Pharmacology

Question 1

Suggamadex dosing is based on:

Answer 1

actual body weight, not ideal body weight.

Question 2

When would you dose suggamadex at 16 mg/kg

Answer 2

After giving 1.2 mg of Rocuronium. KIM that suggamadex should not be the solution in a can’t intubate, can’t ventilate situation.

Question 3

Can naloxone work if the OD is due to too much intrathecal opioid? Hydrophilic or lipophilic move more rapidly? It compared to IV for pruritus? N/V? Can tolerance develop to intrathecal opioids as well?

Answer 3

yes. LIPOphilic moves more rapidly. More itching in Intrathecal compared to IV. N/V same for IV and intrathecal opioids. Tolerance can develop for intrathecal opioids.

Question 4

Duration of rocuronium and vecuronium (SINGLE DOSE) are dependent on what? What about an infusion

Answer 4

single dose vec and roc: redistributiion.

Infustion of vec or roc: 1/2 time of elimination (inversely proportional to volume of distribution)

Question 5

NDNMB in kids: do they last longer or nah? And NDNMB vOd is dependent on what?
So, lets go over this: Kids and lean muscle tissue?
hepatic metabolization? Renal clearance?

Answer 5

they last longer!
Non-depolarizing neurmuscular blockers in general last longer in children. volume of distribution of NDNMB depend on ECF. Although infants have more ECF, and therefore larger vOd, they still need smaller dosing because of the following:
Kids have less lean muscle tissue
Kids have underdeveloped liver=not as much metab of vec (primarily hepatic). There’s a strange metabolite of vec that must be renaly cleared, and they have decreased renal clearance.

Question 6

So, if you need to decrease the dose of vec or roc, what about sux?

Answer 6

To obtain appropriate onset of action, succinylcholine doses are increased in infants due to an increased volume of distribution. However, volume of distribution is not a major contributor to duration of action for non-depolarizing relaxants.

Question 7

Can diffusion hypoxia occur under hyperbaric conditions?

Answer 7

Yes

Question 8

Desflurane in a hyperbaric chamber?

Answer 8

turn it down. Desflurane has a special vaporizer that is heated to 39 degrees Celsius and 1500 mm Hg so that a constant concentration is delivered. When the ambient pressure is increased the partial pressure delivered will increase, resulting in anesthetic overdose if compensation is not made.

Question 9

Does Isoflurane need to be turned down in hyperbaric chamber?

Answer 9

Isoflurane and sevoflurane do not require dial adjustments at varying ambient pressures because they compensate for changes in temperature and pressure to maintain a constant partial pressure. Therefore the dialed concentration does not need to be adjusted as the partial pressure output will be the same.

Question 10

N20 and hyperbaric?

Answer 10

Be careful, because bad things can happen, as N20 is allowed to get to 1 mac. Hyperbaric chambers allow the delivery of 1 MAC of N2O but this is not without consequence as decompression sickness, diffusion hypoxia, and induction reactions such as opisthotonos, hypertension, tachycardia, and muscular rigidity can occur.

Question 11

How does acetazolamide work? Which metabolic derrangements would you see? Acetazolamide and phosphate? Potassium?

Answer 11

Acetazolamide is a potent inhibitor of carbonic anhydrase, which results in wasting of sodium and bicarbonate in the proximal tubule, with subsequent diuresis and also alkalinization of the urine. This results in a hyperchloremic metabolic acidosis.This means, the patient would be hyperchloremic
Hypophosphatemia can happen
Hypokalemia can happen

Question 12

What are some cardiac meds that can be given IM?

Answer 12

Examples of cardiovascular medications that can be given IM include, but are not limited to: atropine, glycopyrrolate, ephedrine, epinephrine, phenylephrine, and hydralazine.

Question 13

Can Norepi be given IM?

Answer 13

NOPE!

Question 14

T/F, Norepi is alpha&raquo_space;»Beta

Answer 14

TRUE

Question 15

When do EKG changes with magnesium begin? And what does Mg do agaiN? what are those EKG changes?

Answer 15

at 6-12. Vasodilates and relaxes uterus (tocolytic) . EKG changes: PR prolongation and QRS widening

Question 16

At what Mg level do you lose DTRs?

Answer 16

2

Question 17

Bioavailability and IV meds:

Answer 17

As a general rule, the bioavailability of any intravenous medication is 1, meaning 100% of the medication given reaches the circulating blood volume.

Question 18

Oral midazolam and bioavailability in adults and chilren’

Answer 18

less than 50% in adults, and less than 30% in kids

Question 19

What type of drug can cross the placenta?

Answer 19

Placental transfer of medications is facilitated by high lipid solubility, low molecular weights and a high maternal to fetal drug concentration gradient

Question 20

What is the maximum dose of Lido with epi that can be administered?

Answer 20

7 mg/kg. And remember to look at the mL of the % to find out exactly how many mg you are giving. And you can use the 1:200,000 epi.

Question 21

Reasons to NOT use bicarbonate in cardiac arrest.

Answer 21

Patient can’t excrete it because they’re not really breathing. Administration of sodium bicarbonate can result in several adverse effects during cardiac arrest. It can cause extracellular alkalosis, which will shift the oxygen-hemoglobin dissociation curve to the left making unloading of oxygen more difficult. It produces hypernatremia and hyperosmolarity. It may inactivate administered catecholamines such as epinephrine by exacerbating venous acidosis. Bicarbonate may compromise cerebral perfusion pressure (CPP) by reducing systemic vascular resistance.

Question 22

When is the only time you would use bicarbonate in cardiac arrest?

Answer 22

There are only a few special circumstances where sodium bicarbonate therapy may be appropriate during CPR, such as known hyperkalemia and known tricyclic antidepressant overdose. For these situations, a dose of 1 mEq/kg is used and therapy should be guided by bicarbonate concentration or calculated base deficit from blood gas measurement. This patient does not have a history of renal failure and has no reason to be hyperkalemic. He also does not have a diagnosis of depression thus TCA overdose is less likely.

Question 23

When to give epi in CPR:

Answer 23

After defibrillation, epinephrine would be an appropriate medication for cardiac arrest. In the setting of an unshockable rhythm (asystole or PEA), epinephrine should be given as early as possible

Question 24

When would you give lidocaine in CPR?

Answer 24

If amiodarone isn’t around

Question 25

Normally, what does the Ed50 and Ed =95 mean? What is the ED95 for non-depolarizing neuromuscular blockers?
What is the pre-curization dose?

Answer 25

The ED50 is the median effective dose that will produce an effect in 50% of the population that it is administered to. ED95 would refer to the median effective dose in 95% of the population, but unfortunately this terminology has a different meaning for nondepolarizing neuromuscular blocking drugs.

The ED95 for nondepolarizing neuromuscular blocking drugs is the dose that causes 95% twitch suppression in 50% of the population. The dose used for tracheal intubation is typically twice the ED95,
The correct precurarization dosage for any nondepolarizing agent prior to succinylcholine administration is 10% of the ED95 dose. For rocuronium, this would be 0.03 mg/kg.

Question 26

How do you know when nitroprusside is starting to get toxic?

Answer 26

Sodium nitroprusside administration has the potential for causing toxicity due to the accumulation of its metabolic byproducts: cyanide and thiocyanate. Common presenting signs of cyanide toxicity include elevated PVO2, tachyphylaxis to SNP, metabolic acidosis, and flushing. Symptoms of thiocyanate toxicity include hypoxia, nausea, tinnitus, muscle spasm, disorientation, and psychosis.

Question 27

What type of drug is phenytoin? it is also similar to:

Answer 27

Phenytoin is an antiepileptic drug with antiarrhythmic properties mediated by blockade of voltage gated sodium channels. Similar to lidoaine

Question 28

Patients who have been receiving echothiophate eye drops are at risk for

Answer 28

significant prolongation of succinylcholine’s effects for up to 2 weeks after therapy is discontinued.

Question 29

Pseudocholinestrase results in problems with whichdrugs?

Answer 29

Remifentanil and esmolol are metabolized by nonspecific blood and tissue esterases and would not be affected by a pseudocholinesterase deficiency. Succinylcholine, mivacurium, ester local anesthetics (2-chloroprocaine, tetracaine, procaine), cocaine, and heroin are metabolized via hydrolysis by pseudocholinesterase, also known as plasma cholinesterase and butyrylcholinesterase. A deficiency or defect in this enzyme would result in decreased metabolism and prolonged effects of the substance.

Question 30

What do hydroxyethyl startch products do?

Answer 30

Hydroxyethyl starch products are known to cause coagulopathy that is typically related to the molecular weight of the specific infused solution and the amount infused. The exact mechanisms are still being elucidated but several factors are known: a dilution of the coagulation factors occurs secondary to increased plasma volume, a decrease in factor VIII (and potentially other factors), and an acquired fibrinogen deficiency.

Question 31

Complications of hydroxyethyl startch products?

Answer 31

Some studies have shown a marked expression of glycoprotein IIb/IIIa on activated platelets and an acquired fibrinogen deficiency (C). All hydroxyethyl starch solutions decrease clot strength and prolong clot formation when measured on thromboelastometry; the degree depends on the specific solution (A). Molecule size and speed of degradation will influence the degree of perioperative blood loss; typically larger, less degraded products result in larger blood loss.

Another major concern with hydroxyethyl starch products is renal dysfunction.

Question 32

What is neuroleptic malignant syndrome? Who gets it? How is it treated?

Answer 32

Neuroleptic malignant syndrome clinically looks similar to MH. Patients often develop a fever and have sustained muscle rigidity. Patients with neuroleptic malignant syndrome (NMS) often develop rhabdomyolysis. NMS is often seen in patients who are taking antipsychotic medication. These patients may have received significant changes in dose or the addition of another antipsychotic medication prior to developing NMS. Treatment for NMS is supportive. Dantrolene has been used but its efficacy is unclear. Bromocriptine a dopamine agonist has been shown to have some effect in the treatment of NMS

Question 33

Which conditions is malignant hyperthermia associated with?

Answer 33

MH is associated with several conditions including: central core disease, multiminicore disease, King Denborough syndrome, and hyper/hypokalemic periodic paralysis

Question 34

Should caffeine halothane test be used as a screening test?

Answer 34

NO d/t low incidence of MH in general population.

Question 35

What is central core disease?

Answer 35

Central core disease is an autosomal dominant myopathy that occurs because of a mutation in the RYR receptor. Of MH patients, 23% have a mutation in the RYR1 receptor. Central core disease often goes undiagnosed for several years before weakness and developmental delays become apparent. Patients often have spine and pelvic weakness with foot deformities. Central core disease has a strong association with MH and thus MH precautions should be taken.

Question 36

INverted t waves can be seen when?

Answer 36

nverted T waves (A) can be seen in several conditions such as hypokalemia, hypocalcemia, and myocardial ischemia.

Question 37

Look at photo of electrolytes and their effects on EKG

Answer 37

OKay

Question 38

Precedex and its affect on EEG waves

Answer 38

Dexmedetomidine produces low-frequency, high amplitude EEG waves and BIS readings consistent with general anesthesia under normal sedation conditions.

Question 39

Side effects of methadone:

Answer 39

Side-effects of methadone include respiratory depression, QT prolongation, nausea/vomiting, constipation, and biliary spasms. Methadone has a black-box warning for:

1) Death from respiratory depression
2) Cardiac effects
3) Arrhythmias (torsades de pointes)

Question 40

Before putting a patient on methadone they must:

Mgmt of patients on methadone

Answer 40

Patients on methadone should have an annual ECG, routine urine drug screening, and a maximum dose of 100 mg per day. Dose adjustments are rarely needed for patients with end-stage renal disease.
Management of a patient on methadone:
- Start with low doses; titrate slowly
- Initial ECG to assess QTc. Repeat ECG 30 days after methadone initiation. Then, repeat ECG annually (A).
- Routine urine drug screen (D).
- Recommended maximum dose of 100 mg per day (C).

Question 41

Lipophilic vs hydrophilic opioids-which one causes more nausea? watch time in both of them?

Answer 41

Use of epidural lipophilic opioids (e.g. fentanyl) is associated with a decreased risk of nausea and vomiting and possibly pruritus compared to epidural use of more hydrophilic opioids (e.g. morphine).

TrueLearn Insight : The ASA recommends a longer period of monitoring for respiratory depression following a single neuraxial dose of morphine compared to fentanyl. For lipophilic opioids: continual monitoring for at least 20 minutes following administration and then at least hourly monitoring for the next two hours. For hydrophilic opioids: at least hourly monitoring for the first 12 hours and then monitoring at least every two hours for the next 12 hours.

Question 42

Can suggamadex help reerse sux?

Answer 42

Sugammadex has no affinity for succinylcholine or benzylisoquinolinium neuromuscular blocking drugs (e.g. cisatracurium) and will not reverse their effects

Question 43

The two MOST IMPORTANT adverse effects of suggamadex: ___ & _____ along with others (but are not considered most important)

Answer 43

The two most important adverse effects of sugammadex include anaphylaxis/hypersensitivity reactions and potentially severe bradycardia. Other important adverse effects include, but are not limited to arrhythmias, tachycardia, hypotension, prolongation of PT/INR and aPTT, and increased risk of unintentional pregnancy due to inactivation of hormonal contraceptives.

Question 44

Deep hypothermic circulatory arrest (DHCA) is used for several different surgical procedures, mostly for ____.
Advantages and disadvantages of DHCa:

Answer 44

Aortic arch surgery It provides major benefits: completely bloodless surgical field due to cardiac arrest (thus no need for intrusive clamps or cannulae) and a significantly decreased brain metabolism that permits longer periods of circulatory arrest. Although these benefits can be significant, the disadvantages are many: edema formation, coagulopathy, organ damage, and longer cardiopulmonary bypass times (to allow for safe rewarming).

Question 45

TArget temperature of DHCA:

Answer 45

Usually the target temperature is between 15 to 19 degree Celsius.

Question 46

Most important factor in reducing cerebral ischemia

Answer 46

The use of barbiturates during deep hypothermic circulatory arrest is controversial. It was previously thought that administration of barbiturates before initiation of DHCA was beneficial to help decrease the risk of cerebral ischemia by further lowering the cerebral metabolic oxygen consumption. This has been called into question and some studies have concluded that it may result in more damage. Hypothermia is the most important factor for decreasing cerebral ischemia.

Question 47

Flumanzenil and benzos-do people like them?

Answer 47

Flumazenil should not be administered for non-iatrogenic or unknown overdoses due to risk of seizure, particularly if the patient has taken additional medications (e.g. alcohol, tricyclic antidepressants) concomitantly. Many feel that the risks of flumazenil usually outweigh any benefit. Further, flumazenil does not consistently reverse central respiratory depression due to benzodiazepines, and over half the patients in a large multicenter study experienced re-sedation after use.

Question 48

Who is sugammadex cool for? Who is it not cool for?

Answer 48

Sugammadex is FDA approved for reversal of neuromuscular blockade by rocuronium or vecuronium in adult patients undergoing surgery. It is contraindicated in patients with known hypersensitivity to sugammadex or its components. Other patient populations or situations in which the use of sugammadex is not recommended and/or not FDA approved include: pediatric patients, patients with severe renal failure, reversal of NBDs other than rocuronium and vecuronium, and for reversal following rocuronium or vecuronium administration in ICUs.

Question 49

Sugammadex is not compatible with which drugs, and need to be flushed?

Answer 49

Sugammadex is physically incompatible with ondansetron, ranitidine, and verapamil and should not be co-administered with these medications. If sugammadex and one of the above drugs are to be administered in the same line, the line should be adequately flushed with saline between administration of the two drugs.

Question 50

Methylene blue and hypotension-what do you have to watch out for?

Answer 50

Methylene blue can block the vasodilatory effect of nitric oxide by inhibiting guanylate cyclase. However, it is usually considered a last-line medication for vasoplegic shock. Also it is contraindicated in patients receiving SSRIs because it is a MAO inhibitor and can cause serotonin syndrome.

Question 51

Intraop hypotension assoc with ACEi/ARB therapy: what to do?

Answer 51

Intraoperative hypotension associated with perioperative continuation of ACEi/ARB therapy: IV hydration, phenylephrine, ephedrine, glycopyrrolate are the early treatments. Refractory hypotension can be reversed with either norepinephrine or vasopressin, but only norepinephrine will do so while maintaining cardiac output and gastric perfusion.

Question 52

Nitric oxide-does it veno or vasodilate more? Does it cause systemic hypotension-why or why not?

Answer 52

It is primarily an arterial dilator (A) by promoting smooth muscle relaxation in arterioles. The venous vascular beds are less sensitive to the effects of NO. Unlike other commonly used intravenous vasodilators, inhaled NO has very limited systemic effects (B) as erythrocytes within the pulmonary circulation rapidly inactivate the gas.

Question 53

Which Local anesthetic crosses the placenta the least?

Answer 53

2-chloroprocaine has the least amount of placental transfer of all local anesthetics because it is rapidly metabolized in the plasma by plasma cholinesterase.

Question 54

Caution with lidocaine and preggo?

Answer 54

Caution should be considered with certain local anesthetics in pregnancy due to the potential for ion trapping. Fetal-maternal lidocaine ratio can reach 1.2 during fetal acidosis, which increases the risk of fetal local anesthetic toxicity. This effect can become more important with large epidural doses, obstetrical blocks (e.g. pudendal, paracervical), or intravenous lidocaine used at intubation. This effect is most likely to be clinically significant in the premature fetus, which has increased blood-brain barrier permeability

Question 55

Be careful with ketamine in which patients?

Answer 55

Ketamine has intrinsic sympathomimetic activity, which can lead to an increased sympathetic outflow. It should be avoided or used cautiously in patients with pheochromocytoma as the sympathetic response can be exaggerated.

TrueLearn Insight : Ketamine should also be used with care in chronically ill patients, as these patients have frequently exhausted their endogenous catecholamine stores. In this circumstance, ketamine’s direct negative inotropic effects can lead to a decrease in blood pressure and cardiac output because there will be no compensatory sympathetic response.

Question 56

Renal compensation for respiratory acidosis: acute vs chronic:

Answer 56

enal compensation for respiratory acidosis occurs at a slow rate. In acute respiratory acidosis, serum bicarbonate levels increase 1 mEq/L for each 10 mm Hg rise in PaCO2. If the respiratory acidosis is chronic, bicarbonate levels increase between 4-5 mEq/L for each 10 mm Hg rise in PaCO2. Hence, in this scenario, early compensation for the acute respiratory acidosis is seen with a bicarbonate level of 26 mEq/L for the PaCO2 level of 70 mm Hg.