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anesthesia pharm final > Anesthesia Pharm Final > Flashcards

Anesthesia Pharm Final Flashcards

1
Q

parenteral routes of drugs

A

IV, IM, SC,etc

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2
Q

volatile anesthetics: cerebral blood flow

A

increase vasodilation, decrease vasc resistance, increase CBF, increase ICP

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3
Q

opioids: metabolism

A

fentanyl 75% lungs, remi=plasma/tissue, morphine= gluc acid hepatic/renal, meperidine 90% hepatic

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4
Q

midazolam: first pass metabolism

A

50% first pass

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5
Q

local anesthetics: target channels

A

Na channels

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6
Q

volatile anesthetics: coronary blood flow

A

iso is a potent coronary vasodilator

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7
Q

desflurane and CO2 absorber

A

carbon monoxide, from dry dessicated absorber

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8
Q

bupivicaine toxicity

A

lower dose of bupivicaine will produce Cardiovascular collapse then lidocaine, pregnant patients may be more sensitive, cardiac resuscitation is more difficult after bupivacaine, cardiotoxicity potentiated by acidosis and hypoxia

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9
Q

uptake and distribution: alveolar PP

A

uptake = solubility x CO x (PA-PV)

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10
Q

opioids: side effects

A

pruritis, N/V, urinary retention, vent despression

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11
Q

local anesthetics: metabolism

A

amides: liver CYP450, esters- cholinesterase enzymes

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12
Q

opioids:best for neurological assessment post-op

A

remifentanyl

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13
Q

inhaled agents: pharmacokinetics

A

highly soluble=less uptake=faster induction

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14
Q

desflurane and heart rate

A

increased due to SNS stimulation

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15
Q

local anesthetics: nodes of ranvier

A

2-3 blocked will stop the action potential

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16
Q

compound A formation

A

sevo interation with CO2 absorbers, higher levels seen in Baralym vs soda lime, nephrotixin in rates, use flows higher than 2

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17
Q

EMLA components

A

5% lidocaine, 5% prilocaine

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18
Q

Induction drugs: hiccups

A

methohexital

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19
Q

benzodiazepine-ion channel effect

A

hyperpolarization

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20
Q

induction drugs: cortisol secretion

A

etomidate

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21
Q

inhaled agents: bone marrow suppression

A

nitrous oxide

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22
Q

Induction drugs: propofol method of action

A

decrease GABA dissociation

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23
Q

opioids: histamine release

A

morphine, meperidine

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24
Q

opioids: potency

A

MMHAFRS

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25
Q

opioids: remi metabolism

A

plasma cholinesterase

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26
Q

opioids: seizure

A

meperidine or normeperidine with renal failure

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27
Q

local anesthetics: cardiotoxicity

A

circumoral numbness, tinitus

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28
Q

dibucaine number

A

80

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29
Q

propofol: additives

A

glycerol burns, disodium edetate is bacteriostatic

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30
Q

opioid: side effects, glucagon

A

tx biliary coloc 2mg IV

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31
Q

ketamine: tx for emergence delirium

A

benzos

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32
Q

thiopental redistribution

A

effects 5-10 minutes bc of redistribution

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33
Q

benzodiazepine: clinical effect

A

20%: anxiolytic, 30% sedation, amnestic 60% unconscious

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34
Q

opioid: dynorphon receptors

A

kappa

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35
Q

inhaled agents: metabolism

A

exhalation, biotransformation, transcutaneous loss(hal - sevo - iso - des - n20)

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36
Q

opioids: renal failure

A

alfentanyl

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37
Q

dose of etomidate

A

0.2-0.3mg/kg

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38
Q

induction drugs: causes analgesia

A

ketamine

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39
Q

duration of naloxone

A

30-45 minutes

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40
Q

local anesthetic: effect of epinephrine

A

increase duration due to vasoconstriction

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41
Q

inhaled anesthetics: MH

A

don’t use

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42
Q

local anesthetics: cauda equina syndrome

A

serious potential complication of spinal anesthesia

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43
Q

local anesthetics: methemoglobemia

A

benzocaine/prilocaine (ortholuidine is the metabolite that causes methemoglobinemia); decreases oxygen carrying capacity of hemoglobin, oxidation of hemoglobin to methemoglobibemia, neonates at higher risk, normal metHbB is less than 1%, pulse ox will read 85, treat with methylene blue 1-2 mg/kg

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44
Q

induction drugs: effect of ICP

A

thio and etom decrease ICP, prop and ketamine increase ICP

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45
Q

chloroprocraine: contraindicated in

A

spinal

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46
Q

premedication in children

A

0.5mg/kg versed PO

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47
Q

midazolam: drug interactions

A

synergistic with opioids

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48
Q

induction drugs: myoclonus

A

etomidate

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49
Q

volatile anesthetics: preservatives

A

halothane has thymol

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50
Q

volatile anesthetics: reactive airway

A

don_t use des, use sevo

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51
Q

maximum dose of bupivacaine

A

225mg with epi, 175 mg w/out epi

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52
Q

flumazenil metabolism

A

quick, doesn_t last = resedation, hepatic enzymes

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53
Q

mechanism of action for barbiturates

A

decrease GABA dissociation

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54
Q

propofol CV effects

A

decrease BP and increase HR

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55
Q

alpha 1 glyco protein (protein binding)

A

basic

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56
Q

benzodiazepine: contraindications

A

PO no grapefruit, pregnancy

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57
Q

division of CO

A

75% VRG (10% of body mass), 19% muscle (50% of body mass) 6% fat (20% body mass) 0% VPG (20% body mass)

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58
Q

isoflurane CV effects

A

decrease SVR, increase HR, no effect of CO, coronary steal

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59
Q

desflurane, physical properties

A

liquid at room temp

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60
Q

iso and des

A

increase heart rate

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61
Q

inhaled anethetics: cerebral metabolic rate of oxygen

A

decrease CMRO2

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62
Q

MAC additive properties

A

MACs are additive

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63
Q

thiopental pH

A

10.5

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64
Q

induction drugs: does not interact with GABA

A

ketamine

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65
Q

thiopental concentration

A

2.50%

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66
Q

inhaled anesthetic: analgesic properties

A

NO only

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67
Q

propfol in ICU

A

3 days then hyper lipidemia

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68
Q

routes of administration: onset times

A

IV, intraosseous, endotracheal, inhalational, sublingual, IM

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69
Q

indirect agonist definition

A

acting receptor agonist _ drug that produces its physiologic response by increasing the concentration of ENDOGENOUS substrate (neurotransmitter or hormone) at receptor site

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70
Q

local anesthetics: ion trapping

A

refers to a phenomenon that occurs when a difference on pH exists in two body compartments. The more acidotic the pH, the greater the fraction of local, which is a basic compound, that ionizes. Ionized compounds are water soluble and cannot easily pass biologic membrands. when a local becomes more ionized and water soluble it becomes less able to leave the body compartment. If a patient who has CNS toxicity due to local overdose, is improperly managed, and becomes hypoxic with accompanying acidosis, the local becomes trapped in the CNS worsening the toxicity. Can also occur in pregnant patients because fetal pH is lower than maternal pH.

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71
Q

racemic mixture

A

50-50 entantiomers

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72
Q

CPP=

A

CPP = MAP - ICP

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73
Q

propofol metabolism

A

hepatic metabolism, glucuronidation is the major pathway

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74
Q

propoful IV sedation dose

A

25-100 mcg/kg/min

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75
Q

propofol GA TIVA dose

A

100-200 mcg/kg/min

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76
Q

solubility definition

A

_Relative affinity of an anesthetic for two phases and therefore the partitioning of that anesthetic between the two phases at equilibrium

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77
Q

inhaled anesthetics: what is equilibrium

A

no difference in partial pressure exists

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78
Q

partial pressure

A

the pressure which is the pressure the gas would have if it alone occcupied the volume

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79
Q

two ways to increase initial concentration of gas and the uptake

A

concentration effect, 2nd gas effect

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80
Q

effect of solubility on gas uptake

A

decreased solubility increases PA/PI so induction is quicker, increased solubility slows induction time

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81
Q

inhaled anesthetics: CO effect

A

increased CO means increased solubility and slower induction

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82
Q

what changes pharmacokinetics?

A

age, lean muscle, body fat, hepatic fxn, pulmonary gas exchange, CO

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83
Q

What do we want GA to do?

A

Minimize deleterious direct and indirect effects of agents, Sustain physiologic homeostasis during procedure, Improve postop outcomes

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84
Q

what MAC prevents mvmt in 95%

A

1.3

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85
Q

MAC and hypothermia

A

For each decrease in core temp 1 degree C_MAC is decreased by 5%

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86
Q

MAC and chronic alcohol abuse

A

MAC unaltered

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87
Q

MAC and acute alcohol intox

A

MAC decreased

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88
Q

Agents that decrease myocardial contractility and CO

A

halothane and enflurane

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89
Q

Which agents decrease SVR?

A

iso, des, sevo

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90
Q

Which agents decrease PVR?

A

all, blunt hypoxic pulmonary vasoconstriction response, (N2O known to increase PVR in pts with hypertension)

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91
Q

Inhaled agents and arrythmias

A

halothane desensitizes the myocardium to catecholamines, exogenous epi can cause vtach and pvc, sinus brady and av rhythms bc of direct depressive effect on SA node / halo, iso, des and sevo prolong QT interval

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92
Q

Inhaled agents and MV

A

increase RR decrease TV, rapid shallow breathing which causes and increase in PaCO2, drugs probably inhibit medullary vent center. Des and Sevo produce apnea around 1.5, 2 mac (decrease in vent response to hypoxemia, decrease in airway resistance, except for des, decrease in FRC)

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93
Q

inhaled anesthetics and renal effects

A

decrease renal blood flow, decrease GFR, decrease urine output, nephrotoxicity

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94
Q

inhaled anesthetics and hepatic effects

A

decrease hepatic blood flow, decrease hepatic clearance, hepatic toxicity

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95
Q

inhaled anesthetics in vitro

A

can cross placenta, baby usually ok until 1 mac

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96
Q

inhaled anesthetics and skeletal muscle

A

ether derived produce more relaxation than halothane, NO does not produce relaxation and may produce rigidity

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97
Q

opioid agonist/antagonist

A

nalbuphine- used for people who are narcotic dependent or weaning off opioids (agonist at kappa, antagonist at mu)

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98
Q

opioid: mechanism of action

A

Bind specific G protein-coupled receptors that are located in brain and spinal cord regions involved in the transmission and modulation of pain

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99
Q

opioid receptors: Mu1

A

analgesia, euphoria, N/V, pruritis, low abuse potential, bradycardia

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100
Q

opioid receptors: Mu2

A

(spinal) hypoventilation, analgesia, euphoria, sdeation, physical dependence, constipation

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101
Q

opioid receptors: kappa

A

(supraspinal, spinal) analgesia, respiratory depression <mu, dysphoria, diuresis, dynorphins, agonist-antagonist work here, resistant to high intensity pain

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102
Q

opioid receptors: delta

A

(supraspinal, spinal) analgesia, resp despression, physical dependence, urinary retention, enkaphalins

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103
Q

opioid overdose triad

A

respiratory depression, CNS depression, pin point pupils

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104
Q

opioid miosos

A

edinger-westphal nucleua of the oculomotor nerve, toolerance does not develop

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105
Q

opioid withdrawal

A

chills, gooseflesh, hyperventialtion, hyperthermia, vomiting, diarrhea, hostility

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106
Q

morphine

A

potency 1, onset 15-30 minutes, 2-10mg, peak effect 45-90 minutes, duration 3-4 hours, metabolized bia conjuction with glucuronic acid, metabolite morphine 6-glucaronide (accumulation in kidney failure pts can lead to prolonged narcosis and vent depression), histamine realease

107
Q

meperidine (demerol)

A

0.1 potency of morphine, peak effect 5-7 minutes, duration 2-4 hours, local/atropine side effects (block Na channels, tachycardia, dry mouth, mydriasis), 90% hepatic metabolism to normeperidine which is renally eliminated, tx for post-op shivering

108
Q

fentanyl

A

75-125 more potent than morphine, peak effect 3-5 minutes, duration 30-50, 75% undergoes 1st pass pulmonary uptake, highly lipid soluble and protein bound, hemodynamic stability,

109
Q

induction dose of fentanyl

A

2-6 mcg/kg with a sedative hypnotic

110
Q

sufentanil

A

5-10x as potent as fentanyl, 1000x more potent than morphine, greater affinity for opioid receptor, peak 3-5 minutes, duration 30-60 (dosing 0.3-1.omcg/kg 1-3 minutes before DL)

111
Q

alfentanyl

A

1/5 to 1/10 as potent as fentanyl, duration 10-20 minutes, peak 1.5-2 minutes, renal failure doesn_t alter clearance, rapid on/off, good for RBB, DL, 5-10mcg/kg

112
Q

remifentanyl

A

similar potency to fentanyl, peak effect 1.5-2 minutes, duration 6-12 minutes, metabolized by plasma and tissure esterases, good for RBB, continuous gtt, MAC vs general, quick recovery cases (0.5-1mcg/kg + propofol for FL then 0.25-.5mcg/kg/min)

113
Q

codeine

A

antitussive, analgesia for mild to moderate pain

114
Q

methadone

A

long term relief of chronic pain and opioid withdrawal

115
Q

hydromorphone

A

8x as potent as morphine but shorter acting

116
Q

pentazocine, butorphanol, nalbuphine

A

partial agonist and or comp antagonist, produce analgesia with limited resp depression, ceiling effect

117
Q

local anesthetics

A

bind Na channels in activated state, rate of depolarization is decreased, resting potential and threshold are not altered, blockade of Na channels prevent achievement of the threshold potential; action potential is not progagated

118
Q

lipophilic groups have a

A

benzene ring

119
Q

hydrophilic groups hav a

A

tertiary amine

120
Q

what effects potency of local

A

fiber size, type, myelination, pH, frequency of stimulation

121
Q

metabolites of esters

A

para-aminobenzoic acid (PABA) **allergies

122
Q

local inj sites and vascularity

A

IV>tracheal>intercostal>caudal>paracervical>epidural>BP>sciatic>subcutaneous

123
Q

toxicity dosages of locals

A

bupi is 2.5, lido is 5, lido with epi is 7

124
Q

CV effects of systemic toxicity

A

hypotension, decreased cardiac conduction, ventricular arrythmias

125
Q

dose of intralipid

A

1.5mg/kg iv over 10 minutes

126
Q

brain stem anesthesia

A

Accidental injection into the CSF can occur during the block due to perforation of the meningeal sheaths that surround the optic nerve. The patient may experience disorientation, aphasia, hemiplegia, unconsciousness, convulsions, and respiratory or cardiac arrest. The incidence of this is estimated in studies to be 0.13%. Direct injection intravascularly via the optic nerve sheath or local anesthesia carried by the ophthalmic and internal carotid artery by retrograde flow to the thalamus and midbrain can also present the same way. This situation requires prompt recognition and treatment (including airway control, respiratory support, possible cardiac intervention, etc.)

127
Q

drugs used for topical anesthesia

A

tetracaine, cocaine, lidocaine (with oxymetazoline)

128
Q

anticholinergic overdose

A

physostigmine?

129
Q

name Beta-1 agonists

A

norepi

130
Q

metoclopramide, contraindications

A

Parkinson’s and GI obstruction

131
Q

diuretics- hyperglycemia

A

HCTZ

132
Q

Reye Syndromw with aspirin

A

kids with flu treated with tylenol not ASA

133
Q

metformin- renal excretion

A

100% unchanged by kidneys

134
Q

zofran, ped dose

A

0.1mg/kg

135
Q

metoclopramide, side effects

A

Prolong QT, dty mouth, ab cramping, extrapyramidal effect (dysphoria, agitation, sedation) RARE side effects: hirsuitism, maculopapular rash Prolactin side effects: breast enlargement, menstrual irregularities FETAL effects = doesn_t cross, no effects on baby

136
Q

cardiac arrhyhmias with lasix

A

hypo K and hypo Mg, increased risk of digitalis toxicity and ventricular arrhythmias

137
Q

H2 blockers as premed

A

˙ˇ pepcid can be used as a premedication. It will decrease hydrogen ion secretion, so the gastric contents in the future hours may be less acidic. However, H2 blockers will not decrease the acidity of what is already in the stomach. Pepcid premed = 20 mg IV, 30 minutes prior.

138
Q

bicitra beneficial preop effects

A

˙ˇ 30 ml cup of nonparticulate antacid. Neutralizes the pH of the stomach contents. If the patient does aspirate it will be a higher pH, but possible more volume (weigh the risks vs. benefits).

139
Q

decadron, peds dose

A

0.1mg/kg

140
Q

droperidol contra

A

dopamine antagonists. 0.625 mg dose. Significant decrease in PONV. Black box warning = Increases QT interval, so contraindicated in patient_s with prolonged QT intervals already. Also contraindicated in parkinson_s disease.

141
Q

amiodorone side effects

A

pulmonary fibrosis

142
Q

side effect of 2nd generation H1 antagonists

A

prolong QT

143
Q

histamine antagonists, mechanism of action

A

competitive inhibition

144
Q

zofran mechanism of action

A

serotonin 5HT3 receptor antagonist

145
Q

Histamine

A

autocoid = naturally occurring endogenous amine. Histamine is a chemical mediator in inflammation. Histamine increases acid production. It is released from mast cells (skin, lungs, GI tract, basophils). Histamine DOES NOT cross the BBB, but some H2 blockers do cross the BBB. Histamine is involved in the antigen-antibody response.

146
Q

H1 receptor

A

respiratory and GI smooth muscle contraction, pruritis and sneezing, nitric oxide release by vascular smooth muscle_ vasodilation_ hypotension.

147
Q

H2 receptor

A

increased GI secretion of H+, increased HR/contractility

148
Q

H3 receptor

A

presynaptic receptors = decreased histamine synthesis and release

149
Q

Generalized effects of histamine

A

dilation of arterioles and capillaries due to NO release, flushing (red/hives), decreased systemic vascular resistance, decreased blood pressure, increased capillary permeability.

150
Q

H1 activation

A

oˇˇ occurs at lower concentrations of histamine than activation of H2 receptors. Decreased AV node conduction, coronary artery vasoconstriction, bronchial smooth muscle constriction.

151
Q

H2 activation

A

oˇˇ CV effects (increased myocardial contractility, increased HR), catecholamine release, coronary artery vasoDILATION. increased gastric hydrogen ion secretion.

152
Q

skin response

A

dilated capillaries in affected area, edema due to increased capillary permability, wheal = dilated arterioles around edema.

153
Q

allergic rxn

A

histamine is one of several chemical mediators released. Histamine antagonists will block edema and pruritis but WILL NOT block hypotension.

154
Q

H1 blocker

A

˙ˇ first generation H1 blockers also activate muscarinic cholinergic, serotonin and alpha receptors and cause significant SEDATION. Second generation H1 blockers only bind to H1 receptors and they are non-competitive at higher doses and they cause much LESS SEDATION.

155
Q

1st generation H1 blocker

A

oˇˇ diphenhydramine (benadyrl) and Dramamine; ˇ Side effects: somnolence, decreased alertness, slowed reaction time, dry mouth, blurred vision, urinary retention, impotence, tachycardia, dysrhythmias. Benadryl inhibits alcohol dehydrogenase

156
Q

2nd generation H1 blocker

A

loratadine (claratin), fexofenadine (allegra); _ Side effects: QT prolongation (at high doses), limited side effects.

157
Q

clinical uses of H1 blockers

A

rhinoconjunctivitis, bronchospasm, anaphylactoid/anaphylactic reactions (most allergic reactions in anesthesia are due to muscle relaxants _ give Benadryl 25 mg), motion sickness.

158
Q

H2 blockers

A

inhibit gastric acid secretion, doesn_t affect what is already in the gut

159
Q

Potency of H2 blockers

A

Cimetidine (tagamet) =1; Ranitidine (zantac) =10; Nizatidine (axid)=10; Famotidine (Pepcid)=50 Iv dose 20mg

160
Q

Pharmacokinetics of H2 blockers

A

rapid oral absorption, extensive 1st pass metabolism, cross BBB and placenta (usually no effects on baby), avoid in patients with renal dysfunction/increased age = decreased elimination time and prolonged effects. Decrease the dose in renal dysfunction and elderly patients.

161
Q

Clincal uses of H2 blockers

A

˙ˇ treatment of duodenal ulcers, active reflux/GERD, allergy prophylaxis (block histamine receptors), preop med (decrease gastric acid secretion, but will not decrease the H+ ions already in the gut). Keep taking H2 blockers up till am of surgery because if they are discontinued there can be a hypersecretion of gasric acid in the stomach.

162
Q

Side effects of h2 blockers

A

˙ˇ diarrhea, headaches. Side effects are usually only present in patients with renal/hepatic dysfunction. Prolonged use may weaken the barrier to bacteria.

163
Q

H2 blockers with drug interactions

A

cimetidine is the most common. Hepatic metabolism of other drugs is affected. Cytochrome P450 system is inhibitedÖ leads to prolonged duration of drugs that are metabolized by P450 enzymes (valium, propanolol). Other H2 blockers (other than cimetidine) do not bind P450 enzymes. Also there is a delayed lidocaine metabolism = increased risk of lidocaine toxicity.

164
Q

Histamine blockers and CYTP450

A

cimetidine (tagamet). Cytochrome P450 system is inhibitedÖ leads to prolonged duration of drugs that are metabolized by P450 enzymes (valium, propanolol). Other H2 blockers (other than cimetidine) do not bind P450 enzymes

165
Q

cromolyn

A

inhibits antigen-induced release of histamine from mast cells (pulmonary mast cells). Administered by inhalation. Used as prophylaxis for bronchial asthma. Patients on cromolyn can actually become allergic to it.

166
Q

proton pump inhibitors

A

˙ˇ prazoles_. They have longer durations than H2 blockers. PPI prolong the inhibition of gastric acid secretion up to 24 hours. Better results that H2 blockers because they increase the gastric pH and decrease the volume of the gastric contents. If a patient is on PPIs, then they probably have GERD and are considered an aspiration risk.

167
Q

PPIs as premed

A

can increase gastric fluid pH if given early enough, can decrease gastric fluid volume, MUST BE GIVEN >3 HOURS PRIOR TO SURGERY

168
Q

Serotonin and 5-HT3 receptor antagonists

A

autocoid Ö cerebral, coronary, and pulmonary vasoconstriction. Oxidized by the liver and lungs and taken up by platelets (stored inactivated in platelets). Many subtypes with greatly varying actions. NT in the CNS. 90% found in enterochromaffin cells of GI tract and the rest are in CNS and platelets.

169
Q

Serotonin and 5-HT3 receptor antagonists; sites of action

A

GI tract, platelets, vascular system (vasoconstriction), CNS (15 sub-types = sleep, cognition, sensory perception, motor activity, temp regulation, nociception, appetite, sexual behavior, hormone secretion.

170
Q

5HT1

A

5 subtypes = cerebral vasoconstriction; _ Agonist: Sumatriptan (imitrex) reverses middle cerebral artery vasodilation to improve migraines and cluster headaches.

171
Q

5HT2

A

3 subtypes, coronary artery and pulmonary vessels, _ Antagonist: Ketanserin attenuates vasoconstriction, bronchoconstriction, platelet aggregation and also acts as an alpha blocker.

172
Q

5HT3

A

nausea and vomiting, appetite, addiction, pain and anxiety. These receptors are predominantly in the chemotaxic center in the brain that causes N/V./ ondansetron (zofran), tropisetron, dolasetron (12.5 mg dose; 0.035 mg/kg), granisetron (0.01 mg/kg).

173
Q

Sumatriptan and receptor interaction

A

˙ˇ 5HT1 receptor agonist. Reverse cerebral artery vasodilation = vasoconstriction.

174
Q

Ondansetron

A

structurally related to serotonin. Therapeutic effects include decreased PONV in susceptible patients _ used prophylactically. Side effects include: headache, diarrhea, increased liver enzymes with chronic use.

175
Q

Antacids

A

tums. Neutralize the acid that is already in the stomach. Antacids are usually a salt and they combine with HCl to neutralize it. As the pH in the gut increases, the gastric emptying also increases. Why use themÖ inexpensive, promote healing (due to increased pH and less reflux), work quickly.

176
Q

Sodium bicarbonate (tums)

A

highly soluble, rapid action in stomach, brief duration, can cause alkalosis. May increase Na+ levels = bad for patients with bad hearts.

177
Q

Magnesium hydroxide (milk of magnesia)

A

oˇˇ no acid rebound when discontinued, laxative effect (osmotic diarrhea), beware of HIGH doses Ö hypermagnesemia can lead to renal dysfunction and neurological/neuromuscular effects.

178
Q

calcium carbonate

A

rapid absorption, metabolic alkalosis with chronic use, hypercalcemia, acid rebound.

179
Q

Aluminum hydroxide

A

minimal absorption, phosphate depletion, decreased gastric emptying = constipation.

180
Q

antacid drug interactions

A

˙ˇ increased delivery of PO medications because of the increased gastric pH. Decreased bioavailability of medications due to increased gut pH

181
Q

Preop use of antacids

A

anecdotal (no real evidence to support/not support). Antacids have no effect on regurgitation and aspirationÖ just make the patient aspirate a higher pH. Non-particulate (sodium bicitrate) is better to use preop than particulate antacids (such as tums).

182
Q

Sucralfate

A

coats ulcerated lesions so the stomach acid doesn_t irritate the lesion. Viscous suspension. Used to treat duodenal and gastric ulcers.

183
Q

Prokinetics

A

˙ˇ increase gastric emptying by increasing peristalsis. Clinically useful prokinetics include metoclopramide, cisapride, domperidone, erythromycin.

184
Q

Metoclopramide

A

dopamine antagonist. Increases gastric emptying, increases lower esophageal tone (decreased aspiration risk), relaxes pylorus and duodenum when the stomach contracts.

185
Q

Who gets metoclopramide?

A

oˇˇ ll stomach, trauma, obese, diabetics, parturient (women at full term). 10mg IV or 0.15mg/kg

186
Q

Domperidone (motilyium)

A

not really used much in anesthesia. Dopamine antagonist. Effects = stimulates peristalsis, increases LES tone, increases gatric emptying. NO cholinergic activity. NO central effects.

187
Q

Cisapride (propulsin)

A

GI prokinetic. Increases ACh and ACh binds to parasympathetic receptors to increase gastric emptying. Treatment of opioid induced gastroparesis.

188
Q

alpha-glucosidase inhibitors, side effects

A

˙ˇ acarbose. Slows digestion and absorption of carbohydrates. Does not induce hypoglycemia. Side effects: flatulence, abdominal cramping and diarrhea.

189
Q

Graniestron dose

A

0.01mg/kg

190
Q

scopolamine patch

A

patch behind the ear. Must go on at least 1 hour preop, but preferably the night before surgery. Antimuscarinic effects. Crosses the BBB = sedation.

191
Q

dolasetron dose

A

12.5mg (o,o35mg/kg)

192
Q

Metoclopramide dose

A

10mg (0.15mg/kg)

193
Q

Decadron dose

A

4-10mg

194
Q

antihypertensives, sites of action

A

Arterioles (resistance), Venules (capacitance), Heart (cardiac output), Kidneys (volume).

195
Q

calcium channel blockers

A

selectively inhibit L-type (slow) calcium channels in the heart. Mechanism of action = decrease phase 4 and depress AV node conduction. Inhibit the flux of calcium across the slow channels of cardiac muscles resulting in decreased rate of spontaneous phase 4 depolarization.

196
Q

types of calcium channel blockers

A

phenylalkylamines, dihydropyridines, benzothiazepines

197
Q

phenylalkylamines

A

intracellular pore blocking of channel at binding site , verapamil

198
Q

Dihydropyridines

A

extracellular allosteric modulation of channel at binding site, “pines”

199
Q

Pharmacological effects of calcium channel blockers

A

decrease contractility, decrease heart rate, decrease SA node activity, decrease AV node conduction, decrease systemic BP (secondary vascular smooth muscle relaxation) / o CLINICAL USES_ coronary artery spasm, stable angina, cerebral vasospasm (after stroke of SAH), HTN (usually in combination with beta blockers or nitrates; CCB+nitrates = synergistic effect for dilating the coronaries).

200
Q

CCB, vasodilation

A

nicardipine has the most, it has no SA/AV node effect, NO mycardial depression, used intraop to treat HTN

201
Q

Tx of cerebral artery vasospasm

A

nimodipine crosses BBB so it is used to treat - verapamil may be used in IR bc it is injected into cerebral arteries

202
Q

antihypertensives and local anesthetic toxicity

A

verapamil has effects on fast Na channels so can get prolonged LA effects

203
Q

effects of verapamil

A

AV node depression, SA node negative chronotrope, negative ionotrope, some vasodilation

204
Q

CCB and drug interations

A

exaggerated response to volatiles (greater decrease in MAP), impaired NMB reversal, increase risk of LA toxicity (verpamil), decrease platelet function, increase plasma concentration of digoxin, CCB + dantrolene = increase K+ and prolonged effect, hyperkalemic effects when used with K+ containing solutions.

205
Q

CCBS in a nutshell

A

___pines_ DILATE, nimodipine = nimoTOP it goes to the head and crosses the BBB, Diltiazem = CARDIzem AV node conduction with little cardiac depression (good for heart failure patients).

206
Q

Peripheral vasodilators

A

sodium nitroprusside, nitroglycerin, hydralizine, papavarine, trimethaphan

207
Q

when to use peripheral vasodilators

A

treat HTN crisis, maintain controlled hypotension ((surgery, ICU post-heart surgery to keep a decreased afterload and give the heart time to recover), improve LV stroke volume for CHF patients or regurgitant valves.

208
Q

how do peripheral vasodilators work?

A

DECREASE SYSTEM BLOOD PRESSURE by decreasing SVR (vasodilation), decrease RA filling (decreased preload), and increase Nitric Oxide production (increased NO = increased cGMP production = vasodilation).

209
Q

nitric oxide

A

NO is an endogenous gas that acts as a chemical messenger. It helps maintain CV tone and CNS signaling (excitatory transmission). NO inhibits platelet aggregation. NO aids in GI relaxation and immune functions.

210
Q

duration of nitric oxide

A

5 seconds

211
Q

pathophysiology related to NO

A

essential HTN is caused due to decreased NO production

212
Q

hypotension and septic shock

A

are caused by increased NO production. Atherosclerosis is due to decreased NO production and thus increased platelet aggregation. Vasospams after SAH is due to not enough production of NO.

213
Q

anesthesia mechanism of action

A

˙ˇ nitric oxide is involved in the excitatory transmission in the CNS. NO is produced by NO synthase. Anesthetic agents may decrease NO synthase Ö decreased excitatory pathway in the brain and increase the inhibitory pathway so that GABA (inhibitory NT) will predominate. Inhibiting nitric oxide may be involved in global suppression.

214
Q

clinical uses of nitric oxide

A

inhaled NO can be used to treat pulmonary HTN (vasodilate the pulmonary vasculature specifically) and to treat ARDS. o Dosing: 1-100 ppm dose. NEED HIGH FGF. The FGF must = Minute ventilation. o Toxicity: NO + O2 _ NO2. Toxicity occurs when NO2 builds up.

215
Q

papaverine, vasodilation

A

from poppy (opium) plant. Used by surgeons to keep the mammary vessels open. There may be a systemic decrease in the BP. Very short half life so the systemic decrease in BP is only transient.

216
Q

Thiocyanate toxicity treatment

A

dialysis

217
Q

Antihypertensives and methemoglobinemia_

A

sodium nitroprusside

218
Q

Treatment of methemoglobinemia

A

sodium nitroprusside

219
Q

Nitroglycerin mechanism of action

A

requires a thio substance to interact with. Increases NO release = increased cGMP = vasodilation (principally a venous dilator).

220
Q

Angiotensin-Converting Enzyme Inhibitors

A

__prils_. Block the coversion of angiotensin IÖ angiotensin II. Prevent angiotensin II vasoconstriction and stimulation of sympathetic system = vasodilation. Angiotensin II is responsible for the secretion of aldosterone, thus ACE-I decrease aldosteroneÖ less vasoconstriction.

221
Q

ACE inhibitor side effects

A

no CNS side effects. COUGH, angioedema, contraindicated in patients with renal artery stenosis because these patients are dependent on Angiotensin II for renal blood flow.

222
Q

angiotensin receptor blockers

A

“sartans” Prevent angiotensin II from binding to its receptor. Clinical uses include: essential HTN and CHF. Side effects: no cough like ace, dizzy from vasodilation, no profound hypotension with GA, losartan

223
Q

labetalol

A

Alpha 1 and nonselective beta 1 and beta 2 antagonist. Beta:alpha is 3:1 oral and 7:1 IV. Works in 5-10 min.

224
Q

beta blockers overdose

A

glucagon

225
Q

nitroprusside cGMP

A

upregulates

226
Q

alpha antagonist, tx of BPH

A

tamulosin (flomax)

227
Q

beta blockers, effects on ECG

A

sotalol - long QT

228
Q

isoproterenol, receptor effects

A

B2

229
Q

beta blocker metabolism

A

liver all but esmolol

230
Q

beta blockers, airway resistance

A

atenalol least likely bc beta 1 specific

231
Q

lab value and ketorolac

A

creatinine

232
Q

toradol IV and morphine doses

A

30 mg toradol = 10mg morhphine

233
Q

diuretic for IOP

A

mannitol

234
Q

hirudin, mechanism of action

A

direct thrombin inhibitor

235
Q

inhaled nitric oxide and fresh gas flows

A

fresh gas flows must be greater than MV

236
Q

naloxone, duration

A

30-60 minutes

237
Q

antidysrhyhthmic, class II mechanism

A

blockade of sympathetic activity, decrease rate of phase 4 depolarization, decreased rate of SA node discharge

238
Q

beta blocker for glaucoma

A

timolol

239
Q

antimicrobial prophylaxis, 2006 medical letter guidelines for bowel procedures

A

cefoxitin

240
Q

thrombolytics

A

-ases break up all clots

241
Q

action of transexamic acid

A

antifibrinolytic agent

242
Q

antidysrhyhthmic, class IV mechanism

A

CCB

243
Q

sulfonylurea mechanism of action

A

promote insulin secretion

244
Q

bupivicaine toxic dose

A

2.5mg/kg

245
Q

ACT normal range

A

90-100

246
Q

vitamin k dependent coag factors

A

2+7,9,10

247
Q

amiodarone infusion rate

A

150mg/10 min then 1mg/min

248
Q

contraindications for acute intermitteny porphyria

A

thiopental

249
Q

gabapentinoids

A

affect Ca channels, do not act on gaba, provides sedation 600-900mg (15mg/kg) , reduction in pain and opoiod use, does help in chronic pain

250
Q

nmda receptor antagonists

A

glutamate-acticated Ca channels, inplicated in neural changes asoociated wth chronic or sustrained pain

251
Q

drugs that block nmda receptors

A

ketamine, memantine hcl, dextrorphan (entantiomer of codeine)

252
Q

ketamine

A

related to PCP, direct inhibition of nmda receptors, augmentation of noradrenergic output from locus ceruleus, weak opoiod receptor agonist, inhibits production of inflamm cytokines; alpha, beta waves predominant; decrease NV, decreases opoiod consumption

253
Q

magnesium

A

competitive antagonist of nmda, clinically significant reduction on pain

254
Q

dexmedetomidine

A

fxns centrally in locus ceruleus, inhibition of descending spinal cord projections likely the mechanism by which drug inhibies nociception, sedation very similar to natural sleep; reduces need for post op opoiods, decreases pain, decrease NV (prob from less opoids) MORE bradycadia and hypotension!

255
Q

uses for precedex

A

tonsilectomy: most widely used pt population, 1mcg/kg over 15 minutes, faster wakeup

256
Q

clonidine in caudals

A

prolongs duration of analgesia

257
Q

precedex and spinal, peripheral nerve blocks

A

prolongs sensory block but 3.7x in bradycardia

258
Q

clonidine as premed for kids

A

improved post-op pain contrl and reduced emergence delirium

259
Q

precedex pharmacokinetics

A

must be started earlier, need loading dose but there are hemodynamic consequences, doesn’t reach peak as fast

260
Q

decadron

A

4mg for PONV, high doses show pain reduction, decrease in bleeding

261
Q

toradol

A

bleeding effects exaggerated / transient reduction in GFR,no sig change in creatinine

262
Q

acetaminophen (paracetamol)

A

antipyretic effect, analgesua, weak peripheral anti-inflamm, must be given prophylatically- about 30 minutes before wakeup

263
Q

acetaminophen, metabolism

A

glucuronidation, sulfation, oxidation to NAPQI (NAPQI is hepatatoxic)

anesthesia pharm final (1 decks)

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