name in order from most potent to least the following
demerol, fentanyl, sufentanyl, remifentanyl, alfentanyl, morphine |
|
Definition
| Sufentanil > remi = fent > alfentanil > morphine >demerol |
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Term
| the elmination 1/2 is greatest in what opioid and why |
|
Definition
| fentanyl has the longest E 1/2 life bc the reason why it acts so fast is due to redistribution to inactive sites. So it take time for the drug to then leave those actve sites and be elminted. |
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Term
| which opioid can be life threatening if given with patients who are on MAOI..what can happen |
|
Definition
| DEMEROL + MAOI = HIGH RISK FOR SEROTONIN SYNDROME |
|
|
Term
| What is the difference between type I and Type II demerol reactions |
|
Definition
Type I
1. HTN
2. Agitation
3. Skeletal Muscle Rigidity
4. Headache
5. Hyperpyrexia
Type II Rx;
1. Hypotension
2. Resp Depression
3. Coma |
|
|
Term
| the elimination 1/2 life of methadone is? |
|
Definition
|
|
Term
| normeperdine is how potent |
|
Definition
|
|
Term
| normeperdine toxicity manifests as? Seen when |
|
Definition
1. myoclonus
2. seziures
Most commonly seen when administered over 3 days with a pt who has impaired renal |
|
|
Term
| why does fentayl have a longer elimination half-time than morphine |
|
Definition
| b/c it has a Larger volume of distribution (INC Vd) due to its lipid solubility and therefore can penetrate lots of areas in various vascular areas than morphine can which is less lipid soluble. |
|
|
Term
| why is fentanyl prolonged in elderly patients |
|
Definition
| bc decreased clearance. Vd is not changed in older adults, but clearnace is thats why |
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|
Term
| which opioid may be associated with a possible acute opioid tolerance syndrome..whats this mean |
|
Definition
| Remifenanil. Has been shown if given in large amounts may cause an acute increase in tolerance in patients. Thefore during your postop check if your pt is in extreme atypical pain this may be related to the remi gtt and they will need more opioids in the interim. |
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|
Term
what opioid is the result of the substitution of a methyl group
for the hydroxyl group on the number 3 carbon of morphine |
|
Definition
|
|
Term
| codeine is metabolized to? Where is it metabolized? |
|
Definition
| 10% of codeine is demehtylated to morphine during 1st pass hepatic metabolism. Another active metabolite is codeine-6-glucuronide. |
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|
Term
| __ mg of codeine is effective at suppressing cough |
|
Definition
| 15 mg oral codeine is effective as a antitussive |
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|
Term
| opioid-agonist/antagonist bind to what recpetors |
|
Definition
|
|
Term
| What is the benefit of agonist/antagonist opoiids |
|
Definition
| causes analgesia without respiratory depression |
|
|
Term
| Describe ceiling effect with agonist/antagonist |
|
Definition
| due to the partial antagonist effect of opioid agonist/antagonist you cannot overdose b/c more you take than more antagonist also binding to sites. |
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|
Term
| What side effect is possible with agonist/antagonist |
|
Definition
|
|
Term
| what agonist/antagonist can be given to reverse fentanyl dperession but preserves the analgesia effect of fent |
|
Definition
| nubain!!! give 10-20mg iv to reverse fentanyl dpression on ventilation due to nubain's antagonist effect. but it will maintain analgesia! |
|
|
Term
| what is the ceiling dose for nubain |
|
Definition
|
|
Term
| Is nubain more or less potent than morphine |
|
Definition
| equal potency nubain = morphine |
|
|
Term
| Is butophanol (stadol) good for acute or chronic pain |
|
Definition
| Acute pain > chronic pain |
|
|
Term
| What are the major S/E of stadol (butorphanol) |
|
Definition
| ATTENUATES OPIOID AGONIST ACTIVITY so you get more sedation, nausea and respiratory depression |
|
|
Term
| what opioid agonist / antag causes attenuation of opiooid agonist |
|
Definition
|
|
Term
| can narcan cross the placenta is this relevant |
|
Definition
| CROSS PLACENTA! CAN CASUE FETAL DEMISE due to fetus withrawing and having increase SNS ect.. |
|
|
Term
|
Definition
| 30-45 min so you need to constantly redose b/c more opioids have doa that are longer |
|
|
Term
| what is the dose of narcan to reverse opioid induced resp depression and analgesia |
|
Definition
|
|
Term
| membrane phopholipids are broken down by ___ to arachidonic acid |
|
Definition
|
|
Term
| Arachidonic acid is broken down into what two groups |
|
Definition
1. Prostaglandins
2. Leukotrienes |
|
|
Term
| prostaglandins are made from? |
|
Definition
| cyclooxygenase enzymes that break down arachindonic acid to form prostaglandins. |
|
|
Term
| what are the negative effects of blocking the cox enzymes by drugs like nsaids |
|
Definition
1. gastric ulceration
2. decreased renal perfusion
3. bleeding |
|
|
Term
| Cox 1 is associated with while Cox 2 is associated with |
|
Definition
Cox 1:
1. GI mucosal integrity
2. Platelet function
3. Renal function
Cox 2:
1. Pain
2. Fever
3. Inflammation |
|
|
Term
| Name four Cox-2 selective inhibitors |
|
Definition
1. celcoxib
2. rofecoxib
3. valdecoxib
4. parecoxib |
|
|
Term
| inhibition of cox 1 or cox 2 is associated with many of the adverse side effects of NSAIDS |
|
Definition
| Inhibition of Cox 1 is associated with the adverse side effects of NSAIDS. B/c by inhibiting Cox 1 you have platelet inhibitiong and therefore more bleeding, you have more acid production nad decrease renal perfusion. |
|
|
Term
| Whats the bad with selective Cox 2 inhibitors |
|
Definition
|
|
Term
| 10 mg of morphine = ___ mg of toradol |
|
Definition
| 30mg toradol = 10 mg of morphine |
|
|
Term
| what is the triad of toradol |
|
Definition
Avoid toradol in:
1. asthmatics
2. pts with nasal polyps
3. ASA allergy |
|
|
Term
| most common side effect of ASA is |
|
Definition
|
|
Term
| ulceration of the GI related to NSAIDs can cause a loss of how much blood daily |
|
Definition
| 3-8 mL of blood loss / day |
|
|
Term
| platelet inhibition of asa lasts how long |
|
Definition
| life of the platelet which is 7-10 days |
|
|
Term
| how does acetaminophen work |
|
Definition
| by central inhibition of prostaglandin synthesis |
|
|
Term
| how is acetaminophen metabolized |
|
Definition
in liver via:
1. conjugation
2. hydroxylation |
|
|
Term
| Treatment of tylenol overdose is with |
|
Definition
|
|
Term
| how long do you have to protect liver from failure of tylenol overdose |
|
Definition
| need to give acetylcysteine within 8 hours of overdose. |
|
|
Term
| what are the signs and sx of ASA allergy |
|
Definition
1. vasomotor
2. laryngeal edema
3. bronchospasm
4. CV collapse |
|
|
Term
| What two NSAIds related drugs can cause or induce bronchospasms via what mechanisms |
|
Definition
| ASA and Toradol. via release of leukotrienes |
|
|
Term
| ASA causes platelet dysfunction due to what mechanism |
|
Definition
| inhibition of thromboxane formation |
|
|
Term
| ASA overdose manifests as |
|
Definition
1. seizures
2. hyperventilation (Due to acidosis from ASA) |
|
|
Term
| The earliest sign of overdose from ASA is |
|
Definition
|
|
Term
| treatment of overdose of asa is |
|
Definition
1. diuretics (preserve kidneys)
2. sodium bicarb (to treat acidosis) |
|
|
Term
| Which NSAID does NOT cause renal failure with chronic use |
|
Definition
| ASA hence why we give it daily to heart patients without that worry |
|
|
Term
| the hallmark sign of tylenol induced nephropathy is |
|
Definition
| renal papillae and papillary necrosis |
|
|
Term
| versed is only lipid soluble if the ring is open or closed? For this to happen what needs to be done |
|
Definition
| CLOSED. So to be closed versed needs to be in a pH >4.0. |
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|
Term
| the faster the onset of versed is directly proportional to what characeristic |
|
Definition
|
|
Term
| versed can't be given to pregnant people because it is associated with what defect |
|
Definition
| cleft lip palate in baby if given in first trimester |
|
|
Term
| the E1/2 of valium compared to versed |
|
Definition
Versed: 1-4 hours
Valium: 21-37 hours |
|
|
Term
| the most potent amnestic of benzo drugs is |
|
Definition
|
|
Term
|
Definition
|
|
Term
| how long does it take for flumazenil to work |
|
Definition
| 1-3 minutes but last an hour |
|
|
Term
| give flumazenil in increments of? Max dose of? |
|
Definition
| 0.2mg /min. Max dose of 3mg in adults |
|
|
Term
| side effects of flumanezenpil |
|
Definition
| 1. anxiety 2. increased ICP 3. redevelop seizures 4. nausea and vomiting |
|
|
Term
| what is the pka of a drug mean |
|
Definition
| it is the ph of the solution when the drug is 50% ionized and 50 non-ionized |
|
|
Term
| if you're in ECT and what to locate seizure foci what is a good drug to use to sedate the patient |
|
Definition
| methohexital which is a barbiturate |
|
|
Term
| Barbiturates work via ____ receptors in this part of the brain |
|
Definition
| GABA receptors in the reticular activating system. also targets the glutamate and adenosine receptors. |
|
|
Term
| most importnat factor determining barbiturate districution is this |
|
Definition
|
|
Term
| early awakening after one time dose of barbiturates is related to what property |
|
Definition
|
|
Term
| the most prominent site of redistribution of barbiutrate is to what area of the body |
|
Definition
|
|
Term
| thiopental is primarily metaoblzied in |
|
Definition
|
|
Term
| long use of barbiturates is associated with |
|
Definition
| enzyme induction. So increase metabolism as a result of increase enzymes of drugs like anticoagulants, dilantin, TCA, and endogenous corticosteroids, and vitamin k |
|
|
Term
| Enzyme induction can persist after d/c of a barbiturate for how long |
|
Definition
|
|
Term
|
Definition
a genetic disease that results in excess porphyrins since the person lacks the specific quanity of enzymes to transform these prophyrins. High concentrations of porphyrins results in neurological and dermatological sx.
Sx: severe abdominal pain, vomiting, neuropathy, mental changes, HTN and tachy. |
|
|
Term
| what triggers porphyria exacerbations |
|
Definition
1. sulfonamides
2. sulfonylureas
3. barbiturates
4. systemic antifungals
5. ketamine
6. etomidate
7. flagyl
8. anticonvulsants: dilantin, valproate, |
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|
