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?
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
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
4
Q
propranolol tell me about the receptor activity
A
nonselective beta antagonist
lacks intrinsic sympathomimetic activity=pure antagonist
5
Q
propranolol effects for beta 1 beta 2
A
antagonism for beta 1 and beta 2 is equal
6
Q
what is the standard drug to which all beta antagonist are compared
A
propanolol
7
Q
propanolol cardiac effects
A
decreases heart rate
decreases myocardial contractility resulting in decreased CO
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
9
Q
what are the sodium changes seen with propanolol
A
sodium retention due to intrarenal hemodynamic changes form decrease co
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
11
Q
metoprolol which receptors
A
selective beta 1 antagonists
12
Q
metoprolol responses
A
prevents inotropic and chronotropic responses
less likely to cause beta 2 issues
13
Q
what is the concern with large doses of metoprolol
A
it will becomes nonselective exerting antagonist effects on beta 2 receptors.
14
Q
how do you reverse the effects of (bronconstriction) metorpolol
A
terbutaline
15
Q
labetalol which receptors
A
beta 1 beta 2 alpha 1
nonselective beta antagonist
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
17
Q
labetaolol elimination half time
A
5-8 hours
18
Q
labetaolol side effects
A
orthostatic hypotension most common side effect
bronchospasm
fluid retention -possibly need a diuretic
19
Q
labetalol dose per hammon
A
10-20mg
20
Q
clinical uses for labetalol
A
HTN emergency
angina pectoris
switching IV to po
type B thoracic aneurysm
21
Q
verapamil describe it
supplied as?
A
derivative of papaverine
supplied as a racemic mixture
22
Q
verapamil dextroisomer=
A
acts on fast sodium channels accounting for the local anesthetic effects of verapamil
23
Q
verapamil levoisomer=
A
specific for slow calcium channel channels as a calcium channel blocker
1.6 as potent as procaine
24
Q
verapamil side effects
A
negative inotropic
negative chronotropic
25
who should NOT get verapamil
heart failure
severe bradycardia
sinus node dysfunction/av nodal block
may precipitate ventricular dysrhythmias in WPW
26
clinical use of verapamil
SVT
vasospastic angina pectoris
essential HTN
lateral and fetal tachydysrhythmias
premature labor
decreases uterine blood flow
27
elimination half time of verapamil
6-12 hours
28
lidocaine, diazepam, propranolol increase the unbound portion of which drug
verapamil
29
diltiazem clinical use
SVT
HTN
30
what are the effects of diltiazem
the effects of diltiazem and its vasodilation properties appear to be intermediate between those of verapamil and dihydropyridines
31
dose of diltiazem
| protein binding of diltiazem
70-80% protein bound
0.25-0.35mg/kg
32
giving verapamil and diltiazem in the presence of dantrolene will result in
hyperkalemia and cardiovascular collapse
33
daily dose of clonodine
0.2-0.3mg
34
name the drugs in class IA
quinidine
procainamide
disopyramide
35
name drugs in class IB
lidocaine
tocainide
mexiletine
36
name drugs in class IC
flecainide
| propafenone
37
name the drugs in class III
amiodarone
sotalol
bretylium
38
name the drugs in class IV
verapamil
| diltiazem
39
propfafenone side effects
proarrythmic-vtach
40
digoxin what does it do
depresses sa node
used for afib-atrial tachycardia
slows av node conduction
41
digoxin toxicity
NVD, yellow vision, increase pr, decrease QT, t wave inversion and arrythmias
42
dig toxicity treatment
anti dig fab fragment
43
verapamil dose
5-10mg
44
amiodarone toxicity
pulmonary fibrosis
hepatotoxicity
hypo/hyperthyrodism
corneal deposit
skin deposit
45
what is amiodarone used for
supra ventricular and ventricular tachyarrythmias /fib
preop oral administration decreases the incidence of afib after cardiac surgery
effective for suppression of WPW
46
when will amiodarone decrease mortality
after MI
47
class III to include amiodarone will have what affect on ap and ERP
increase AP duration
| increase effective refractory period
48
blood volume total
| plasma volume total
5L
3plasma
2 erythrocytes
49
what is the 60-40-20-15-5 rules
```
60% water
40% intravascular
20% extravascular
15% interstitial
5% plasma
```
50
minute ventilation=
tidal volume x breaths per minute
51
alveolar minute ventilation=
(tidal volume- deadspace) x RR
52
masseter spasm with succs seen in what age group and why?
seen in children because we didn't give them enough
53
```
succs
classification
dose
onset
duration
bottle
```
```
depolarizing neuromuscular blocker
1-15.mg/kg-adult
2-4mg/kg-child
onset immediate
duration 10min
20mg/ml
```
54
adverse effects of succs
```
muscle pain
increased gastric pressure
increase intraocular pressure
cardiac arrythmias
sudden cardia arrest
braydcardia
antithymocyte globulin
```
55
precautions for succs
not to be used routinely for children less than 12 due to undiagnosed duchenne muscular dystrophy
MH
hyperkalemia
56
drugs that prolong succs?- from apex
metoclopramide
esmolol
neostigmine
echothiophate
oral contraceptives
MAOI
nitrogen mustard
57
stage 1
Stage I
Begins with induction of anesthesia
Ends with loss of consciousness (no eye-lid reflex)
Still can sense pain
58
stage 2
```
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
59
stage 3
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
Stage IV
```
Stage IV
Stay away from. Too deep
Apnea
Non reactive dilated pupils
Hypotension resulting in complete CV collapse if not monitored closely
```
61
sugammadex for what three drugs greatest to least
roc-vec-pan
62
two things important about des
transient tachycardia
| airway irritant
63
things that make you increase MAC
```
hyperthermia
red hair
drug induced catecholamines level
cyclospirine
hypernatremia
chronic alcoholism
```
64
things that make you decrease MAC
```
hypothermia
increasing age
preop meds
acute alcohol
pregnant
lithium
hyponatremia
```
65
which gas potentiates which neuromuscular
des- roc
66
succs administration after already giving it will produce
possibly bradycardia-asystole- give atropine
67
how many L of plasma are there
3 l
68
first pass effect
drugs absorbed from the GI tract enter portal venous blood and pass through the liver before entering the systemic circulation.
69
name two drugs that undergo extensive hepatic extraction and metabolism
propranolol
lidocaine
70
ester vs amide
1 eyed ester
| 2 eyed amide
71
pharmacodynamics
what the drug does to the body
72
pharmacokinetics
```
what the body does to the drug
absorption
distribution
metabolism
excretion
```
73
therapeutic index
LD50/ED50
74
what index do we use in anesthesia
LD1/ED99
75
potency refers to where on the graph
potency is the position on the x graph
76
efficacy refers to where on the graph
refers to the position of the maximum effect on the Y axis.
77
** roc elimination
metabolized in the liver and excreted in the bile
78
how is remifentanil metabolised
nonspecific plasmaesterase hydrolysis
79
if you give NSAIDS with what two drugs will make you toxic
lithium
| digoxin
80
neuraxial opioids issues
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
where is mu 1 a dominant receptor
supraspinal
82
where is mu2 a dominant receptor
spinal
83
substantia gelatinosa is found
lamina II lamina III
84
remifentanil is quick on quick off what do we give to cover
longer acting pain meds
85
interesting things about NE-
cautiously in RV failure exacerbate right sided heart failure
86
codeine
less potential for abuse- half that of morphine
is a prodrug- demethylated in the liver to morphine
-less euphoria than morphine
87
tell me about morphine 6 glucuronide
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
how is morphine eliminated
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
how does suggamadex work
hydrophobic cavity with a hydrophilic exterior that encapsulates steroidal neuromuscular blocking drugs
90
how is suggamadex eliminated
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
sugammadex how do we dose it and what do we tell young women
dosed off actual body weight
| inhibits BC for 1 week.
92
which blockers release histamine
atricurium
mivacurium
tubocurarine
93
what are the histamine effects seen
skin flushing
decreases in blood pressure
SVR- increase in pulse rate
94
pancuronium has what effect
vagolytic effect
95
what does dibucaine number tell us
it inhibits normal PCHE around 80% inhibited
| if its only 20 - then it only inhibited 20 meaning there is atypical PCHE.
96
if a patient experiences prolonged apnea after succs what do you need to determine about the pseudocholinesterase
differentiate between atypical and low levels.
97
volume controlled ventilation (VCV)=
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
what is the concern with volume controlled ventilation (VCV)
the peak inspiratory pressure is monitored but not controlled.
99
pressure controlled ventilation (PCV)
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
patients with low compliance benefit from PCV mode- name some conditions
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
synchronized intermittent mandatory ventilation
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
pressure controlled ventilation with volume guarantee
PCV-VG
| it delivers a volume breath- inspiratory pressure is adjusted based off the patients compliance.
103
pressure support ventilation
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
volume of distribution of opioids- greatest to least- (flood pg 226)
fentanyl>meperidine>morphine>sufentanil>remifentanil>alfentanil
105
rate the neuromuscular blocking drugs from highest to lowest for risk of anaphylaxis
succs>atracurium>cisatracurium>roc>vec
106
most local anesthetics are considered-
| this local anesthetic is different and considered
weak bases
| benzocaine is a weak acid
107
what is the main difference in all beta blockers
| which beta blocker lasts the longest
elimination half times
nadolol
108
which inhaled gas is MOST potent
Isoflurane
109
what is the second gas effect
reflects the ability of high volume uptake of one gas(first gas) to accelerate the rate of increase of the PA
110
MAC of each gas
```
halothan 0.75
enflurane 1.63
isoflurance 1.17
desflurane 6.6
sevoflurance 1.8
nitrous 104
```
xenon 63-71-if anyone cares
111
MW of each gas
```
nitrous 44
halothan 197
enflurane 184
isoflurance 184
desfluance 168
sevoflurane 200
```
112
boiling point of each gas C
```
nitrous---
halothane 50.2
enflurance 56.5
isoflurane 48.5
desflurane 22.8
sevoflurane 58.5
```
113
vapor pressure of each gas mmhm 20C
```
nitrous
halothane- 244
enflurane 172
isoflurane 240
desflurane 669
sevoflurane 170
```
114
odor of each gas
halothane = organic
nitrous =sweet
the rest are ethereal
115
which gases need a preservative
halothane
116
which gases are not stable in soda lime
halothane and sevo
117
blood:gas of all gases
```
nitrous 0.46
halothan 2.54
enflurane 1.90
isoflurane 1.46
desflurane 0.42
sevoflurane 0.69
```
118
mac + nitrous
```
nitrous
halothane 0.29
enflurane 0.57
isoflurane 0.50
desflurane 2.83
sevoflurane 0.66
```
119
what are the analgesic effects of nitrous oxide- how long do they last
analgesic effects are prominent, but short lived and dissipate in 20 minutes
120
what is the negatives of nitrous oxide
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
how long does IPC last-
persist for 1-2 hours
reoccurring 24 hours
second or late window may last for as long as 3 days
122
what is IPC
brief episodes of myocardial ischemia occurring before a subsequent longer period of myocardial ischemia providing protection against myocardial dysfunction and necrosis
123
how is ischemic preconditioning mediated
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
oxidation, reduction and hydrolysis refers to
phase 1 metabolism
125
conjugation refers to
phase 2 metabolism
126
what does the concentration effect state
the higher the PI, the more rapidly the PA approaches the PI
127
explain partial pressure of gases
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
is MAC additive
yes
129
what is mac bar
block autonomic response/following a supra maximal painful stimulus- 1.5MAC
130
what mac is awareness and recall prevented
0. 4-0.5 mac
| 0. 7 MAC or more to prevent conscious recall
131
what is mac awake
0.15
132
movement can be prevented in 95% of patients at what mac level
1.3mac
133
hydralazine
direct systemic arterial vasodilator- hyper polarizes smooth muscles cells and activates guanylate cyclase to produce vasorelaxation.
134
long term use of hydralazine
systemic lupus syndrome
135
is hydralazine good for MI patients? why?
No, increases HR and myocardial contractility - but a good afterload reducer.
136
what are the 5 subunits for the slow L type channel
```
A1
A2
B
Y
D
```
137
what subunit do calcium channel blockers bind to
alpha 1 subunit of the L type calcium channels thus diminishing entry of calcium ions into the cell.
138
```
duration of
Pancuronium
rocuronium
vecuronium
atracurium
cisatracruium
mivacurium
```
```
pancuronium 86
rocuronium 36
vecuronium 44
atracurium 46
cisatracrium 45
mivacurium 16
```
139
nagelhout page 149 drugs that may inhibit cholinesterase
donepezil (aricept)
| rivastigmine (exelon)
140
diseases with markedly decrease pseudocholinesterase
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
toxic plasma concentrations of lidocaine are greater than
5-10mcg/ml
142
what are the effects of toxic lidocaine
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
what is corticosteroid therapy used with
local anesthetics
144
what can corticosteroid do with local anesthetics
it can prolong the block
prolong analgesia with ropiviacaine and bupivicaine for 22 hours. stronger with ropiviance.
145
secondary treatment dose for corticosteriods
Corticosteroids (0.25–1 g hydrocortisone; alternatively, 1–2 g methylprednisolone)a
146
abrupt d/c of corticosteroids
addisonian crisis
147
what does dexamethasone minimize
opioid doses and decreases post op pain
