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Spring '20/ L. BASICS/PHARM FINAL > pharm > Flashcards

pharm Flashcards

1
Q

beta blocker protein binding

A 
propranolol 90-95
esmolol 55
pindolol 40-60
nadolol 30
acebutolol 25
metoprolol=timolol- 10
atenolol- 5
betaxolol-0?
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2
Q 
clonodine
receptor?
a2-a1?
admin routes
metabolized
terminal half life
regular half life
is it variable with certain patients?
A 
alpha 2
400:1
IV, Oral, transdermal 
metabolized liver
excreted urine less in bile
terminal half life- 12-16hrs
half life 9-12 hours
variable with liver or kidney dysfunction
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3
Q

dexmedtomidine

receptor

a2-a1

terminal half life

dose

side effect when turned off

large bolus produces?

A

alpha 2 agonist

1600:1

terminal half life- 2 hours

dose 0.1-1.5mcg/kg/min

produces dependence and

can result in tachycardia

HTN anxiety when turned off

large bolus will result in HTN
and bradycardia

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4
Q

propranolol tell me about the receptor activity

A

nonselective beta antagonist

lacks intrinsic sympathomimetic activity=pure antagonist

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5
Q

propranolol effects for beta 1 beta 2

A

antagonism for beta 1 and beta 2 is equal

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6
Q

what is the standard drug to which all beta antagonist are compared

A

propanolol

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7
Q

propanolol cardiac effects

A

decreases heart rate

decreases myocardial contractility resulting in decreased CO

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8
Q

when are the effects of propanolol on the heart most prominent

A

during exercise or in the present of increased sympathetic nervous system activity

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9
Q

what are the sodium changes seen with propanolol

A

sodium retention due to intrarenal hemodynamic changes form decrease co

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10
Q

what is the effect of fentanyl administered to a patient being treated chronically with propanolol

A

pulmonary first pass uptake of fentanyl is substantially decreased two to 4 times as much injected fentanyl enters the systemic circulation

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11
Q

metoprolol which receptors

A

selective beta 1 antagonists

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12
Q

metoprolol responses

A

prevents inotropic and chronotropic responses

less likely to cause beta 2 issues

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13
Q

what is the concern with large doses of metoprolol

A

it will becomes nonselective exerting antagonist effects on beta 2 receptors.

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14
Q

how do you reverse the effects of (bronconstriction) metorpolol

A

terbutaline

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15
Q

labetalol which receptors

A

beta 1 beta 2 alpha 1

nonselective beta antagonist

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16
Q

with labetaolol what is the response of alpha two receptors

A

presynaptic alpha 2 receptors are spared such that released NE can continue to inhibit further release of catecholamines via negative feedback mechanism

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17
Q

labetaolol elimination half time

A

5-8 hours

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18
Q

labetaolol side effects

A

orthostatic hypotension most common side effect

bronchospasm

fluid retention -possibly need a diuretic

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19
Q

labetalol dose per hammon

A

10-20mg

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20
Q

clinical uses for labetalol

A

HTN emergency

angina pectoris

switching IV to po

type B thoracic aneurysm

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21
Q

verapamil describe it

supplied as?

A

derivative of papaverine

supplied as a racemic mixture

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22
Q

verapamil dextroisomer=

A

acts on fast sodium channels accounting for the local anesthetic effects of verapamil

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23
Q

verapamil levoisomer=

A

specific for slow calcium channel channels as a calcium channel blocker
1.6 as potent as procaine

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24
Q

verapamil side effects

A

negative inotropic

negative chronotropic

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25
Q

who should NOT get verapamil

A

heart failure

severe bradycardia

sinus node dysfunction/av nodal block

may precipitate ventricular dysrhythmias in WPW

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26
Q

clinical use of verapamil

A

SVT

vasospastic angina pectoris

essential HTN

lateral and fetal tachydysrhythmias

premature labor

decreases uterine blood flow

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27
Q

elimination half time of verapamil

A

6-12 hours

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28
Q

lidocaine, diazepam, propranolol increase the unbound portion of which drug

A

verapamil

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29
Q

diltiazem clinical use

A

SVT

HTN

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30
Q

what are the effects of diltiazem

A

the effects of diltiazem and its vasodilation properties appear to be intermediate between those of verapamil and dihydropyridines

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31
Q

dose of diltiazem

protein binding of diltiazem

A

70-80% protein bound

0.25-0.35mg/kg

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32
Q

giving verapamil and diltiazem in the presence of dantrolene will result in

A

hyperkalemia and cardiovascular collapse

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33
Q

daily dose of clonodine

A

0.2-0.3mg

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34
Q

name the drugs in class IA

A

quinidine
procainamide
disopyramide

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35
Q

name drugs in class IB

A

lidocaine
tocainide
mexiletine

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36
Q

name drugs in class IC

A

flecainide

propafenone

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37
Q

name the drugs in class III

A

amiodarone
sotalol
bretylium

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38
Q

name the drugs in class IV

A

verapamil

diltiazem

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39
Q

propfafenone side effects

A

proarrythmic-vtach

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40
Q

digoxin what does it do

A

depresses sa node

used for afib-atrial tachycardia

slows av node conduction

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41
Q

digoxin toxicity

A

NVD, yellow vision, increase pr, decrease QT, t wave inversion and arrythmias

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42
Q

dig toxicity treatment

A

anti dig fab fragment

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43
Q

verapamil dose

A

5-10mg

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44
Q

amiodarone toxicity

A

pulmonary fibrosis

hepatotoxicity

hypo/hyperthyrodism

corneal deposit

skin deposit

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45
Q

what is amiodarone used for

A

supra ventricular and ventricular tachyarrythmias /fib

preop oral administration decreases the incidence of afib after cardiac surgery

effective for suppression of WPW

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46
Q

when will amiodarone decrease mortality

A

after MI

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47
Q

class III to include amiodarone will have what affect on ap and ERP

A

increase AP duration

increase effective refractory period

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48
Q

blood volume total

plasma volume total

A

5L
3plasma
2 erythrocytes

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49
Q

what is the 60-40-20-15-5 rules

A 
60% water
40% intravascular
20% extravascular 
15% interstitial
5% plasma
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50
Q

minute ventilation=

A

tidal volume x breaths per minute

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51
Q

alveolar minute ventilation=

A

(tidal volume- deadspace) x RR

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52
Q

masseter spasm with succs seen in what age group and why?

A

seen in children because we didn’t give them enough

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53
Q 
succs
classification
dose
onset
duration
bottle
A 
depolarizing neuromuscular blocker
1-15.mg/kg-adult
2-4mg/kg-child
onset immediate 
duration 10min
20mg/ml
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54
Q

adverse effects of succs

A 
muscle pain
increased gastric pressure
increase intraocular pressure
cardiac arrythmias
sudden cardia arrest
braydcardia
antithymocyte globulin
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55
Q

precautions for succs

A

not to be used routinely for children less than 12 due to undiagnosed duchenne muscular dystrophy
MH
hyperkalemia

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56
Q

drugs that prolong succs?- from apex

A

metoclopramide

esmolol

neostigmine

echothiophate

oral contraceptives

MAOI

nitrogen mustard

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57
Q

stage 1

A

Stage I
Begins with induction of anesthesia
Ends with loss of consciousness (no eye-lid reflex)
Still can sense pain

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58
Q

stage 2

A 
Stage II
Delirium Excitement
Uninhibited excitation
Pupils dilated, divergent gaze
Potentially dangerous response to noxious stimuli:
Breath holding
Muscular rigidity
Vomiting
Laryngospasm

this is when we tell everyone to be quiet in the OR

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59
Q

stage 3

A

Stage III
Surgical Anesthesia
Centralized gaze with constriction of pupils
Regular respirations
Anesthesia depth is sufficient for noxious stimuli when the noxious stimuli dose not cause increase sympathetic response

60
Q

Stage IV

A 
Stage IV
Stay away from.   Too deep
Apnea
Non reactive dilated pupils
Hypotension resulting in complete CV collapse if not monitored closely
61
Q

sugammadex for what three drugs greatest to least

A

roc-vec-pan

62
Q

two things important about des

A

transient tachycardia

airway irritant

63
Q

things that make you increase MAC

A 
hyperthermia
red hair
drug induced catecholamines level
cyclospirine
hypernatremia
chronic alcoholism
64
Q

things that make you decrease MAC

A 
hypothermia
increasing age
preop meds
acute alcohol 
pregnant
lithium
hyponatremia
65
Q

which gas potentiates which neuromuscular

A

des- roc

66
Q

succs administration after already giving it will produce

A

possibly bradycardia-asystole- give atropine

67
Q

how many L of plasma are there

A

3 l

68
Q

first pass effect

A

drugs absorbed from the GI tract enter portal venous blood and pass through the liver before entering the systemic circulation.

69
Q

name two drugs that undergo extensive hepatic extraction and metabolism

A

propranolol

lidocaine

70
Q

ester vs amide

A

1 eyed ester

2 eyed amide

71
Q

pharmacodynamics

A

what the drug does to the body

72
Q

pharmacokinetics

A 
what the body does to the drug
absorption 
distribution
metabolism
excretion
73
Q

therapeutic index

A

LD50/ED50

74
Q

what index do we use in anesthesia

A

LD1/ED99

75
Q

potency refers to where on the graph

A

potency is the position on the x graph

76
Q

efficacy refers to where on the graph

A

refers to the position of the maximum effect on the Y axis.

77
Q

** roc elimination

A

metabolized in the liver and excreted in the bile

78
Q

how is remifentanil metabolised

A

nonspecific plasmaesterase hydrolysis

79
Q

if you give NSAIDS with what two drugs will make you toxic

A

lithium

digoxin

80
Q

neuraxial opioids issues

A

respiratory depression
younger guys get urinary retention- (interaction of opioid with opioid receptors in the sacral spinal cord)

itchy nose
pruritus - most common side effect- may be generalized but more likely to be localized to the face, neck, upper thorax- more likely to occur in obstetric patients. (interaction of estrogen with opioid receptors)

viral reactivation -2-5 days after epidural administration of the opioid.

sedation- most commonly associated with use of sufentanil

81
Q

where is mu 1 a dominant receptor

A

supraspinal

82
Q

where is mu2 a dominant receptor

A

spinal

83
Q

substantia gelatinosa is found

A

lamina II lamina III

84
Q

remifentanil is quick on quick off what do we give to cover

A

longer acting pain meds

85
Q

interesting things about NE-

A

cautiously in RV failure exacerbate right sided heart failure

86
Q

codeine

A

less potential for abuse- half that of morphine
is a prodrug- demethylated in the liver to morphine
-less euphoria than morphine

87
Q

tell me about morphine 6 glucuronide

A

analgesia and depression of ventilation via mu receptors
duration of action is greater than morphine.

650 fold higher potency than morphine.
low permeability to BBB

88
Q

how is morphine eliminated

A

conjugated in liver to active metabolite
excreted in urine

impaired in renal failure causing an accumulation of metabolites and unexpected ventilatory depression. greater than 7 days.

89
Q

how does suggamadex work

A

hydrophobic cavity with a hydrophilic exterior that encapsulates steroidal neuromuscular blocking drugs

90
Q

how is suggamadex eliminated

A

in the urine 75% - avoid with a creatine clearance less than 30. reverses within 3 minutes- no twitches needed
90% gone in 24 hours

91
Q

sugammadex how do we dose it and what do we tell young women

A

dosed off actual body weight

inhibits BC for 1 week.

92
Q

which blockers release histamine

A

atricurium
mivacurium
tubocurarine

93
Q

what are the histamine effects seen

A

skin flushing
decreases in blood pressure
SVR- increase in pulse rate

94
Q

pancuronium has what effect

A

vagolytic effect

95
Q

what does dibucaine number tell us

A

it inhibits normal PCHE around 80% inhibited

if its only 20 - then it only inhibited 20 meaning there is atypical PCHE.

96
Q

if a patient experiences prolonged apnea after succs what do you need to determine about the pseudocholinesterase

A

differentiate between atypical and low levels.

97
Q

volume controlled ventilation (VCV)=

A

the desired tidal volume is delivered at a constant flow.
inspiration is terminated when the desired tidal volume is delivered or if an excessive pressure is reached (60-100cm h20)

98
Q

what is the concern with volume controlled ventilation (VCV)

A

the peak inspiratory pressure is monitored but not controlled.

99
Q

pressure controlled ventilation (PCV)

A

peak inspiratory pressure is limited and the cycle is controlled by time. inspiratory flow is strongest early and increases lung inflation and oxygenation at the lowest PIP.

Tidal Volume is uncontrolled and increases if compliance increases.

100
Q

patients with low compliance benefit from PCV mode- name some conditions

A

pregnancy, laparoscopic surgery, morbid obesity, or adult respiratory distress syndrome. it can also compensate for leaks. and provide effective ventilation during one lung ventilation

101
Q

synchronized intermittent mandatory ventilation

A

used for short ambulatory or office based procedures, during spontaneous unassisted breathing.

SIMV- intermittent mandatory breaths are delivered in synchrony with the patients spontaneous efforts. SIMV-PS provides pressure support breathing when the patient is making an attempt.

102
Q

pressure controlled ventilation with volume guarantee

A

PCV-VG

it delivers a volume breath- inspiratory pressure is adjusted based off the patients compliance.

103
Q

pressure support ventilation

A

this mode offers a RR of zero. only useful for patients who are breathing spontaneously. some vents do allow a minimum back up ventilation.

104
Q

volume of distribution of opioids- greatest to least- (flood pg 226)

A

fentanyl>meperidine>morphine>sufentanil>remifentanil>alfentanil

105
Q

rate the neuromuscular blocking drugs from highest to lowest for risk of anaphylaxis

A

succs>atracurium>cisatracurium>roc>vec

106
Q

most local anesthetics are considered-

this local anesthetic is different and considered

A

weak bases

benzocaine is a weak acid

107
Q

what is the main difference in all beta blockers

which beta blocker lasts the longest

A

elimination half times

nadolol

108
Q

which inhaled gas is MOST potent

A

Isoflurane

109
Q

what is the second gas effect

A

reflects the ability of high volume uptake of one gas(first gas) to accelerate the rate of increase of the PA

110
Q

MAC of each gas

A 
halothan 0.75
enflurane 1.63
isoflurance 1.17
desflurane 6.6
sevoflurance 1.8
nitrous 104

xenon 63-71-if anyone cares

111
Q

MW of each gas

A 
nitrous 44
halothan 197
enflurane 184
isoflurance 184
desfluance 168
sevoflurane 200
112
Q

boiling point of each gas C

A 
nitrous---
halothane 50.2
enflurance 56.5
isoflurane 48.5
desflurane 22.8
sevoflurane 58.5
113
Q

vapor pressure of each gas mmhm 20C

A 
nitrous 
halothane- 244
enflurane 172
isoflurane 240
desflurane 669
sevoflurane 170
114
Q

odor of each gas

A

halothane = organic
nitrous =sweet
the rest are ethereal

115
Q

which gases need a preservative

A

halothane

116
Q

which gases are not stable in soda lime

A

halothane and sevo

117
Q

blood:gas of all gases

A 
nitrous 0.46
halothan 2.54
enflurane 1.90
isoflurane 1.46
desflurane 0.42
sevoflurane 0.69
118
Q

mac + nitrous

A 
nitrous
halothane 0.29
enflurane 0.57
isoflurane 0.50
desflurane 2.83
sevoflurane 0.66
119
Q

what are the analgesic effects of nitrous oxide- how long do they last

A

analgesic effects are prominent, but short lived and dissipate in 20 minutes

120
Q

what is the negatives of nitrous oxide

A

it increases the risk of post op nausea and vomiting. it inactivates vitamin b12. and increases the gas in open space- bowels- middle ear- expands pneumo

121
Q

how long does IPC last-

A

persist for 1-2 hours
reoccurring 24 hours
second or late window may last for as long as 3 days

122
Q

what is IPC

A

brief episodes of myocardial ischemia occurring before a subsequent longer period of myocardial ischemia providing protection against myocardial dysfunction and necrosis

123
Q

how is ischemic preconditioning mediated

A

release of adenosine - binds to adenosine receptors- increases protein kinase C activity. Resulting phosphorylation of adenosine triphosphate (ATP) sensitive mitochondrial potassium channels results in the channels being less sensitive to inhibition by ATP.

124
Q

oxidation, reduction and hydrolysis refers to

A

phase 1 metabolism

125
Q

conjugation refers to

A

phase 2 metabolism

126
Q

what does the concentration effect state

A

the higher the PI, the more rapidly the PA approaches the PI

127
Q

explain partial pressure of gases

A

a high PI delivered from the anesthetic machine is required during initial administration of the anesthetic.

a high initial input off sets the impact of uptake, acceleration induction of anesthesia as reflected by the rate of rise in the PA and this in the Pbrain.

128
Q

is MAC additive

A

yes

129
Q

what is mac bar

A

block autonomic response/following a supra maximal painful stimulus- 1.5MAC

130
Q

what mac is awareness and recall prevented

A
  1. 4-0.5 mac

0. 7 MAC or more to prevent conscious recall

131
Q

what is mac awake

A

0.15

132
Q

movement can be prevented in 95% of patients at what mac level

A

1.3mac

133
Q

hydralazine

A

direct systemic arterial vasodilator- hyper polarizes smooth muscles cells and activates guanylate cyclase to produce vasorelaxation.

134
Q

long term use of hydralazine

A

systemic lupus syndrome

135
Q

is hydralazine good for MI patients? why?

A

No, increases HR and myocardial contractility - but a good afterload reducer.

136
Q

what are the 5 subunits for the slow L type channel

A 
A1
A2
B
Y
D
137
Q

what subunit do calcium channel blockers bind to

A

alpha 1 subunit of the L type calcium channels thus diminishing entry of calcium ions into the cell.

138
Q 
duration of 
Pancuronium
rocuronium
vecuronium
atracurium
cisatracruium
mivacurium
A 
pancuronium 86
rocuronium 36
vecuronium 44
atracurium 46
cisatracrium 45
mivacurium 16
139
Q

nagelhout page 149 drugs that may inhibit cholinesterase

A

donepezil (aricept)

rivastigmine (exelon)

140
Q

diseases with markedly decrease pseudocholinesterase

A

acute or chronic liver disease, organophosphate poisoning, chronic renal disease. late stage pregnancy newborns, acute infections, pulmonary embolism, muscular dystrophy, myocardial infarction, and after certain surgical procedure

141
Q

toxic plasma concentrations of lidocaine are greater than

A

5-10mcg/ml

142
Q

what are the effects of toxic lidocaine

A

produce peripheral vasodilation and direct myocardial depression, resulting in hypotension. In addition, slowing of conduction of cardiac impulses may manifest as bradycardia, a prolonged P-R interval, and widened QRS complex on the ECG

  1. 1-5mcg/ml: Analgesia
  2. 5-10mcg/ml: Tinnitus & myocardial depression
  3. 10-15 mcg/ml: Seizures
  4. 15-25 mcg/ml: apnea
  5. > 25 mcg/ml: CV depression
143
Q

what is corticosteroid therapy used with

A

local anesthetics

144
Q

what can corticosteroid do with local anesthetics

A

it can prolong the block

prolong analgesia with ropiviacaine and bupivicaine for 22 hours. stronger with ropiviance.

145
Q

secondary treatment dose for corticosteriods

A

Corticosteroids (0.25–1 g hydrocortisone; alternatively, 1–2 g methylprednisolone)a

146
Q

abrupt d/c of corticosteroids

A

addisonian crisis

147
Q

what does dexamethasone minimize

A

opioid doses and decreases post op pain

Spring '20/ L. BASICS/PHARM FINAL (3 decks)

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