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Intervenous Drugs > IV drugs Hall > Flashcards

IV drugs Hall Flashcards

1
Q

How Succinylcholine metabolized

A

by plasma cholinesterase

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2
Q

Metabolism of atracurium & Cisatracurium

A

by Hofmannn elimination & ester hydrolysis

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3
Q

Vecuronium & rocuronium metabolism

A

Hepatic & biliary excretion, limited renal excretion 10-25%

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4
Q

The only NMB excreted in urine are?

A

the long acting NMB; d-tubocuraine, pancuronium, doxacurium, & pipecuronium

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5
Q

Of the long acting NMB, which one is the most eliminated by renal?

A

Pancuronium (80%), the others are 70%, and D-tubocuriane has little liver excretion which makes it the least excreted by renal.

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6
Q

Are IV anesthetics safe in prophyrias?

A

Yes to most drugs, local anesthetics are avoided to avoid the confustion if neurologic complications devopls in postop period.

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7
Q

What special attention should be paid for in prophyria noninduciable form (non-drug induced)?

A

avoid excessive pressure or irritation to skin (during mask ventilation or taping, IV cath….) because their skin is very friable.

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8
Q

What are selective vs non-selective B-adrenergic receptors?

A

Propranolol, nadolol, pindolol & timolol.

B1 selectives are; Esmolol & metoprolol.

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9
Q

What is the preferred anti-emetic medication in Parkinson disease patients?

A

Zofran. Drugs that can produew extrapyramidal effects are C/I such as droperidol, promethazine, & thiethylperazine & metoclopramide

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10
Q

Succinylcholine is more resistance to MG or mysthenic syndrome (Eton-Lambert syndrome)?

A

MG (they have fewer Ach Recp, which occupied by Ab’s, however they are more sensitive to NDNMB).
Patients with Mysthenic syndrome are sensitive to both DNMB & NDNMB

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11
Q

Why succunylcholine is CI in ptn’s with Duchenne’s, Hunttingto’s?

A

_ risk of rhabdo, hyperkalemia, & cardiac arrest. CI in hunttingtons because these ptn’s have decreased plasma cholinesterase and can prolong response of succ

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12
Q

Dopamine dose effect?

A

0.5-3 ug/kg/min -> renal vasodilation & increase RBF.
3-10 ug/kg/min -> above effect + B-adrenergic.
10-20 ug/kg/min -> Beta & alpha
> 20 ug/kg/min -> Alpha predominate.

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13
Q

Which IV anesthetic changes from water soluble to lipid soluble upon interning exposure to blood pH?

A

Midazolam.

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14
Q

What is the max dose for epi to avoid ventricular arrhythmia?

A

5 ug/kg.

In patient undergoing halothane anesthesia are more sensitive to ventricular arrhythmia and dose should be < 2 ug/kg.

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15
Q

Anticholinesterase drug that crosses BBB?

A

Physistigmine; makes it useful in treating central anticholinergic syndrome (also called postop delirium, or atropine toxicity).

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16
Q

MOA of ketamine?

A

Interact with NMDA recp also monoaminergic, muscarinic, opoid recp as well as voltage sensitive Ca ion channels.

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17
Q

Which opioid has antcholenergic properties?

A

Meperidine.
its structully similar to Atropin, in contrast to other opoids it can cause tachycardia. its metabolites (normrperidine) a CNS-stimulant and can cause delirium & seizures esp in RF patients and long exposure.

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18
Q

Direct-acting sympathomimetic drugs?

A

Dobutamine, Dopamine, Epi, Isoprpterenol,Methocamine, Norepi, Phenylephrine

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19
Q

Indirect-acting sympathomimetic drugs?

A

Amphetamine & Mephentermine

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20
Q

Indirect-acting & some direct sympathomimetic drugs?

A

Ephedrine & Metaraminol

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21
Q

Opioid that cause greatest myocardial depression with large dose?

A

Meperidine.
it rarely cause bradycardia but can cause tachycardia with high doses. a decrease in contractility seen with large doses maybe related to local anesthetic properties.

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22
Q

Ketamine effects?

A

1) Hypertonus purposeful movements.
2) Increased salivation.
3) Amnesia.
4) Analgesia (Somatic > visceral).
5) + sympathetic (increase pulm artery pressure, HR, CO, myocardial o2 requirement & bronchodilation).

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23
Q

Ketamine metabolism?

A

by liver ctyochrome P-450 enzymes to norketamine, which is as potent as ketamine.

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24
Q

IV anesthetic can cause myocardial depression?

A

Thiopental. by decreasing ca influx into myocardial cells.

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25
Q

What NMB should be avoided in patients taking Echothiophate eye drops for ttx on glucoma?

A

This drug inhibits acetylcholinesterase, therefore succinylcholine & mivacurium should be avoided to avoid prolongation of their affect. its recommended to wait 3 wks after stopping Echothiphate.

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26
Q

In TOF stimulation, how much reduction of twitch height is a good indicator for intubation?

A

at 90-95%

if there is single twitch, the twitch height is depressed at least 85%, 2-4 twitches 70%-85% depression is seen.

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27
Q

Name the 2 major chemical classes of NDNMB?

A

Aminosteroids (-onium drugs) & Benzylisoquinolinium (-urium)

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28
Q

Histamine release by which NMBs?

A

1) Mivacurium
2) Atracurium ( with rapid and >2 doses administration).
3) D-Tubocuronium
4) Succinylcholine

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29
Q

Termination of norepi achieved by …?

A
  • 80% by re-uptake into postganglionic sympathetic & reenters storage vesicles for future release. (small amount undergo metabolism by MAO instead oof storage)
  • 20% diluted by diffusion away from receptors & can go circulation, finally metabolized by COMT in liver.
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30
Q

The incidence of ketamine emergence delirium can be decreased by administering … ?

A

Midazolam 5 minutes before induction.

Atropin & droperidol may increase ketamine emergence delirium if given periopertively.

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31
Q

How much increase in K after succinlycholine administered in RF patients?

A

~ 0.5 mEq/L which is similar in normal patients.

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32
Q

Name few drugs that enhance NDNMB?

A

Volatiles, IV local anesthetics, CCB, dntrolene, Mg, aminoglycosides antibiotics, litium.

Calcium dose not, in fact it antagonizes Mg.

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33
Q

Will patients with hyperparathyrodisim enhance NDNMB?

A

No, Hypercalcemia decreases sensitivity to NDNMB and shortens its duration of action.

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34
Q 
Following medications are not recommended to DC periopertively due to
Clonidine ...
BB ....
MAOI inhibitors ....
TCA ....
A
  • Rebound hypertenstion can develop after DC clonidine & BB.
  • Risk for suicide with DC MAOI (-), keep in minde certain meds interact with MAOI (-) such as meperidine (ms rigidity & hyperpyrexia, and ephedrine (exaggerated hypertensive response).
  • Withdraw sx can occur from DC chronic TCA therapy (such as malaise, chills, coryza & ms aching).
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35
Q

Since atracurium metabolized by Hoffmann & plasma choliinesterase, will ptn’s with atypical pseudocholinesterase experince prolonged paralysis after administration?

A

No. the plasma chollinesterase is different from pseudocholinesterase that metabolize succinylcholine.

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36
Q

If both cicatracurium and atracurium metabolized by Hoffmann elimination (pH & temp dependent) & ester hydrolysis, why atracurium not preferred in RF ptn’s compered to cicatracurium?

A

Atracurium also metabolized by plasma cholenisterase and its metabolite (Laudanosine) can pass BBB and cause CNS stimulation . this metabolite is kidney and liver dependent for excretion. Cicatracurium is more potent and has lower levels of laudanosine at equivalent ms relaxation dose

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37
Q

Pretreatment with NDNMB attenuate which side effects of succinylcholine?

A

Cardiac dysrhythmias, elevation of intragastric pressure & ICP, or mylagia can be attenuates them bu t not eliminates them.
However, Increase K, MH, or prolonged Ms paralysis from abnormal pseudocholinesterase are not attenuated by pretretment.

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38
Q

Antibiotics potentiate NMB?

A

1) Aminoglycosides (neomycin, streptomycin, gentamicin, & tobomycin).
2) Lincosamines (Clindamycin, & lincomycin).

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39
Q

Antibiotics would not affect NMB?

A

Erythromycin, tetracyclines, penicillins, & cephalosporins.

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40
Q

Name anticholinesterase commonly administered with atropin/glycopyrrolate, and which one is fastest?

A

Endrophonium (1-2 min) > neostigmine (7-11 min) > Pyridostigmine (16 min).

Because Atropin has faster action then glyco, Endrophonium used with atropin. if for example glyco given with endrophonium, a marked bradycardia will initially develop.

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41
Q

When is peak time after injury is a risk for hyperkalemia after succinylcholine administration?

A

10 - 50 days after initial injury and may persist for 6 months or more.

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42
Q

The most common S/E of flumazenil is …?

A

Nausea & Vomiting.

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43
Q

Whats the best combination of anticholenergic drugs (Atropi, glycopyrolate) with cholegergic drugs (Endrophonium, neostgmine, pyridostigmine)?

A

Depends on onset of action, the goal not to give a faster anticholenergic drugs than cholenergics and avoid marked bradycardia.

  • Glycopyrrolate with Neostgmine (7-11 min)/pyridostigmine 16 min).
  • Atropin + Edrophoniumv (1-2 min)
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44
Q

What are anesthetics that are contraindicated in patients with prophyria?

A
  • Barbiturates
  • Etomidate -> potentially porphyrinogenic in animals
  • BZDs (diazepam)
  • Anagisics (ketorolac, pentazocine)
  • Hydonation anticonvulsants.
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45
Q

What is the first step if etomidate accidentally injected in artery?

A

Observe.

Although it causes pain on IV injection ~80%, it dose not result in detrimental (harm) effects to artery.

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46
Q

The combination of dentrolene and verapmil risk for?

A

Hyperkalemia.

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47
Q

What makes fentanyl faster then morphine?

A

its more lipid soluble. it rabidly redistributed from brain to inactive site (lipid tissues).

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48
Q

What is Azerotrope term refer to?

A

Mixture of 2 volatile anesthetics.

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49
Q

Volatile agent that is avoided in prolonged closed cranium procedures?

A

Enflurane & Desflurane-> they increases CSF secretion but decreases its absorption.

Halothane: decreases CSF secreation & increases its absorption.

Isoflurane: no effect on secretion but increases its absorption

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50
Q

What makes (RO)curonium a unique advantage then other NDNBM?

A

Its rapid onset (Rapid Onset = ROcuronium)
1.5-3 minutes with 0.3 mg/kg (other NDNMB ~3-7 min).
a larger dose 0.6 mg/kg the onset reduced to 1-1.5 min

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51
Q

What is the effect of acute hypokalemia on NMB?

A

Hypokalemia causes hyperpolarization and this cases resistance to DNMB and increase sensitivity to NDNMB.

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52
Q

What NMB causes significant release of histamine?

A

D-tubocurarine. (can result in significant hypotension and that is why is not given in large doses).

in general succinyl and benzylisoquinolinium (attracurium but not cisattracurium or doxacurim) risk for histamine release.

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53
Q

DUMBBLESS are symptoms of …. and treated with …?

A

Cholinergic stimulation (increased Acho levels) that occur with anticholinesterase poisoning leading to parasympathetic nerves system activation (Diarrhea, urination, Miosis, Bronchoconstriction, Bradycardia, Lacrimation, Emisis, Salivation, Sweating). ttx with Atropin. (Pralidoxime added to ttx nicotinic effects of elevation of Acho at neuromascular junction of Muscles such as wakness and apnea

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54
Q

Flumazenil can cause seizures in patients with …?

A

On chronic BZDs for long term sedation, and in patients with serious antidepressent overdose (twitching, rigidity, wide QRS, hypotension).

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55
Q

Duration of action of Flumazenil? route of administration?

A

0.7-1.3 hours (which is shorter than midazolam 2-2.5 hours). IV, and its poorly absorbed orally.

56
Q

What is the percentage of occupied NM receptors that is adequate recovery from NMB? and what test or physical exam consist to it?

A

50% or less.

sustained tetanus at 100 Hz (but its painful) Head lift for 5 seconds in supine position

57
Q

What medication can prevent tachyarrythmias in WPW syndorme patients?

A

Droperidol.
in addition to its antidopaminergic effect, it protect against epinephrine-induced dysrhthmias by blocking alpha receptors and mild local anesthetic effect.

58
Q

where is Pseudocholinesterase (plasma cholinesterase) production and what its half life?

A

Produced by liver (and that explaines its reduction in advanced liver disease patients). Half life ~ 8-16 hours.

It metabolizes ACho at NM junction and certain drus (succinyl, mivacurium & ester-type loval anesthetics)
significant prolongation of NMB occur with succinyl if this ezyme is deficient more than 75% of it normal levels.

59
Q

MoA of Ketorolac?

A

It is a NSAIDS, which inhibits the enzyme cyclooxygenase which is necessary for prostaglandin synthesis. PGs are mediators of pain and inflammation and act at the site of injury, therefore its inhibition at the level of peripheral sensory receptors.

60
Q

What are the steroid drugs that has only glucocorticoid activity?

A

Triamcinolone (Kenalog), Betamethasone (Celestone), Dexamethasone (Decadron).

They have 0 Mineralcorticoid activity (Na retaining potency)

61
Q

2 NDNMB are not affected by age for its spontaneous recovery (Recovery Index “RI” which is the time needed for a twitch hieght from 25% to 75% of the baseline height)?

A

The 2 NDNMB that are not liver or kidney dependent for elimination (Aging reduces renal & hepatic function), which they are atracurium & cisatracurium (they are broken down in plasma).

62
Q

What is the predominant effect of succinyl on cardiovascular system in adults vs children? tachycardia or bradycardia?

A

in general; 1) histamine release. 2) +autonomic ganglia which stimulates the release of neurotransmitors at para & sympathetic system. 3) direct + postjunctional cardiac muscarinic receptors.

The effect on heart rate (dierect + cardiac muscarinic) is variable and depends on non dominant autonomic system; when sympathetic tone is high (in CHILDREN) BRADYCARDIA will develop. when parasymathtic tone is high (in ADULTS) TACHCARDIA will occur mostly esp with second dose

63
Q

Why Succinyl is contraindicated in children for routine tracheal intubation?

A

Risk for Hyperkalemia 2/2 undiagnosed Duchenne nuscular dystrophy

64
Q

From most to least (faster to slower) muscles to be blocked by NMB after administration?

A

Central muscles of airway (larynx, jaw, diaphragm) = orbicularis oculi > abductor muscle of thumb.

  • When oebicularis oculi maximally relaxed = intubation is optimal.
  • when adductor thumb function return to normal, the diaphram amd layngeal muscles will have recovered.
65
Q

What effect of volatiles on NMB and reversal agents?

A

it enhances NMB and slows the reversal agents. (therefore, vapor % should be decreased at the end of case to help ensure adequate reversal).

66
Q

Meoeridine is CI in patients who is taking which anti-Parkinson medications?

A

Selegiline (MAOI) because of the risk of excitation (agitation, rigidity, hyperpyrexia) or depression (hypotension, depressed ventilation, coma).

67
Q

Side effects of Etomidate? and which one is the most reported unsatisfactory by patient?

A 
N/V (modt reported, its even greater than thiopental).
pain in injuction
thrombophelbitis
myoclonic movements
hiccups.
68
Q

A NMB that can inhibit the re-uptake of NE by adrenergic nerves?

A

Pancuronium.
it can cause tachycardiaa, increase CO & MAP by 1) vagolytic effect. 2) NE release. 3) decrease re uptake of NE by adrenergic nerves.

69
Q

MoA Dantrolene? and its side effects? which one is most common SE?

A

it directky affect Musles by decreasing the amount of calcium released from sacroplasmic reticulum which reselt in decrease excitation-contraction coupling needed for contraction.

  • Ms weakness (most common).
  • N/diarrhea & blurred vision.
  • if given IV, it can cause diuresis due to the co-administered mannitol to make IV solution isotonic
  • Hepatitis & pleral effusions with chronic oral use (in case of ttx patients with ms spasticity 2/2 UMN lesion)
  • Hypothermia may occur but it is mostly due to cooling (ice pack) process, therefore cooling should be stopped with temp reaches 38 C.
70
Q

When is metformin induced lactic acidosis is a risk for patients going to elective surgery?

A

if it was taken within 48 hours of surgery.

71
Q

Recovery of neuromuscular function after NDNMB occurs when ….?

A

the drug diffuses from nueomuscular junction into plasma to be metabolized and eliminated from body.

Termination = diffusion
Elemination = liver/kidney or other specific process
72
Q

Which opioid is not reversed by naloxone and therefore iin cases where respiratory depression opioid indiced can be challenging?

A

Buprenorphine (Buprenex) a mixed agonist-antagonist opioid. because of its strong affinity (50 times greater than morphine) and slow dissociation from receptor, it has prolonged duration (>8 hours) and shows resistance to Naloxone.

73
Q

Which IV anesthetics has the highest association with Nausea & vomiting?

A

Etomidate ~ 40%

74
Q

Off the intravenous dilators medications, one has no affect on systemic artery dilatation? all has affect on venous, pulm artery, CO, & systemic artery (except one)

A

Niric oxide affect only pulm artery.

others (nitrogylcerin, nitroprusside, phentolamine, milrione, and PG E1) has affect on systemic artery along with venous & pulm artery affect.

75
Q

Termination of succinyl by ….?

A

diffusion into extracellular fluid. (psudocholinesterase present in blood, not at the NMJ, that also explains why large dose required for intubation).

76
Q

Dexemdetomidine onset? peak? and affect on BP, HR, and respiratory?

A

Onset; <5 minutes
Peak: 15 minutes
HR: Bradycardia and can cause sinus arrest.
BP: It increased BP initially (due to + peripheral alpha) then in 15 minutes returns to normal and is followed by 15% decrease in BP by an hour (due to CNS alpha + overriding peripheral affect).
RS: minimal, with high doses (1-2 mcg/kg/min) it can decrease TV but without RR changes.

77
Q

Whats the advantage of Fospropofol over propofol?

A

Its water soluble that is prodrug converted to propfol after IV administration.
Because its a water soluble, the problem of lipid vehicle (pain on injection, hypertriglceridemia, risk of pulm embolism and sepsis) are gone.

78
Q

What are the tow symptoms of morphine therapy that are not at risk to develop tolerance?

A

Miosis & constipation.

Analgesia, RS depression, nausea, ephoria, and sedation are subject to tolerance after 2-3 weeks of morphine therapy.

79
Q

H2 receptor antagonists (cimetidine, ranitidine, famotidine, niatidine) side effects to consider when given as premedication?

A

Its given to increase gastic fluid pH before induction (above 2.5) to decrease the incidence and severity of lung damage if aspiration occur. but its not commonly applied to patients with very high acidic fluid (obese, symptomatic GERD)

side effect occurs more in patients with renal/hepatic dysfunction and if administered as IV.

  • Bradycardia (H2 effect on heart).
  • Elevation of liver enzymes (reversible)
  • Confusion and delayed awakening (it crosses BBB).
  • It binds to C P-450 and Impairs metabolism on propofol, diazepam, lidocaine.
80
Q

Antidote or treatment of Sarin poisoning?

A

Atropin.
its a poisin gas acts on nerve cells same as organophosphate and blocks nerve endings from allowing muscle to contract (it act by inhibiting acetylcholinesterase enzyme).

Pralidoxime added to remove the poison from acetylcholinesterase enzyme.
BZD often administered to counter the effect of poison on GABA system.

81
Q

Compare Alfentanil to fentanyl in onset and potency?

A

Alfentanil less potent but has more rapid onset (1.5 minutes) and shorter duration due to redistribution to inactive tissue sites & rapid hepatic metabolism (96% cleared within 1 hr).

82
Q

Clonidine MoA?

A

alpha 2 AGONIST. it stimulates central adrenergic receptors and decreases the sympathetic response.

  • Decreases MAC & extremes in BP during anesthesia.
  • reduce opioids requirement
  • Can decrease postanesthetic shivering. (IV 75 mcg)
  • decrease periop MI when given preop and 4 days postop
83
Q

Stiff chest syndrome can develop with large & rapid dose of opioid to the point cant venitalte, how would you reverse it?

A

Muscle relaxant or naloxone.

choosing Ms relaxant may be desired if pain control needed for surgery.

84
Q

Which type of metabolic acidosis can be caused by propofol infusion syndrome?

A

High anion gap acidosis due to lactic acidosis

85
Q

Dibucaine test results? and paralysis time with succinyl

  • Normal …
  • Heterozygous …..
  • Homozygous ….
A
  • 80%, up to 10 min paralysis.
  • 50-60%, 30 min
  • 20%, >3 hours.
86
Q

Remifentanil breakdown mechanism? elimination? and dosage?

A

by nonspecific plasma and tissue esterases. eliminated t 1/2 less than 6 minutes.

  • 0.05-0.1 mcg/kg/min for sedation.
  • 0.05-2 mcg/kg/min for analgesia.
  • 1 mcg/kg for loading dose (or 0.5 mcg/kg if premedicated with BZDs) given over 60-90 seconds prior infusion.
87
Q

Whats the max single dose of lidocaine given by infiltration?

A

4.5 mg/kg

7 mg/kg with epi.

88
Q

Causes of postop shivering and risk? medication options to treat?

A

Unclear mechanisim but commonly caused by anesthetics, hypothermia, transfusion reactions, and pain.

risk for increase O2 consumption & making monitoring difficult.

Clonidine, dexmedetomidine, propfol, ketanserin, tramadol, physostigmine, Mg sulfate, meperidine.

89
Q

Main disadvantage of sugammadex?

A

Not affective against Benzylisoquinolinium relaxants (-urium).

90
Q

Treatment of accidental intra-arterial thiopental injunction?

A
  • dilution with saline or drug produce vasodilation (lidocaine, papaverine, phenoxybenzamine).
  • intra-arterial injection of heparin, or urokinase.
  • stellate ganglion or brachial block if the affected artery in UE.
91
Q

At which rate of sodium nitroprusside would be a risk for cyanide toxicity? and what are first signs?

A

> 2 mcg/kg/min (esp 10 mcg/kg/min for 10 min).

  • resistance to the hypotensive effect of nitroprusside
  • metabolic acidosis.
  • increased mixed venous PO2 values.
92
Q

What the effect of patients on TCA on IV anesthetics?

  • MAC?
  • Vassopressors?
A

the drug inhibits reuptake of released Norepi & erotonin.

  • Increase MAC due to available neurotransmitters in CNS.
  • Exaggerates BP after indirect vassopressors (ephedrine). the risk of hypertensive crisis is greatest with acute TCA treatment (14-21 days).
93
Q

Careful taken with adminstering Meperidine in patients taking MAOIs or TCA?

A

With MAOIs because the possibility of inducing seizures, hyperpyrexia or coma.

94
Q

The most rapid action insulin?

A

Lispro & Aspart “the -log -> Humalog/Novolog” (15 minutes)

95
Q

Which Beta Blockers and treat hypertension & tachycardia in asthmatic patients?

A

The selective B1 blockers (Atenolol, acebutolol, betaolol, bisoprolol, emolol, metoprolol) however, they are not always 100% selective and so some B2 blockade may occur and bronchoconstriction my still be possible.

96
Q

MoA of alpha & beta BLOCKERS?

A

Alpha1 : decrease PVR but leads to reflex tachy ( phentolamine).
Beta 1: Cardiac muscles -> decrease HR & BP
Beta2: smooth muscles such as bronchus, leads to bronchoconstriction & vasodilation

97
Q

Remifentanil metabolism?

A

By nonspecific plasma & tissue esterase (t1/2 <6 min) and not affected by liver/renal failure.

98
Q

Pain after injuction is least with ?

A

Thiopental & ketamine.

common with diazepam, etomidate, methohexital & propofol.

99
Q

Alpha blocker examples?

A

Alpha 1: prazosin
Alpha2: yohimbine.
Nonselective: phentolamine & Phenoxybenzamine

100
Q

Which alpha blocker is irreversible?

A

Phenoxybenzamine. even with massive smpathomimetics are ineffective until its terminated by metabolism.

101
Q

Treatment of symptomatic bradycardia induced by excessive beta blocker?

A
  • Atropin first.
  • if not effective then beta agonists: if selective B1 used then try Dobutamine. if nonselective used then try Isoproterenol.
  • Glucagon is drug of choice for BB overdose (initial dose 1-10 mg then infusion of 5 mg/hr).
  • Aminophylline and Ca chloride can be tried.
  • finaly a pacemaker is the ultimate treatment.
  • Dopamine is not recommended because the high dose of dopaime that is needed to reverse the blockade is significant that cause induce vasoconstriction through alpha stimulation.
102
Q

Dantrolene therapy expected consequence?

A

Diuresis.
It is formulated with mannitol (300 mg mannitol/20 mg danttrolene) to avoid AKI or failure caused by myoglobinuria from MH-associated muscle breakdown

103
Q

Dose Dantrolene affect heart or cause cardiac dysrhythmis?

A

little effect, however in fulminant MH, dysrhythmias may occur but this is related to preturbations in pH & electrolytes.

You must know to avoid verapmil in this situation because it can interact with dantrolene an dmay produce hyperkalemia & MI (instead using lidocaine is safer).

104
Q

Differences between atracurium & cic-atracurium?

A

They both have same molecular weight, both undergo hoffman elemination & form laudanosine, and neither undergo liver/renal degradation.

but atracurium resales histamine and undergo metabolism via ester hydrolysis catlayzed by nonspecific plasma esterase (not psudocholinesterase).

105
Q

Opioids withdrawal onset?

A

6-12 hours with short-acting
72-84 after long acting.
Heroin 5-10 days for and methadone is way longer.

106
Q

Opioids withdrawal s&s?

A

Craving, restlessness, anxiet, irritability, jerkiny legs, N/V,vabdominal cramps, muscle aches, insomnia,sympathetic stimulation (tachy, hypertension, mydriasis, diaphoresis), & hyperthermia.

  • seizures not expected and if it occurs then suspect withdrawal from other medications (barbiturates) or underlying seizure disorder.
107
Q

Which IV anesthetic associated with adrenal suppression?

A

Etomidate.

it inhibits conversion of cholesterol to cortisol with single dose and can persist up to 24 hours.

108
Q

Anesthetic associated with thrombosis, phlebitis and has specific antidote?

A

Diazepam and that why it replaced with midazolam.

109
Q

Anesthetic causes pain on injection with hemodynamic instability?

A

Propofol.

Diazepam & Etomidate can cause it but without HD instability.

110
Q

IV anesthetic decreases ICP and which increases ICP?

A

Thiopental, etomidate, & propofol and can either decrease or unchange with BZDs.

Ketamine increase ICP and should be avoided in intracranial mass lesion or elevated ICP patients.

111
Q

IV anesthetic associated with lactic acidosis?

A

Propofol infusion syndrome (> 75 mcg/kg/min) if infused for > 24 hours.

112
Q

What are the early signs of propfol infusion syndrome?

A

Tachycardia.

113
Q

What are later signs of propofol infusion syndrome?

A

metabolic acidosis, bradyarrythmias, and MI.

114
Q

What is the cause behind propfol infusion syndrome?

A

Impaired fatty acid oxidation in the mitochondria

115
Q

What are side effect of Minoxidil?

A

Pulm hypertension, pericardial effusion, cardiac tamponade, and hair growth.

116
Q

Medication that causes alpha and beta blockade?

A

Labetalol

117
Q

Which catacholemine lowere SVR at low doses and increase SVR at high doses and CO increase at all doses?

A

Epi.
it also tends to decrease RBF, and oth the all 5 catacholamines it causes the most significant effect on metabolism (hyperglycemia for example).

118
Q

Which catacholamine at low doses increaase RBF but at high doses it decreases RBF?

A

Dopamine.
at low doses it act like Epi
at high dose it accts like NorEpi

119
Q

Opioid receptor types in

  • Spinal & supraspinal
  • increase prolactin release
  • depress respiration
  • constipation
  • Dysphoria & diuresis (inhibition of ADH)
  • ADH stimulation
A
  • Mu, Kappa, delta
  • Mu1
  • Mu2 & delta
  • Only Mu 2
  • Kappa
  • Mu 2
120
Q

Phase 1 vs phase 2 blockade of DNMB?

A

Phase 1: occurs with depolarization of postjunctional membrane.

Phase 2: blockade occur when the postjunctional membrane have become repolarized but do not response to normal actylcholine (often called desenstization) and it occurs with doses >2-4 mg/kg. the response to twitch monitor is similar to NDNMB.

121
Q

When post-tetanic facilitation occur?

A

With NDNMB & phase 2 DNMB

122
Q

Sustained response to tetanic stimulation occur …? (decrease height but no fade)

A

With phase 1 DNMB.

where marked fade occur with NDNMB & phase 2 DNMB.

123
Q

TOF response with DNMB vs NDNMB?

A

All twitches same but decrease in height with DNMB. where in NDNMB marked fade.

124
Q

TOF ratio in phase 1 vs phase 2 vs NDNMB?

A

> 0.7 …… <0.4 ……. <0.7

125
Q

Factors increase MAC?

A

Anything that increase metabolic function of the brain like hyperthermia or in patient with increase brain catecholmines (MAOIs, TCA, cocaine, acute amphetamine)

chronic alcohol

126
Q

Factors decrease MAC?

A

Factors that decrease brain metabolic function (IV anesthetics, acute alcohol, narcotics, hypothermia).

chronic amphetamine

127
Q

Will hyper/hypothyroidism affect MAC?

A

No. however the cardiovascular effects of volatile is altered with thyroid function.

128
Q

Lithium effect on MAC?

A

Decreases it due to decreasing brain catecholamine.

129
Q

Pregnancy effect on MAC?

A

Decrease. due to progesterone sedative effect. pregnant also sensitive to local anesthetics.

130
Q

Anemia & hypoxia effect on MAC?

A

Both decreases it.

131
Q

Main differences between glycopyrolate and atropin/scopolamine?

A

Glyco do not cross BBB therefore has no sedative or amnesic effects and therefore no CNS toxicity (central anticholenergic syndrome). it also dose not prevent motion induced nausea, neither mydriasis or cycloplegia

What is left out of anticholenirgic effect that glyco dose are; decreasing airway secretions (by inhibiting salivation), can cause tachycardia, and decrease LE sphincter & gastric pH, also increases temp (by inhibity sweating).

132
Q

What anticholenergic has the least effect on inhibiting salivation and decreasing airway secretions?

Best at sedation?
Best increasing gastic pH?
Produces Mydriasis & cycloplegia when applied topical

A
  • Atropin
  • Scopolamine ) atropin (glyco dose not cross BBB).
  • None! they all do but need way higher doses than clinically used.
  • Scopolamine & atropin (glyco dose not)
133
Q

Why advising patients who receive scopolamine to not rub their eyes and you should wash your hands after applying it?

A

scopolamine can cause mydriasis & cycloplegia if applied topically and since touching the pad your at risk to have unilater mydriasis.

134
Q

Ketamine dosage that won’t be a risk for dissociative??

A

5 mcg/kg/min

135
Q

β1-selective blockers?

A 
Acebutolol 
Atenolol
Betaxolol
Bisoprolol
Celiprolol
Esmolol
Metoprolol
Nebivolol
136
Q

B antagonist meds nmonics

A

Medications starts with letter A to M are selective

Carvidolol and labetalol has alpha blockade too

Intervenous Drugs (13 decks)

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