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Pharmacology II > Medication Exam > Flashcards

Medication Exam Flashcards

1
Q

Midazolam Class

A

Benzodiazepine

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2
Q

Midazolam Glucuronidation leads to

A

active metabolite 1- hydroxymidazolam

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3
Q

Efficacy measures intrinsic ability of a drug to produce clinical effects. What is the intrinsic ability of Midazolam ?

A

Full effect

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4
Q

In selected patient ____or opioid maybe added to propofol for continuous IV sedation .

A

Midazolam

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5
Q

Cerebral blood flow velocity changes in______direction with changes in PCO2 in the presence of propofol and _______

A

Parallel ; Midazolam

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6
Q

At equal sedation level _____produces same degree of memory impairment as ______ , while ______produces less and fentanyl produces none.

A

Propofol ; Midazolam; Thiopental

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7
Q

Cerebral vasomotor response is preserved during propofol and Midazolam Anesthesia in humans . True or False.

A

True

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8
Q

Imidazole nucleus renders etomidate and Midazolam water soluble at ___pH and Lipid soluble at ___pH

A

Acidic; physiologic

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9
Q

Most commonly used benzo in the perioperative period is…because …

A

Midazolam ; because diazepam and Lorazepam have a prolonged context 1/2 life

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10
Q

Which is the only benzo used for prolonged administration when rapid recovery is desired ?

A

Midazolam

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11
Q

___in contrast with barbituates and propofol is unable to produce isoelectric EEG.

A

Midazolam

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12
Q

Although clinical significance is unclear, This drug’s inhibition of platelet aggregation reflects conformational changes in platelet membranes

A

Midazolam significantly inhibits platelet aggregation

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13
Q

Midazolam is a —-soluble drug with a ——ring that contribute to its stability in ——solution and rapid metabolism

A

Water soluble; imidazole ; aqueous

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14
Q

Which benzo has replaced diazepam in the periop ?

A

Midazolam

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15
Q

with Midazolam and other benzo the amenesic effect is _____than the sedation effect .

A

More

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16
Q

Midazolam is unlike other benzo because it has a

A

Subtituted imidazole ring

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17
Q

What happens to Midazolam at physiological pH in the bloodstream

A

90% of midazolam is unprotonated and lipid soluble

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18
Q

Does Midazolam cause IV discomfort ? And compatible with what ?

A

No IV or IM discomfort , ok with LR, can be mixed with acidic drugs i.e: opioids and anticholinergic

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19
Q

Midazolam PO has substantive first pass effect : meaning

A

Only 50% of PO dose of Midazolam reaches the systemic circulation

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20
Q

Midazolam absorption

A

Rapid absorption in GI tract

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21
Q

Midazolam BBB

A

Crosses BBB but has a slow effect site equilibrium compared to thiopental and propofol

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22
Q

Midazolam and plasma protein binding

A

Extensive ; 98%; its protein binding is independent to its plasma concentration

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23
Q

Midazolam has an extensive protein binding yet a short DOA( like diazepam ) why ?

A

98% protein binding , but high lipid solubility = fast high redistribution from the brain to inactive tissue

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24
Q

Metabolism of Midazolam is done by the

A

Hepatic and small intestine cytochrome P450 CYP3A4 to active and inactive metabolites
1 hyrdoxymidazolam is rapidly glucorunated to 1 hydroxymidazolam glucuronide and is then excreted by the kidneys .
4- hydroxymidazolam is the other active metabolite ..but so little

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25
Q

1 hydroxymidazolam has ____ the activity of the parent drug

A

1/2

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26
Q

Midazolam metabolism is slowed in the presence of which other drugs ?

A 
Cimetidine 
Erythromycin 
CCB
Antifungal meds 
* they inhibit P-450 enzymes = unexpected CNS depression !!
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27
Q

What medication inhibits the hepatic clearance of Midazolam

A

Fentanyl

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28
Q

Hepatic clearance of Midazolam is ____greater than Lorazepam and ____greater than diazepam

A

5; 10.

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29
Q

What is the elimination halt time of Midazolam and what can prolong it .

A 
2 hours (1.9) 
May be doubled in elderly= bc of decreased hepatic blood flow
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30
Q

What happens to Volume distribution of elderly and obese ?

A

It’s increased

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31
Q

Elderly and Obese have increased Vd of Midazolam . True or False ?

A

True

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32
Q

Midazolam has extensive hepatic metabolism . Therefore renal failure will not alter Midazolam’sm

A

1) Vd
2) t1/2
3) clearance

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33
Q

Paradoxical excitement of versed . Give

A

Flumazenil . Benzo antagonist .

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34
Q

CRMO2 and CBF effects of Midazolam

A

Decreased
the same as propofol and barbituates .
Acceptable induction alternative to barbiturates in patients with increased ICP

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35
Q

Midazolam and anticonvulsion

A

Potent anticonvulsant; good status epilecticus

Can outcome in incomplete ischemia but no neuroprotective properties .

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36
Q

We know Midazolam is ok to use in increased ICP but it can increased ICP when

A

Severe head trauma + ICP is less than 18 ( open circles )

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37
Q

Benzodiazepines and swallowing reflex and upper airway activity

A

Decreased

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38
Q

What benzo can you give for paradoxical vocal cord motion ?

A

0.5mg- 1 mg of Midazolam

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39
Q

Midazolam induction dose

A
  • 0.1 - 0.2 mg/Kg IV
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40
Q

Does CO increase or decrease with Midazolam

A

Neither. BP drops because Midazolam causes decreased SVR.

Actually improved CO in CHF

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41
Q

Does Midazolam prevent BP and HR changes due to Intubation ?

A

No.

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42
Q

Oral Midazolam syrup concentration , and effects

A

2mg/ml.syrup
Max 20 mg PO( 1mg/kg)
Sedation + anxiolysis at dose 0.25mg/kg plus minimal ventilatory and O2 sat effects
0.5mg/kg to children 30 minutes before induction= sedation + anxyiolysis w/ no delayed awakening .

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43
Q

How long before surgery recommended to give PO Midazolam

A

20 minutes before induction

But 10 minutes produces best antregrade amnesia

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44
Q

Midazolam Sedation dose ( regional or therapeutic procedures )

A

1 - 2.5 mg IV
Onset : within 1 minute ( 30s-60s)
DOA: 15 - 80 minutes
Peak 1/2t : 6 minutes(5.6)

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45
Q

Midazolam + opioids or other CNS depressant =

A

Exaggerated ( synergistic ) Midazolam -induced ventilation depression ( decreased Hypoxic drive ) esp COPD

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46
Q

Hypnotic effect of midazolam on the elderly .

A

Increased sensitivity to the hypnotic effects in the elderly .
Also increased pharm variability

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47
Q

Midazolam seldom for induction but you would give how much

A

0.1- 0.2mg/kg over 1 minute

1-3 minutes before giving it , give 50 - 100 mcg of Fentanyl to facilitate onset of unconsciousness

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48
Q

When Versed caused increased CV responses it’s because of

A

Peripheral vasodilation

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49
Q

Yes! You can supplement use ____to supplement opioids, Inhaled anesthetics, and propofol

A

Midazolam

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50
Q

Emergence time from Midazolam infusion is increased in the presence of

A

Elderly
Obese
Liver disease

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51
Q

Butorphenol given with Fentanyl =

A

Will partly reverse the fentanyl analgesia in pts taking chronic opioids

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52
Q

Redistribution of drugs from Highly perfused tissue to fat =

A

Offset of drug effect following a bolus or IV infusion of lipid soluble drugs like fentanyl

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53
Q

Which drugs have pulmonary 1st pass effects that exceed 65% of the dose

A

1) Fentanyl
2) Sufentanil
3) Alfentanil
4) Meperidine
5) Lidocaine
6) Propranolol

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54
Q

Most abundantly expressed P450 isoform is

A

CYP3A4
Opioids( Fentanyl, alfentanil, Sufentanil) , LA, Anti-histamines( terfenadine), Benzodiazepines, Immunosupressant(Cyclosporin)

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55
Q

Fentanyl peak effect after injection is

A
  1. 5 minutes

* Morphine is 90 minutes .

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56
Q

Opioids decrease MAC of inhaled anesthetic required to suppress noxious stimuli . 1/5 ng/ml of fentanyl plasma concentration decreases MAC by

A

50%

After the initial reduction in MAC there is limited benefit from additional fentanyl

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57
Q

Clearance of high extraction drugs fentanyl and sufentanil is minimally influenced by

A

Changes in the rate of metabolism

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58
Q

In elderly , decreased co= decreased hepatic blood flow + decrease hepatic enzyme =

A

Prolonged DOA in lidocaine and Fentanyl

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59
Q

Fentanyl and morphine____effect on somatosensory sensory evoked potential

A

Decreases SSEP . Less than volatiles though !

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60
Q

On a neuro aspect ECG changes support a ____% dose reduction of opioid for the elderly

A

50

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61
Q

Droperidol + fentanyl =

A

Neuroleptalnagesia .

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62
Q

Droperidol does what to Fentanyl ?

A

Does not enhance it’s analgesia but prolongs it’s DOA

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63
Q

Derivatives of Meperidine

A

Fentanyl , Sufentanil, alfentanil

When pt get Meperidine and derivatives with MAOI = adverse reactions (toxicity )

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64
Q

Fentanyl first pass uptake is

A

Variable, up to 90%

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65
Q

BB + nifedipine and high dose fentanyl.

A

Patients tolerate high dose fentanyl , and do not show cardiac depressive effects when using verapamil added

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66
Q

BB blocker and high dose fentanyl

A

No alteration in CV response even in presence of pre existing BB

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67
Q

Which drugs prevent tachycardia vs increase SBP in tracheal intubation

A

Fentanyl, Lidocaine and Esmolol ( Attenuates the HR )

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68
Q

Pulmonary First pass uptake is decreased in patients taking

A

Propranolol chronically .

= 2 to 4 times as much fentanyl enters the systemic circulation

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69
Q

What drugs protect against digitalis- enchance automaticity

A

Fentanyl , Enflurance , to a lesser extent Isoflurane

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70
Q

PONV is much less than inthratecal midazolam than with inthratecal …

A

Fentanyl

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71
Q

After administration of Fentanyl epidural in parturient , the opioid in breast milk is

A

Negligible

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72
Q

Early depression of ventilation in Fentanyl happens in _____

A

2 hours

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73
Q

After epidural fentanyl , it peaks in the CSF in ____minutes

A

20 minutes

Sufentanil- 6 minutes

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74
Q

Lidocaine dose

A

1 - 1.5 mg/kg IV for indication

Class 1b antidysrrhythnmic

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75
Q

Lidocaine 0.5% + Epinephrine Submucosally =

A

Doubles the dose of epinephrine necessary to provoke ventricular dysrhythmia.

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76
Q

Mixing propofol with lidocaine can lead to

A

Coalescence of oil droplet= risk of PE

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77
Q

Accidental intraarterial injection of barbituates . What do you do?

A

1) Immediately try to dilute the drug
2) prevent arterial spasm with vasodilator such a s lidocaine or papaverine
3) general measures to sustain adequate blood flow

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78
Q

Adding 0.5 mcg/kg of dexamedetomidine to lidocaine =

A

Improves quality of anesthesia and post op analgesia without side effects

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79
Q

Lidocaine produces analgesia by

A

Suppressing activity of sodium channels in neurons that respond to noxious stimuli . Preventing nerve conduction and pain transmission . VGSC play a role in neuronal excitability . Abolish pain temporarily

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80
Q

Lidocaine was synthesized as an ____local anesthetic in 1943. Produces more____than procaine.

A

Amine , rapid , intense , longer lasting conduction blockade than procaine. Cardiac antidysrhythmic , effective topically = that’s why all LA are compared to Lidocaine

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81
Q

Lidocaine Potency, onset, duration , max dose , pka, protein binding , toxic plasm concentration

A 
Potency : 1 
Onset : rapid 
DOA : 60- 120 minutes 
Max single dose for infiltration: 300mg 
Pka: 7.9 
Protein Binding : 70%
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82
Q

Intrisic vasodilation of lidocaine influences potentcy. Lidocaine more vasodilation than mepivicaine =

A

Greater systemic absorption and shorter DOA of lidocaine .

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83
Q

Lidocaine has high uptake into the lung =

A

Rapid decreased in plasma concentration initially.

* the concentration also decreases bc of rapid distribution to heart , brain , kidneys( high perfused tissues )

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84
Q

What drug decreased plasma clearance of lidocaine

A

Propranolol

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85
Q

Anesthesia which may decrease the hepatic blood flow and hepatic disease can affect lidocaine metabolism how?

A

Decrease the rate of metabolism . Especially when volatiles are used

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86
Q

Liver disease and Lidocaine …

A

Elimination half time increase 5 folds

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87
Q

Lidocaine can cause depressed myocardial contractility without arrhythmia. True or False

A

True

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88
Q

The seizure threshold for lidocaine in related to

A

Serotonin. Accumulation of serotonin lowers the threshold for seizures for lidocaine, and prolongs the DOA of seizures

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89
Q

Lidocaine to pt with mexelitine ( antidysrhythmic) =

A

Lowers threshold for neurotoxicity

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90
Q

EMLA

A

2.5% lidocaine combined with 2.5% prilocaine cream

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91
Q

Onset of action of Lidocaine

A

1- 3 minutes

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92
Q

For spinal anesthesia using lidocaine , limit dose to

A

60 mg

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93
Q

Lidocaine and requirement for volatile drugs

A

Decreased volatile requirement

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94
Q

Dose of lidocaine to decreased cough reflex during tracheal intubation

A

> 2 mcg/ml

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95
Q

Stump pain but not phantom pain is temp diminished buy IV lidocaine

A

True

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96
Q

Lidocaine may _____defibrillation threshold

A

Increase

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97
Q

LA significant antibiotic effect

A

Tetracaine>Bupivicaine>Lidocaine

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98
Q

Tumescence

A

5L of subQ infiltration of 0.05 - 0.10% of Lidocaine with epinephrine 1: 100,000
Slow and sustained release of Lidocaine < 1.5mcg/ml peak at 12- 14 hours then decline gradually over the next 6- 14 hrs
Dose 35-55mcg/kg of highly diluted Lidocaine aka mega dose

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99
Q

Inhaled Lidocaine attenuates

A

Histamine related Bronchospasm

Mild bronchodilation but constriction in asthma patients

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100
Q

Treatment of PVC

A 
Lidocaine 
BB
CCB
Amiodarone 
Radioactive ablation
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101
Q

How much Lidocaine to suppress Ventricular dysthymia by digitalis

A

1-2mg/kg

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102
Q

Lidocaince, Diazepam and propanol can do what to Verapamil

A

Can increase the pharmacologically active unbound portion of verapamil

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103
Q

Lidocaine class IB. MOA

A

Less SCB than IA, shortens the duration of action potential and refractory period in normal heart

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104
Q

Lidocaine terminates Vtach

A

Yes

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105
Q

Lidocaine can decrease conduction in the

A

AV node and His- Purkinje

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106
Q

Etomidate is good for __(3 things)but terrible for(7things)______

A

Good for

1) hemodynamically unstable. Minimal CV effects
2) Lowers ICP and CBF and CRMO2
3) Status epilepticus : bc has anticonvulsant properties

Not good for

1) not a very good analgesic or anesthesic ( only 15 minutes )
2) Painful on injection
3) Suppression of adrenal function and immune system : inhibits cortisol
4) acute intermittent porphyria
5) high risk of PONV
6) do not give to patient with sepsis
7) Not for patient with hx of seizures . Activity of seizure Foci

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107
Q

MOA of etomidate

A

Interacts with specific GABAa , appears to decrease the rate of dissociation of inhibitory NT = increased DOA of GABA activated opening of Cl- channels= Hyperpolarization ( propofol and barbiturates do the same )

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108
Q

Etomidate change in BP and HR how ?

A

No change!!!

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109
Q

How is Etomidate unique among injected and inhaled anesthetics ?

A

It’s administered as a single isomer

Anesthetic effect is R + isomer which is 5 times more potent than the S - isomer

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110
Q

Etomidate effects on GABAa

A

Binds to a specific site on the protein and increases the affinity of the inhibitory NT GABA for these receptor
Increases GABA affinity to GABAa receptor

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111
Q

Steroid-induced psychosis is inhibited by which drug

A

Etomidate ( it enhances GABA receptor function)

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112
Q

Etomidate has a ____Vd, a _____Lipid solubility , and is a weak base

A

Large, moderate and is a weak base

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113
Q

What has abolished pain on IV injection of etomidate

A

It was changed to a fat emulsion from it’s previous preparation with 35% propylene glycol with pH 6.9
* but myoclonus still not changed

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114
Q

Is Etomidate a potent cerebral vasodilator?

A

No . it’s a direct cerebral vasoconstrictor.

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115
Q

Etomidate decreases Intraocular pressure same as which drug?

A

Thiopental , propofol

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116
Q

Etomidate is used when maintenance of spontaneous ventilatory response because

A

It stimulates ventilation independently of the medullary center

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117
Q

Spontaneous movement particularly myoclonus occurs in 50- 80 % of patients receiving

A

Etomidate . But this happens in the absence of premedication.

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118
Q

Albumin level effect on Etomidate

A

Low plasma albumin level= dramatic increased in unbound, active etomidate

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119
Q

Etomidate distribution

A

99% unionized at physiological ph ( pka 4.9, ph 8) = crosses lipid membranes easily, and rapidly peaks in brain within 1 minute.

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120
Q

Etomidate metabolism

A

Rapidly metabolized by ester hydrolysis( to carboxylic acid ester = now water soluble = now inactive ).
Hydrolysis by 1) hepatic P450 microsomal enzymes 2) plasma esterase

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121
Q

Etomidate elimination

A

Urine (86%) and small amount in bile (10-13% bile )
Half time 2- 5 hours. 5 times more clearance than Thiopental.
Etomidate is a high hepatic extraction drug

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122
Q

How to attenuate etomidate myoclonic activity

A

With premedication using an opioid

Ex: Fentanyl 1-2 mcg/kg IV or a Benzo

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123
Q

Etomidate produces analgesia. True or False?

A

False

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124
Q

Alternative drug to propofol and thiopental ( they decrease seizure duration) in patients undergoing Electroconvulsive therapy is…

A

Etomidate

125
Q

Etomidate and PONV

A

Increased risk when used for anesthesia induction.

Thats just a view but doesn’t actually show increased PONV when compared to propofol

126
Q

What is the main limiting factor of etomidate in it’s use for induction of anethesia ?

A

It has the ability to transiently suppress adrenocortical function= inhibits conversion of cholesterol to cortisol( inhibits 11 b-hydroxylase) = low cortisol . ( stress-free anesthesia )
So sepsis and hemorrhage patients need cortisol = do not give the etomidate !

127
Q

Etomidate vs propofol in 30 day mortality

A

Etomidate has increased 30 day mortality in non cardiac surgery pts

128
Q

Etomidate and allergy

A

It does not release histamine from mast cells

Low allergy risk .

129
Q

Patient with history of seizure , can you give them Etomidate. Why?

A

Try not to . Because etomidate disinhibits subcortical structures that normally suppresses extrapyramidal motor activity .

130
Q

What can explain myoclonus upon awakening with etomidate administration?

A

The extrapyramidal system emerge before the cortex that normally inhibits it .

131
Q

What can rapid injection fo Etomidate do to your ventilation

A

Apnea
Etomidate = low tidal volume ( vent depressant < barbiturates) but etomidate = increased frequency of breathing : the decreased tV is then offset
Etomidate ventilation effect is transient and only lasts 3- 5 minutes
Depression of vent by etomidate may be more frequent and more intense when combined with inhaled anesthetic or opioid

132
Q

Patient with no cardiac reserve , what to give for induction :

A

Etomidate

133
Q

Dose adjustment in elderly for etomidate

A

Decrease by 20%

134
Q

Total Volume distribution of propofol ( vast

A

5,000L

135
Q

Propofol IV maintenance

A

100- 300mcg/kg/min

136
Q

Propofol anti pruritic dose
Anti emetic Dose
Maintenance dose

A

10mg
10- 15 mg
100- 300mcg/kg/min

137
Q

How long can open bottle of propofol be used for. Why

A

6 hours

E. coli and Pseudomanas aeruginosas and Candice albican

138
Q

Patient movement , deepen the anesthesia with bolus of____ and that will do what to their recall

A

Bolus of propofol , the recall from short term memory will not go to the long term memory and patient will be amnestic

139
Q

Propofol infusion syndrome is

A 
>75mcg/kg/min
1) lactic acidocis 
2) Bradydysrhythmias 
3) Rhabdo 
Metabolic acidosis, severe refractory bradycardia(in children ), unexpected tachycardia on infusion ( adults )= look for metabolic lactic acidosis
140
Q

Propofol and BIS numbers for rapid recovers

A

Titrate propofol to 45 to 60 BIS then allow it to increase 60-75 in the last 15 minutes of surgery.

141
Q

Two drugs that increase SSEVP

A

Ketamine and etomidate

142
Q

Propofol and opioids lower the SSEVP , yes or no

A

Yes !

143
Q

Lowers threshold of vasoconstriction and Sweating

A

Propofol and Alfentanil.

144
Q

Propofol and platelet aggregation

A

1) Propofol is pro inflammatory
2) inhibits aggregation of platelets by inducing pro inflammatory lipid mediated thromboxane A2 and PAF
3) * does not affect the platelet function only the aggregation

145
Q

Propofol is antioxidant and resembles which vitamin?

A

E

146
Q

Prolonged profolol turn urine___ color because

A

Green;

Because of phenols in the urine

147
Q

Name of propofol chemical name

A

2, 6 diisopropylphenol

148
Q

Propofol onset duration and Clearance

A 
Onset: 30- 60 minutes 
DOA : 30- 60 seconds 
Duration 5- 10 minutes 
Clearance : Extrahepatic clearance in the lungs ( Apex) 
Liver P-450 , 
Clearance exceeds liver blood Flow
149
Q

Propofol anticonvulsant dose

A

> 1mg/kg

150
Q

Propofol more Myocardial Injury in Cardiac surgery patient than SEVO

A

True

151
Q

Does Propofol cause drug-induced spinal cord depression ?

A

No, volatile anesthetics do

152
Q

Propofol increases uterine contractility at anesthetic concentrations by how much ?

A

Only slightly

153
Q

Propofol airway protection .

A

Decrease pharyngeal contraction force . Thats we give it in laryngospasm

154
Q

Propofol and Parkinson’s

A

abolition of their tremors short term

155
Q

Ketamine decreases activity of what receptor

A

NMDA. It’s an NMDA antagonist
Other receptors it acts on : Mu Delta Kappa ( directly )
Anti Nociceptive because it acts on the descending inhibitory monoaminergic pain pathways

156
Q

Ketamine produces Delirium, Brondilation and emergence delirium because ….

A

Because its an ANTAGONIST at Muscurinic receptors

157
Q

Ketamine is administered as a racemic mixture …elaborate

A

The S+ enantiomer is more potent than the R-enantiomer and is less like to cause emergence delirium

158
Q

Doses of Ketamine

A 
Analgesia: 0.20- 0.50 mg/kg
Induction : 1-2 mg/kg IV
IM Induction : 4-8mg/kg 
0.3/mg/kg/hr = improves analgesia reduces opioid tolerance 
Post-Op infusion for pain : 1-2mgkg/hr
Concentration : 50mg : 1 ml *
159
Q

Ketamine can cause funky s/e :

A

Nystagmus

Sialhorrea

160
Q

Ketamine inhibits platelet aggregation along with

A

Propofol and Midazolam

But Ketamine : contributes to Known bleeding undergoing surgery

161
Q

Ketamine plus Nitrous =

A

Neurotoxicity .

162
Q

Intermittent treatment of ketamine for OCD

A

Decreases OCD

163
Q

Thiopental, Diazepam , or Midazolam blunt _____increased in Cerebral blood flow

A

Ketamine

164
Q

What type of anesthesia does Ketamine produce. Describe

A

Dissociation between of Thalamocortical and Limbic system.

165
Q

Dissociative Anesthesia of Ketamine resemble

A

Cataleptic state : eyes remain open with slow nystagmus gaze.
Various degree of hypertonus & skeletal movement independent of surgical stimulation

166
Q

Ketamine properties

A

Amnesic
Intense analgesic
Anticholinergic

167
Q

Ketamine + Heart that is Beta Blocked=

A

Heart Failure . Activate SNS = increase SVR = high afterload + BB reduced Myocontractility = HF
BB will decrease Ketamine induced increase in SBP and HR*

168
Q

Ketamine is a myocardial depressant, that myocardial depressant is unmasked with Patient with depleted catecholamine source .

A

That is true

169
Q

Ketamine + volatile or + Verapamil

A

Decreased BP

170
Q

Ketamine alone ( effects on BP )

A

Increased BP

171
Q

Ketamine Anesthesia is partially antagonized by

A

Anticholinesterase drugs

Think of Ketamine effects anticholinergic symptoms : emergency delirium , Bronchodilation, and the sympathomimetic

172
Q

Ketamine mine inhibits Plasma cholinesterase =

A

Prolong duration of Sux

173
Q

Atropine what type of muscurinic agonist

A

Broad spectrum

174
Q

Isoflurane induced decrease in Heart rate is attenuated by

A

Atropine and Pancuronium( because they are vagolytic )

175
Q

Propofol causes profound ______and _____ even in healthy patient treated with prophylactic IV anticholinergic

A

Bradycardia and asystole.

176
Q

Propofol attenuates the the heart rate response to IV _______ . What to give instead in case of proprofol induced bradycardia. Why?

A

Atropine . Even giving larger dose of atropine with not help
Give epinephrine instead bc it is a direct beta agonist
Propofol suppresses SNS activity thats why you have to give direct acting

177
Q

Atropine can ____spike of EEG

A

Decrease

178
Q

Atropine and Ketamine

A

Ketamine cause salivation + increase risk laryngospasm
Give antisialogogue but Glyco preferred over Scopolamine and atropine because the cross the BBB and may increase incidence of Ketamine emergence delirium

179
Q

Scopolamine is ____times more potent than atropine at decreasing the activity at the reticular activating system

A

100.

And 3 times more potent antisioliguoge

180
Q

IM atropine antisiologuoge dose

A

.4-.6 mg IM

Less effect than Scopolamine 0.3 - 0.5 mg IM

181
Q

Atropine Fever happens more in

A

Small children

182
Q

Opioid induced ureter tone and peristalsis increase can be reversed with anticholinergic

A

Atropine

183
Q

What is atropine effect on analgesia

A

Antagonizes analgesia

184
Q

Meperidine structurally resembles atropine . That is why

A

It has anti spasmodic effect and increased HR unlike other opiods
Causes Mydriasis ( not miosis like the others )
And caused dry mouth

185
Q

Atropine is effective at ____and ____ bradycardia

A

Treating and preventing

186
Q

Atropine should be paired with ? What dose ? And why ?

Anticholinesterase + anticholinergic agent in reversal of NMB

A

7-10 mcg/kg of atropine matches the onset of edrophonium 0.5-1mg/kg
Administer anticholisterases over 2- 5 minutes

187
Q

Glyco + Neostigmine

A

Glyco : 7-15 mcg/kg
Neo 40 - 70 mcg/kg
NEO max dose per Flood : 60-80mcg/kg

188
Q

Patient with pre existing cardiac disease, do you use atropine or glyco ?

A

Glyco preferred over atropine

189
Q

Drugs to treat dig toxicity

A

Phenytoin
Lidocaine
Atropine ( 35 - 70 mcg/kg IV)

190
Q

Timolol bradycardia and hypotension is refractory to

A

Atropine

191
Q

BB induced excessive bradycardia and hypotension should initially be treated with

A

7mcg/kg atropine

192
Q

Amiodarone prolongs QTc and causes Bradycardia that does not respond to

A

Atropine

193
Q

For 40 minutes Atropine can ____LES pressure and _____barrier pressure and ____resistance to reflux

A

Decreases, decreases , decreases .

* Glyco does it too for 1 hour

194
Q

Atropine opposes Reglan increased LES time . What dose

A

0.6mg/kg IV

195
Q

Pg 839

A

X

196
Q

Atropine bronchodilation is by inhibiting

A 
Muscurinic 3 (M3) 
like atrovent
197
Q

Atropine has sedative and amnesic action : true or false

A

True

198
Q

Atropine has the least antisiologuoge than

A

Glyco and scopolamine

199
Q

You should avoid _____in patients with Cystic Fibrosis

A

Atropine

200
Q

Avoid ____in beta blocked patients

A

Ketamine

201
Q

Propofol is a weak acid or weak base ?

A

Weak acid

202
Q

Propofol t 1/2

A

0.5 to 1.5 hrs . 30- 90 minutes
11.6 hours for thiopental
More rapid and complete awakening

203
Q

Cv effects of propofol m

A

Both BP and SVR are decreased
More ventilatory effect than Thiopental
Antiemetic via CTZ and the vomiting center : 10- 15 mg
Anticonvulsant : 0.5- 1 mg/kg
Antipruritic Dose : 10mg
Decreased cerebral blood flow and cerebral metabolism

204
Q

Propofol induction vs infusion which to use : LBW to TBW ?

A

Induction : Lean

Infusion : Total

205
Q

Which anesthetic is by TBW?(4)

A

Versed (except 50% dose reduced in elderly)
Fentanyl
Maintenance propofol
Sux

206
Q

Tylenol

A 
NMDA antagonist
Substance P 
nitric oxide 
NMDA 
Cox 3 
PG
Descending seratonergic pathways pain by ...
207
Q

Propofol receptor activation

A

GABAa and little glycine

208
Q

Low lipid emulsion version of propofol is

A

Ampofol 5% soybean and 0.6% egg lethicin

209
Q

Alternative lipid emulsion propofol preperation

A

Aquavan . Propofol sulfate progrug that results in propofol = no pain on injection but burning in genitalia

210
Q

Unconsciousness reached in how long with propofol

A

30 seconds

211
Q

What is the conscious dose of propofol?

A

25mcg- 100mcg/kg/min
Or
0.7mg/kg with 3 minute lockout using a pump = continuous IV sedation *

212
Q

Maintenance propofol

A

100- 300mcg/kg/min

213
Q

Antiemetic dose of propofol

A

10- 15 mg *** in the PACU
1- 1.5ml
Or
10 mg IV followed by 10mcg/kg/min to achieve antiemetic propofol plasma concentration

214
Q

Greater than 1 mg/kg of propofol has ____property

A

Anticonvulsant

215
Q

Metabisulfite is a preservative of generic propofol and cause

A

Bronchoconstriction in asthamatic and healthy patient .

216
Q

Propofol augments pressor response of

A

Ephedrine

217
Q

Norketamine

A

Demethylated by P450 enzyme of Ketamine

218
Q

Ketamine doses

A

Intrathecal : 5 - 50mg in 3 ml saline

219
Q

Ketamine dose in coronary artery Disease ?

A

Diazepam .5 /mg + ketamine .5mg/kg then 15 -30 mcg/kg/min

220
Q

TIVA Ketamine + proprofol better than

A

Prop and Fent .

221
Q

Reversal of opioid tolerance dose of Ketamine

A

0.3mg/kg/hr

222
Q

Ketamine blocks NMDA and mentally leads to

A

Less depression and OCD.

And less restless leg syndrome by the way !

223
Q

Mechanically vented neonate and ketamine

A

2mg/kg of ketamine = dexcreased ant. Fontanelle pressure (ICP)

224
Q

Ketamine + inhaled anesthetics

A

Depression of hemodynamics bc CNS no longer intact by inhaled anesthetic

225
Q

Ketamine plus NMB

A

Enhance of NMB

226
Q

Ketamine + BB

A

Reduce ketamine induced HR and BP= lower BP and low HR

227
Q

Ketamine + verapamil

A

Low BP High HR

228
Q

Ketamine + Sux

A

Prolongs Sux apnea bc ketamine decreased pseudocholinesterase

229
Q

Ketamine + volatile anesthetic

A

Hypotension because : volatile stops CNS fromworking = no sympathetic outflow = ketamine myocardial depression is unmasked = low BP

230
Q

ROCURONIUM DOA , onset

A

36 minutes

231
Q

What is structure of Sux ?

A

two molecules of acetylcholine linked through the acetate methyl groups

232
Q

Sux 1/2 life

A

Succinylcholine has an elimination half-life of 47 seconds

233
Q

What is dose of succinylcholine causing on average 95% suppression of twitch height

A

(the ED95) is approximately 0.3 mg/kg

234
Q

time to recovery to 90% muscle strength following administration of 1 mg/kg succinylcholine ranges from

A

9 to 13 minutes.

235
Q

Why sux short DOA?

A

rapid hydrolysis by butyrylcholinesterase (plasma cholinesterase) to succinylmonocholine and choline, such that only 10% of the administered drug reaches the neuromuscular junction.

236
Q

Factors that have been described as lowering butyrylcholinesterase activity are

A

advanced liver disease, advanced age, malnutrition, pregnancy, burns, oral contraceptives, monoamine oxidase inhibitors, echothiophate, cytotoxic drugs, neoplastic disease, anticholinesterase drugs, metoclopramide, and bambuterol.

237
Q

Esmolol inhibits, effects on sux

A

esmolol inhibits butyrylcholinesterase but causes only a minor prolongation of succinylcholine block.

238
Q

Explain pregnancy decrease of butyrylcholinesterase

A

High estrogen levels, as observed in parturients at term, are associated with up to 40% decreases in butyrylcholinesterase activity

239
Q

CV effects of SUX

A

Sinus bradycardia, junctional rhythm, and even sinus arrest may follow administration of succinylcholine.

240
Q

Cardiac dysrhythmias are most likely to occur when a second dose of succinylcholine is administered approximately

A

Cardiac dysrhythmias are most likely to occur when a second dose of succinylcholine is administered approximately 5 minutes after the first dose. Sinus bradycardia (resulting from stimulation of cardiac muscarinic receptors) is frequently seen in children49 and in adults after a repeated dose of succinylcholine.50

241
Q

The administration of succinylcholine is associated with approximately_____increase in plasma potassium

A

0.5 mEq/dL increase in the plasma potassium concentration in healthy individuals, which is well tolerated and generally does not cause dysrhythmias.

242
Q

Why not give SUX to children

A

Because of the risk of massive rhabdomyolysis, hyperkalemia, and death in children with undiagnosed muscle disease, succinylcholine is not recommended for use in children except for emergency tracheal intubation.

243
Q

Sux IOP increase , describe

A

The intraocular pressure peaks at 2 to 4 minutes after administration and returns to normal by 6 minutes.

244
Q

Atracurium metabolism : 2 mechanisms

A

Hofmann elimination, yielding laudanosine (a tertiary amine) and a monoquaternary acrylate as metabolites.
Furthermore, atracurium can undergo ester hydrolysis.

245
Q

Cistratricurium elimination

A

Hoffman elimination
No ester hydrolysis
Yield Laudosine too. But 5 times less than atricurium bc cistratricurium is 4-5 times more potent

246
Q

Which has Histamine release. Atricurium vs Cistratricurium

A

Atricurium ,

Also : Mivacurium,

247
Q

Cistratricurium Induction dose ?

A
  1. 1mg/kg *

0. 03mg/kg/min

248
Q

Pancuronium is potent long acting NMB with ______and ______properties .

A

a p otent long-acting neuromuscular blocking drug with both vagolytic and butyrylcholinesterase-inhibiting properties

249
Q

Why is Pancuronium DOA long ?

A

Accumulation of the 3-OH metabolite is responsible for prolongation of the duration of block induced by pancuronium

250
Q

Pancuronium in renal failure …

A

40 - 60 % elimination in kidneys…so , avoid

251
Q

Vecuronium elimination

A

T he liver is the principal organ of elimination for vecuronium, and renal excretion accounts for excretion of approximately 30% of the administered dose

252
Q

Vecuronium Duration of NMB depend on

A

Hepatic function , to lesser extent renal

253
Q

Vecuronium structure is

A

Vecuronium is simply pancuronium without the quaternizing methyl group in the 2-piperidino substitution

254
Q

What is The rank order of potentiation of NMB by anesthetic drugs

A

The rank order of potentiation is desflurane >sevoflurane > isoflurane > halothane> nitrous oxide–barbiturate–opioid or propofol anesthesia.

255
Q

Antibiotic that potentiate NMB

A 
Aminoglycosides ( both)
Tetracycline ( post Junction )
Lincomycin (both)
Clindamycin (both ) 
Polymyxin ( both )
256
Q

Most local anesthetics when given in large doses do not potentiate neuromuscular block. True or False ?

A

False ! They do :)

257
Q

what type of patient is phenylephinre useful for

A

coronary artery disease and in patients with aortic stenosis because it increases coronary perfusion pressure without chronotropic side effects, unlike most other sympathomimetics.

258
Q

what strange heart rate might occur when giving phenylephinre

A

reflex bradycardia

259
Q

phenylephinre overdose results in blood pooling in the pulmonary vasculatore- what medication must be avoided

A

beta blockers- they will go into heart failure as the heart is unable to pump out the backed up fluid

260
Q

infusion of phenylephrine + potassium- what occurs

A

potassium doesn’t shift intracellulary

261
Q

phenylephrine continuous infusion dose

A

20-100mcg/min

262
Q

phenylephrine push dose

A

50-100mcg

263
Q

ephedrine push dose

A

5-10mg

264
Q

ephedrine antiemetic dose

A

Ephedrine, 0.5 mg/kg intramuscularly, has an antiemetic effect

265
Q

ephedrine dose can result

A

tachyphylaxis after 1st dose form inhibition of alpha receptor.

266
Q

ephedrine

A

Ephedrine is an indirect-acting synthetic sympathomi- metic that stimulates a- and b-adrenergic receptors. The pharmacologic effects of ephedrine are partly due to di- rect stimulation of adrenergic receptors (direct-acting)64 and partly due to stimulation of release of endogenous norepinephrine (indirect-acting)

267
Q

oral ephedrine

A

bronchodilation

268
Q

norepinephrine infusion dose

A

A continuous infusion of norepinephrine, 2 to 16 mcg per minute

269
Q

norepinephrine is poorly tolerated by

A

Both of these may be poorly tolerated by patients with right heart failure

270
Q

ephedrine has what with the eye

A

mydriasis

271
Q

ephedrine is resistant to metabolism by

A

Ephedrine is resistant to metabolism by monoamine oxidase (MAO) in the gas- trointestinal tract, thus permitting unchanged drug to be absorbed into the circulation after oral administration

272
Q

where is NE stored

A

postganglionic sympathetic fibers

273
Q

Epinephrine is the prototype

A

sympathomimetic

274
Q

neostigmine works by

A

nhibiting acetylcholinesterase

binding to muscarinic (but not nico- tinic) cholinergic receptors

275
Q

Ketamine is unique because

A

it produces intense analgesia at low dose and produces prompt induction of anesthesia at higher doses

276
Q

Preservative in ketamine

A

is benzethonium chloride

277
Q

Esmolol Typical INITIAL Dose is

A

0.5mg/kg over seconds
full effect within 5 minutes
out of your system in 10 - 30minutes

278
Q

Esmolol 150 mg IV over 2 minutes before DL and ET provides

A

reliable protection against both increase in SBP and increase HR which predictably accompanies tracheal intubation .

279
Q

Lidocaine and Fentanyl blunts increased SBP accompanied by DL but not the HR. True or False

A

True

280
Q

What other dose of esmolol give prevent tachycardia and HTN by DL ?

A

you give 100-200 mcg over 15 seconds .

281
Q

When you 500 mcg/kg/minute of Ketamine ( aka 0.5mg/kg over 60 seconds) during electroconvulsive therapy with anesthesia by methohexital + SUX will result in

A

1) attenuation of heart

2) decreased legth of electrically induced seizure !!!

282
Q

What other conditions can you use Esmolol for ?

A

1) Pheochromocytoma
2) Thyrotoxicosis
3) Pregnancy induced HTN
4) epinephrine or cocaine induced cardio toxicity ( but you can have fulfillment pulmonary edema + coronary vasospasm and irreversible CV collapse = NTG and SNP and Phentolamine would better )
5) TOF when having hypercyonotic spells
6) HOCM

283
Q

Esmolol 1mg/kg followed by 250 mcg/kg/min effect on propofol

A

you need less propofol to prevent movement . but no one knows how this happens

284
Q

Pain on injection with esmolol ?

A

yes , because its buffered to a ph 4.5 to 5.5 ( one factor that causes the pain )

285
Q

Esmolol metabolism is independant of

A

renal or hepatic

286
Q

Esmolol metabolism is in done where and by what ?

A

in the BLOOD by plasma esterases. ( a little methanol can also occur from it’s metabolism )

287
Q

Return of predrug HR within____minutes after stopping Esmolol

A

15 minutes . can’t find the drug in the plasma after 15 minutes

288
Q

What is the 1/2 life of esmolol?

A

9 minutes

289
Q

For intraoperative myocardial ischemia what is the dose of esmolol?

A

1 - 1.5 mg/kg IV followed by continuous infusion

50- 300mcg/kg/min

290
Q

Esmolol continuous infusion dose

A 
50-300 mcg/kg/min -
onset is 1-2 minutes
full effect in 5 minutes 
half life 9 minutes
DOA: 10 30 minutes but it's gone from your system by 15 min
291
Q

What is the beta to alpha ratio of labetalol

A

B:a is 3:1

292
Q

Esmolol acts in what phase Action Potential

A

Decrease Phase 4 rate of depolarization

293
Q

Suggamedex structure ….elaborate

A

1) modified Y-cyclodextrin - 4 gylcosyl bond.
2) produced from starch
3) its 3 dimensional structure = hollow /truncated cone or doughnut.
4) Hydrophobic cavity + Hydrophillic exterior

294
Q

How Suggamedex trap the drug it is reversing

A

the hydrophic cavity traps the drug into the doughnut hole = now you have a guest-hole complex that is water souble.
now you have a guest in the hole :)
1:1 ratio of encapsulation

295
Q

For 30 million complex of suggameddex only ___ dissociates

A

1

296
Q

Does Suggamedex binds to plasma protein ?

A

NO

297
Q

Rocuronium mainly eliminated in the

A

biles >75 %

only 10- 25%

298
Q

Suggamedex -rocuronium complex is water soluble and therefore major route of elimination is

A

kidney : 65- 97% is recovered in the urine .

* predominantly unchanged in urine bc metabolism is so limited

299
Q

Renal impairment and Suggademex

A

1) clearance is decreased.
2) elimination half life increased
3) dialyzing won’t work , its not constistant

300
Q

Suggamedex should be avoided in patient with creatinine clearance of ?

A

<30ml/min

301
Q

TOF 1-2 give ___Suggamedex
TOF 2 give
TOF 0 give

A

4mg/kg for 1-2 twtiches
2mg/kg - 2 twitches
8- 16 mg/kg- 0 twitches

302
Q

Neostigmine in inthratecal

A

analgesia

303
Q

Neostigmine can cause Bronchospasm because

A

it stimulates muscarinic receptors in brinchial smooth muscles

304
Q

Neostigmine is unpopular choice for neuraxial adjuvent therapy because

A

Adverse GI effect . but epidural neostigmine does not cause nausea .

305
Q

Neostigmine to a lesser degree edrophonium causes profound ( decrease or increase) in butyrylcholinesterase activity

A

decrease !!

306
Q

Neostigmine effect on acetylcholinesterase

A

it has a ceiling effect.

307
Q

Maximum depth of block that can be antagonized by neostigime is a TOF of

A

TOF of 4 twitches

308
Q

Neostigmine and _____prolongs duration of SUX

A

pyridostigmine

Pharmacology II (7 decks)

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