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Pharm Semester 2 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Anesthesia

A

artificially induces loss of ability to feel pain

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2
Q

Anesthesia purpose

A

to permit the performance of surgery or painful procedures. not ANS, no movement, not aware

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3
Q

GA

A

drug induces loss of consciousness
patient is not arrousable event to painful stimuli
don’t have to intubated/ vent or on volatile anesthetics

independent ventilatory function often impaired; airway, ventilation, cv support

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4
Q

Regional/ peripheral anesthesia

A

Insensibility caused by interrupting the sensory nerve conduction of a particular region of the body
Peripheral
spinal
epidural

LOC is unchanged (unless sedatives are used)

ventilatory/airway protection is maintained

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5
Q

Sedation

A

3 levels
spectrum of consciousness between awake and unconscious

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6
Q

minimal sedation

A

anxiolysis
ex; 2mg of versed
“I dont care” meds
responsive to verbal commands
airway, spont ventilation, cardiac function are unaffected

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7
Q

moderate sedation

A

ex; 5mg of versed
responsive to verbal/touch
no assistance needed with the pts airway
spont ventilation is adequate
cardiac function is usually maintained

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8
Q

Deep sedation

A

responsiveness after repeated or painful stimulations
assistance might be required for airway
spont ventilation is possible inadequate
cardiac function is usually maintained

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9
Q

What methods were used between 4000BC and 400 BC

A

Poppy, cocoa leaves
acupuncture
ethylene fumes from geological fault lines beneath apollos temple
cannabis vapor
carotid compression

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10
Q

Hippocrates

A

accommodate the operator/ surgeron
avoid sinking down and turning away

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11
Q

1st Pharm book

A

Materia medica
written by Discorides - surgeon in Neros army
5 volumes; plants, animal and mineral products
360 medical properties; antiseptic, anti-inflammatory, mental cramps, psych problems

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12
Q

Mandragora (mandrake) and wine

A

used in the early days as hallucinogenic, human shaped, considered to have magical properties

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13
Q

soporifices

A

liquid on sponge- inhalations/ smell and breathe it in

in the middle agest they used;

1/2 ounce of opium
juice of mandrake leaves
juice of hemlock
3 oz of hyposycamus
sufficient water

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14
Q

reversal for soporifics

A

vinegar

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15
Q

hyposcyamus

A

L- isomer of atropine

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16
Q

1st inhalation anesthetic

A

Diethyl ether
made from sulfuric acid and ethyl alcohol
named ether; greek for ignite/ explode
tested on chickens
recreation d/t whiskey tax

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17
Q

Valerius Cordus

A

made the first inhalational anesthetic, diethyl ether
German botanis/ physician

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18
Q

Sir christopher Wren and Robert Boyle

A

Created IV therapy using a good quill and bladder as bag
administered alcohol into a dogs vein
witnessed metabolism of drugs
was a member of the royal society of London

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19
Q

Joseph priestly

A

English chemist
discovers oxygen and nitrous oxide
discovered photosynthsis

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20
Q

Humphry Davy

A

British chemist
discovered the elements; k, na, ca, mg
Suggested to use N2O for surgical pain control (not appreciated)- didn’t help with movement

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21
Q

Horace wells

A

dentist
noticed that a man under the influence of N2O had no recall of pain/ injury
self administered for tooth extraction and uses on several dental patients
Public demonstration at mass general for arranged administration of N2O for amputation but pt moved “humbug?”

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22
Q

Andrews

A

Chicago surgeon
N2O and oxygen anesthesia without cyanosis= dec mortality

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23
Q

Hewitt

A

1st anesthesia machine with N20/ O2

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24
Q

Crawford long

A

delivered Ether for a pt with 2 vascular neck tumors
continued use of whiskey

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25
Q

William morton

A

Dentist
needed anesthesia for denture fitting (made of wood at the time)

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26
Q

1st public demonstration of ether

A

1846
called it Letheon….made it to england in 60 days
didnt have; iv access, prolonged emergence, variable quality, proper filling mask

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27
Q

Dr Robinson squibb

A

developed process for pure ether
founded squibb pharmaceuticals…leading manufacturer

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28
Q

disadvantages of ether

A

flammable
prolonged induction (long on and off set)
unpleasant, persistent odor
high incidence of N/V

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29
Q

Sir James simpson

A

OB in scotland
experimented w/ chloroform following dinner parties
defined pain; actual or potential tissue damage
religious opposition

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30
Q

Bible quote used against religious opposition

A

Genesis 2;21

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31
Q

John snow

A

Fill time anesthetist
used chloroform for queen victory; prince leopold and princess beatrice

disc epidemiology when he traced London cholera outbreak to water sources

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32
Q

Hyderbad commissions

A

said chloroform was safe with their methods
respiratory and cardiac paralysis convinced them chloroform might not be safe
430 cases w/o recording devices + 157 cases with recording devices

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33
Q

Guthrie

A

Discovered delayed chloroform hepatotoxicity in children

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34
Q

Levy

A

light chloroform anesthesia and adrenaline, fatal vf in adults, half awake; sleep->ans->NE-> vf

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35
Q

What was cocaine used for

A

sinus/nasal surgeries-> local anesthetic

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36
Q

Dr Koller

A

Viennese opthamologist (colleague of Sigmund Freud)
Used cocaine for anesthetic for eye surgery

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37
Q

dr Halsted

A

first regional (mandibular) nerve block w/ cocaine

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38
Q

dr august bier

A

1st spinal anesthetic with cocaine
developed Bier block

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39
Q

sister mary bernard

A

low pay
intelligent
focus/ attentive

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40
Q

Alice Magaw

A

Mother of anesthesia
14,000 open drop ether cases w/o death

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41
Q

Agatha Hodgins

A

worked for crile brothers
opened on of 1st nurse anesthesia schools
taught in france during WW1
developed N2O/ O2 techniques
founded AANA

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42
Q

Cyclopropane

A

violently explosive/ hospital explosions

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43
Q

Halothane

A

developed Hepatitis
slow onset

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44
Q

Isoflurane

A

Relatively safe/ cheap
Less N/v
Quicker onset than Halothane.
slow onset/ slow offset-> use for icu/ not extubating pts
Turn off 20 min before bandage

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45
Q

Furane

A

Desflurane
rapid uptake and distribution (most rapid onset and offset)
High vapor pressure- almost same as atm (vaporizes quickly)
large quantitiy to achieve anesthesia
good for out pt sx

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46
Q

Edmund Egar

A

Did all of the experimentation on desflurane
developed the end- tidal concentration correlated to movement (MAC

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47
Q

MAC

A

minimal alveolar concentration; dose of volatile anesthetic

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48
Q

Sevoflurane

A

intermediate action between iso and forane

unstable in soda lime; toxic degradation product concerns (CO2 absorber Pellets)—-disproven

good for asthmatics/ kids because it doesnt cause airway irritation

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49
Q

Triad of anesthesia

A

Amnesia
analgesia
muscle relaxation

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50
Q

Preemptive Anesthesia/ analgesia

A

given before causing pain

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51
Q

Amnesia

A

Stimulation of inhibitory Transmission; ach
inhibit stimulatory transmission; GABA

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52
Q

Analgesia

A

morphine from Opium
not favored at first because of high death rate
Synthetic derivatives; demerol, fent, sufent, remi fent, hydromorphone

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53
Q

Todays analgesics

A

Narcotics (opioids)
Cox inhibitors
Gabapentins (pregaline)
Acetaminophen
Peripheral nerve blocks

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54
Q

Curare

A

muscle relaxation
from plant in south america/ blow darks
decrease amount of anesthesia due to relaxation decreased mortality

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55
Q

Balanced anesthesia

A

Muscle relaxatoin, amnesia, analgesia, homeostasis

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56
Q

Dr liston

A

3 death 1 operation (300%) mortality rate. in an attempt to quickly amputate in 2.5 minutea
hand washing, washing clothes, washing instruments

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57
Q

George crile

A

cleveland clinic
light N2O/O2 anesthesia
local infiltration of procaine/ preemptive anesthesia
helped w/ homeostasis

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58
Q

harvey cushing

A

Regional blocks prior to emergence from ether
anesthetic records, BP/HR measurements

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59
Q

Neolept Anesthesia

A

high amnestic dose, little volatile/ muscle relaxant
opiods, antiphsychotics (aldol, droperidol), nitrous
Block Autonomic and endocrine response to stressed,

high incidence of awareness, dysphoria, extrapyramidal movements

surgical stimulation produced despite lack of movement
tachycardic
htn
problem with CAD pts….Beta blockade
high dose opioid technique - had its own problems

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60
Q

surgical stimulation produced despite lack of movement

A

tachycardia

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61
Q

Preoperative period phase

A

BZD, H1 and H2 blockers, bronchodilators

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62
Q

Induction of anesthesia

A

Eomidate, ketamine, propofol, narcotics

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63
Q

maintenance of anesthesia

A

inhalation drugs, nm blockers, pressors, blockers

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64
Q

Emergence from anesthesia

A

NMB reversal, local anesthetics

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65
Q

Dr guedels

A

Reference chart for stages of anesthesia
also made oral airways

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66
Q

Stage 1

A

Beginning of induction of general anesthesia to loss of consciousness (sternal rub and no movement)

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67
Q

Stage 1 1st plane

A

no amnesia or analgesia- normal

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68
Q

Stage 1 2nd plane

A

amnestic but only partially analgesic- still remember hurting

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69
Q

Stage 1 3rd plane

A

Complete analgesia and amnesia

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70
Q

Stage 2

A

Loss of consciousness to onset of automatic breathing
eyelash reflex disappears
coughing, vomiting, stuggling to occur
irregular respirations w/ breath holding

dangerous stage
high risk for aspiration and bronchospasms- dont extubate
dont touch, dont move, be quiet

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71
Q

Stage 3

A

onset of autonmatic respiration to respiratory paralysis (surgical plane)

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72
Q

Stage 3 1st plane

A

automatic respiration to cessation of eyeball movment

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73
Q

Stage 3 2nd plane

A

Cessation of eyeball movement to beginning of intercostal muscle paralysis; secretion of tears increase

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74
Q

Stage 3 3rd plane

A

beginning to completion of intercostal muscle paralysis; pupils dilate; desired plane prior to muscle relaxants

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75
Q

Stage 3 4th plane

A

complete intercostal paralysis to diaphragmatic paralysis (apnea)

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76
Q

Stage 4

A

stoppage of respiration till death

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77
Q

Drug effects to the number of _______

A

bound receptors
greatest effect = all receptors bound

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78
Q

Agonists

A

Activates receptor by binding to receptor

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79
Q

Hydrogen bonding

A

binding to a very electronegative atom

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80
Q

Ion/ electrocovalent binding

A

Oppositely charged ions

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81
Q

Van der alls interactions

A

the sum of attractive or repulsive forces; creates orbital shift

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82
Q

antagonist

A

binds to a receptor but does not activate the receptor
get in the way of the agonist.

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83
Q

Competitive antagonism

A

Increasing amounts progressively inhibit the agonist
Shifts dose response curves to the right
inc competitive antagonism = dec agonist response

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84
Q

Non-competitive antagonism

A

Even high concentrations of agonist cannot cause the agonist effect

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85
Q

Partial agonist

A

Binding to a receptor (usually at agonist site)
causes less response than the agonist even at supramaximal doses

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86
Q

Inverse agonist

A

Compete for the same site as the agonist but produce the opposite effect

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87
Q

Meds that use lipid bilayer R

A

Opioids, bzd, b-blockers, catecholamines, nmbd

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88
Q

meds that use intracellular proteins

A

Insulin, steroids, milrinone

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89
Q

Meds that use circulating proteins

A

anticoagulants

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90
Q

Pharmacokinetics

A

Quantitative study-Of injected and inhaled drugs (and their metabolites)
ADME

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91
Q

Central compartment

A

What dilutes the drug in the first minute following injection
Venous blood in arm, inferior vena cava, right heart, pulmonary vessels, lungs, left heart, aorta
Then mix with “vessel rich group”

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92
Q

Acidic drugs bind primarily to

A

albumin

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93
Q

Alkalotic bind drugs primarily to

A

a1-acid glycoprotein

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94
Q

Only______drug can cross cell membranes (distribution)/ dtermine concentration available to R (potency)

A

free/unbound

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95
Q

Causes of decreased plasma proteins

A

Age
Hepatic disease
Renal failure
Pregnancy

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96
Q

Thiopental and diazepam are ____protein binding

A

poor

they are also lipophilic
Big volume of distribution

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97
Q

Warfarin is_____protein bound to plasma proteins

A

highly

Small volume of distribution
decreased free drug

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98
Q

What metabolizes drugs in the liver

A

hepatic microsomal enzymes
most anesthetics

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99
Q

Examples of drugs that have active metabolites

A

diazepam (valium)
propanolol (inderal)
morphine
prodrugs such as codeine

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100
Q

Examples of drugs that have active metabolites

A

diazepam (valium)
propanolol (inderal)
morphine
prodrugs such as codeine

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101
Q

What metabolizes drugs in the plasma

A

Hoffman elimination and ester hydrolysis

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102
Q

what metabolizes drugs in the GI tract/ placenta

A

Tissue esterase

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103
Q

Phase 1 metabolic reaction

A

increase polarity through; Oxidation, Reduction, or Hydrolysis

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104
Q

Phase 2 metabolism

A

covalently link with a highly polar molecule to become water soluble
Conjugation

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105
Q

Cyp450

A

10 isoforms
Membrane bound
Contains a heme cofactor
Involves oxidation and reduction

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106
Q

CYP2

A

40% homologous

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107
Q

CYP2A

A

55% homologous

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108
Q

Cyp2a6

A

the individual enzyme

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109
Q

Cyp3a4

A

most common
Up to 60% of cyP450 activity
Metabolizes > 50% of drugs: opioids, BZP, LA, immunosuppressants, antihistamines

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110
Q

Induction of metabolic enzymes……

A

Increased amount of enzyme/ metabolism

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111
Q

Inhibition of metabolic enzymes

A

Decreased activity of enzyme

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112
Q

Hepatic clearance

A

For most anesthetic drugs clearance is constant
Rate is proportional to concentration- More drug/more clearance

At some point metabolism is exceeded since liver capability is not unlimited

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113
Q

Rate of drug metabolism equation

A

R = Q (C inflow- C outflow)

CO x (concentration in - concentration out)

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114
Q

Flow limited hepatic clearance

A

Q limits metabolic rate
cardiac output?

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115
Q

Capacity limited

A

liver’s ability to metabolize is limiting factor

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116
Q

Glomerular filtration and renal clearance

A

GFR and amount of protein bound drug controls amount of drug entering tubule

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117
Q

Passive tubular reabsorption

A

Increased if drug lipid soluble, ie. thiopental (reabsorbed)

Almost zero for water soluble drugs are reabsorbed, they are excreted in urine

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118
Q

Active tubular secretion

A

From peritubular capillaries
Active transport process
penicillins

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119
Q

Elimination ½ time

A

Time necessary to eliminate 50% of drug from plasma after bolus dose

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120
Q

Elimination ½ life

A

Time necessary to eliminate 50% of drug from body.

cant be measured

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121
Q

Context sensitive half-time

A

Time to a 50% decrease after infusion discontinued
Assumes a constant concentration
Roughly relates to ½ life
Increases the longer the infusion increases
Accumulation in peripheral tissues

122
Q

When the pk (dissociation constant) and ph are identical

A

50% of drug ionized, 50% of drug non-ionized

123
Q

Acid drugs are ionized in____ ph

A

Alkaline

124
Q

Bases are ionized in ____ph

A

acid

125
Q

Ionized molecules / drugs are…..

A

inactive
water soluble
dont cross lipid barriers
are excreted in the kidneys
and do not undergo hepatic metabolism

126
Q

non-ionized drugs

A

active
lipid soluble (get to R)
cross lipid barriers
are not excreted in the kidney’s
and do undergo hepatic metabolism

127
Q

Weak acids ionization formula (barbituarates)

A

pk after ph

So if a weak acid (pk 7.6) is put in a basic ph (blood 7.8)
7.8 – 7.6 = +0.2 acid drugs are ionized at basic ph

128
Q

Weak bases ionization formula (LA or opioids)

A

pk before ph

If weak base (pk 8.0) is put in an acid ph (Blood 7.2)
8.0 – 7.2= +0.8 weak bases are ionized at acid ph

129
Q

What numbers are non ionized?

A

nicely negative numbers are non ionized

130
Q

pharmacodynamics

A

“what the drug does to the body”
drug effects

131
Q

Potency

A

concentration vs response….less drug with more effect = more potent

least amount of drug needed for effect

132
Q

Efficacy

A

the ability of a drug to produce a clinical effect

how much of the effect can I get.

133
Q

ED50

A

dose required to produce effect in 50% of patients

134
Q

LD50

A

Dose required to produce death in 50% of patients

135
Q

Therapeutic index

A

ratio between (LD50/ED50 )

136
Q

Stereochemistry

A

How drug molecules are structured In 3 dimensions

137
Q

Chiral compounds

A

Molecules with asymmetric centers
Usually related to way carbon molecules are bonded

138
Q

Usually related to way carbon molecules are bonded

A

Chemically identical
Mirror images
Can’t be superimposed

139
Q

Right Enantiomers

A

Dextrorotatory
R: Rectus

140
Q

Left enantionmers

A

Levorotatory
S: Sinister

141
Q

50/50 mixture of enantiomers

A

racemic
Optical activity equal
Can exhibit different ADME
One enantiomer is active; other inactive or side effects

142
Q

S-enantiomer of ketamine

A

more potent with less delirium

143
Q

L-bupivicaine

A

less cardiac toxicity

144
Q

Cisatracurium, the isomer of atracurium

A

lacks histamine effects

145
Q

Pharmacogenetics/pharmacogenomics

A

How a single gene or all genes (genome) influences responses to drugs

146
Q

Pharmacogenetic testing

A

Look for variants in genes that code for;
Drug-metabolizing enzymes
Drug targets
Immune proteins

147
Q

Phenobarbital_____enzyme

A

induces = increased metabolism of drugs (benzos/opioid) = dec drug effect

148
Q

Grape fruit juice _____ enzymes

A

inhibits = decreased activity of enzyme = increased concentration of drugs/ toxicity levels

149
Q

Alcohol impairment requires more or less anesthesia?

A

Less

150
Q

Marijuana requires more or less anesthesia

A

more

151
Q

medications that do not increase half time with infusion

A

prop
sufentanil
alfentanil

152
Q

medications that increase half time with infusion

A

fent
thiophental
midazolam

153
Q

Relative potency

A

lag time between administration (plasma concentration and effect)

154
Q

Enantiomers

A

chemically identical
mirror images
cant be superimposed

155
Q

Sedatives

A

a drug that induces calm or sleep

156
Q

Hypnotics

A

a drug that induces hypnosis or sleep

157
Q

Sleep share what similarities with anesthesia

A

Both inhibits mid-brain reticular activating system in the thalamus

and reversible inhibit the CNS

158
Q

EEG is related to

A

Cerebral Blood flow
CMRO2- cerebral metabolic requirement of oxygen (metabolic activity)

anesthesia alters these

159
Q

medications with less correlation between BIS and movement

A

High dose narcotic

160
Q

BIS < 58

A

not conscious

161
Q

BIS < 65

A

had less than 5% chance of return to consciousness within 50 sec

162
Q

Signal quality index

A

SQI
good signal or lot of artifact

163
Q

EMG

A

are they going to move, are their muscles tightening up?

164
Q

EEG

A

Electroencephalograms

165
Q

Suppression Ration

A

how many seconds in the last minute has the eeg been flat. should be 0.

166
Q

GA BIS range

A

40-60

no movement or recall

167
Q

Ketamine and BIS

A

false high number on BIS because its a sympathomimetic and its responding to the metabolic activity on the ketamine

168
Q

Beta Blockers and BIS

A

dec hr = dec CO = dec CBF = dec bis (false low)

169
Q

Benzo effect

A

anxiolytics

sedation (decrease alpha activity)

anterograde amnesia (lasts longer than sedative effects)

anticonvulsant

Spinal cord mediated skm relaxation

unable to produce isoelectric state (ceiling effect)

170
Q

MOA for benzos

A

Gamma-aminobutyric acid mediated
Facilitates action of GABA at GABAA chloride ionophore
Enhance affinity of receptor for GABA
Enhanced opening of Cl- channels
Hyperpolarization of postsynaptic membrane…more resistant to depolarization

171
Q

Benzo R site

A

Between the gamma and alpha subunits on GABA R

172
Q

Alpha 1 subunit

A

EFFECTS: sedative, amnestic, anticonvulsant
most abundant type
Cerebral cortex, cerebellar cortex, thalamus

173
Q

alpha-2 effect and location

A

EFFECTS: Anxiolytic, skeletal muscle

Hippocampus, amygdala

174
Q

GABA A receptor binding sites other than benzodiazepines

A

Barbiturates
Etomidate
Propofol
Alcohol

175
Q

Benzo VOD

A

Highly lipid soluble (large volume of distribution)
highly protein bound (96-98%)(albumin)- not alot to cross the lipid bilayer

works and goes away quickly

176
Q

Benzos and platelets

A

inhibits plat aggregation/ inhibits conformational change in plat membrane

(increased bleeding time)

177
Q

Versed is ____ as potent as Diazepam (valium)

A

2-3 x

greater affinity for the R

Clearance 5x faster than lorazepam
10x faster than diazepam

178
Q

Versed effects

A

amnesia > sedation

179
Q

Midazolam is _____soluble

A

water

doesnt burn when injected and dont need additive

180
Q

Midazolam IV solution PH

A

3.5

181
Q

Versed imidazole ring is open when….

A

ph < 3.5 = water soluble/ pronated

182
Q

Versed imidazole ring is closed when……

A

ph > 4.0= lipid soluble = unprotonated

183
Q

Solubizing additive

A

Propylene glycol

184
Q

Midazolam onset

A

1-2 min

185
Q

midazolam peak effect

A

5 minutes

186
Q

Why does midazolam have a short duration?

A

doesn’t stay on R long because lipid solubility = rapid redistribution

187
Q

Midazolam elimination half time

A

2 hours
Doubled in elderly patients…hepatic flow/enzyme activity

188
Q

Midazolam VOD

A

1-1.5 L/kg (large)
because its so lipid soluble

> Vd in Elderly and morbidly obese…peripheral tissues

189
Q

Midazolam metabolism

A

CYP3A4
Active and inactive metabolites

190
Q

midazolam active metabolite

A

1-hydroxymidazolam

½ the activity of the parent

191
Q

Drugs that cause inhibition of P-450 enzymes

A

Decrease BZD metaolism / prolong effect

Cimetidine
Erythromycin
Calcium channel blockers
Antifungal
Fentanyl

192
Q

midazolam CNS effects

A

dec CMRO2, CBF
Preserves vasomotor rsp to CO2
no change in ICP

193
Q

vasomotor response to CO2

A

inc co2= vasodilation
dec co2 = vasoconstriction

194
Q

Midazolam Pulmonary effect

A

Dose-dependent decreases in ventilation
Decreases hypoxic drive
> depression with COPD
Transient apnea if rapid IV esp. with opioid
Depresses swallowing reflex
Decreases upper airway activity

195
Q

Midazolam effect on the CV system

A

inc hr (maintains CO)
dec bp
dec SVR

Does NOT inhibit BP/HR response to intubation

196
Q

Midazolam child dose

A

0.25-0.5 mg/kg oral syrup
Peak 20-30 minutes

197
Q

Midazolam adult dose

A

1-5 mg IV

Elderly require decreased doses…..Greater CNS sensitivity

198
Q

Midazolam for induction

A

0.1-0.2 mg/kg IV over 30-60 seconds

Facilitated by preceding dose of opioid
1-3 minutes
Fentanyl 50-100 mcq

199
Q

Midazolam infusion dose

A

1-7mg/hr IV
Markedly delayed awakening
Active metabolites accumulate
Clearance depends on hepatic metabolism not redistribution

200
Q

Midazolam and SE from sedation drips

A

dont run for more than 2-3 days
alteration in the ability of T cells to amount an immune response (inc risk of infection)

201
Q

Diazepam (Valium) VOD

A

Highly lipid soluble

202
Q

Diazepam (Valium) preparation

A

Propylene glycol…pain on injection; glycol toxicity

203
Q

Valium onset

A

1-5 min

204
Q

Valium E ½ time

A

20-40 hours….extensively protein bound

shorter duration of action than lorazepam (Dissociates from GABAa faster)

205
Q

Valium metabolism/ metabolites

A

CYP3A
Active metabolites
Desmethyldiazepam* (48-96 hours) and oxazepam
Nearly as potent as diazepam
Return of drowsiness 6-8 hours

206
Q

Valium anticonvulsant effects/dose

A

Potent anticonvulsant
0.1 mg/kg IV
Abolishes DT’s, status epilepticus, lidocaine toxicity related seizures
Longer acting antiepileptic drug also administered (fosphenytoin…cerebyx)

207
Q

Valium SE

A

Can produce isoelectric EEG

208
Q

Valium effects on pulmonary system

A

Slight decrease in Vt
After 0.2mg/kg IV increases in PaCO2

209
Q

Valium nm effects

A

Decreases tonic effect on spinal neuron
skeletal muscle tone decreased
Develop tolerance to skeletal muscle relaxant effects

No action at neuromuscular junction

210
Q

Valium induction dosing

A

0.5-1.0 mg/kg IV

Decrease dose by 25-50%
Elderly, Liver disease, Presence of opioids

211
Q

Lorazepam (Ativan) effect

A

More potent sedative and amnestic

212
Q

lorazepam preparation

A

Insoluble in water
Requires solvents: polyethylene glycol

Lower lipid solubility

213
Q

Lorazepam onset

A

Slower onset of action Then midazolam or diazepam because less lipid soluble

214
Q

Ativan peak effects

A

20-30 min

215
Q

ativan dose

A

1-4mg IV

216
Q

Ativan E1/2

A

14 hours
Slower than midazolam

217
Q

Ativan metabolism

A

Conjugated to inactive metabolites
Glucuronidation slower than oxidative hydroxylation
Not entirely dependent on hepatic enzymes
Less affected by hepatic function, age, drugs (cimetidine)
Not as affected by blood flow

218
Q

Flumazenil (Romazicon)

A

Competitive antagonist: high affinity for BZD receptor
Prevents/reverses all agonist activity of BZD

219
Q

Flumazenil (Romazicon) derivative

A

1,4 imidazobenzodiazepine

220
Q

Flumazenil (Romazicon) metabolism

A

Hepatic microsomal enzymes

Inactive metabolites

221
Q

Flumazenil (Romazicon) dose

A

0.2 mg IV and titrated to consciousness
Repeated 0.1mg q 1 minute to 1 mg total

Reversal within 2 minutes
0.3-0.6 mg to reverse sedation
0.5-1.0 mg to abolish therapeutic dose

222
Q

Flumazenil (Romazicon) duration of action

A

Duration 30-60 minutes
Supplemental doses vs continuous infusion (0.1-0.4 mg/hr)

223
Q

Flumazenil (Romazicon) contraindicated

A

Antiepileptic drugs

Precipitates acute withdrawal seizures

224
Q

Histamine induces….

A

Contraction of smm in airways
increases secretion of acid in the stomach
release nt in the cns (ach, ne, 5ht)

225
Q

Histamine induces….

A

Contraction of smm in airways
increases secretion of acid in the stomach
release nt in the cns (ach, ne, 5ht)

226
Q

Drugs that induce histamine release

A

morphine
mivacurium (mivacron)
protamine
attacurium, (Tracrium)

227
Q

H1 receptors can also activate…..

A

muscarinic, cholinergic, 5-HT3, and Alpha adrenergic

228
Q

H2 can also activate….

A

5-HT3 and B-1

229
Q

Histamine on H1 receptor causes

A

Hyperalgesia and inflammatory pain (insect stings)
Allergic rhino-conjunctivitis symptoms

230
Q

Histamine on H2 receptor causes

A

Elevates camp (B1-like stimulation)
Increases acid/volume production

231
Q

H1 and h2 receptor activation:

A

Hypotension (release of nitric oxide)
Capillary permeability
Flushing
Prostacyclin release
Tachycardia

232
Q

H1 R location

A

Receptors in vestibular system, airway smooth muscle, cardiac endothelial cells etc

233
Q

H1 R antagonists are used for…..

A

Effective for motion sickness (but cause sedation- cross bbb)
Possible protection against bronchospasm
Provides some cardiac stability (indicated in anaphylaxis)

Little tachyphylaxis

234
Q

H1 receptor antagonists SE

A

Blurred vision
Urinary retention
Dry mouth
Drowsiness (1st generation)

235
Q

Examples or H1 receptor antagonists

A

diphenhydramine (Benadryl)
Promethazine (Phenergan)
Cetirizine (Zyrtec)
Loratadine (Claritin)

236
Q

Diphenhydramine (Benadryl) uses

A

Mostly used as Antipruritic
pre-treat procedure related allergies….IVP dye

Also anaphylactic indications

Stimulates ventilation- Augments relationship of hypoxic and hypercarbic drives if Administered solo

N/V

237
Q

Diphenhydramine (Benadryl) E1/2

A

7-12 hrs

238
Q

Diphenhydramine (Benadryl) and N/V

A

May inhibit afferent arc of oculo-emetic reflex (salt dimenhydrinate)

why its good to protect against N/V

239
Q

Diphenhydramine (Benadryl) dose

A

25-50 mg IV

240
Q

Promethazine (Phenergan) uses

A

anti-emetic
sedation

Effective As rescue Reduce peripheral pain levels (anti-inflammatory effects)

241
Q

Promethazine (Phenergan) SE

A

Black box warning
children under 2yo = deaths
caustic to veins/ IV extravasation-> tissue necrosis

242
Q

Promethazine (Phenergan) dose

A

12.5-25mg iv

243
Q

Promethazine (Phenergan) onset

A

5 min

244
Q

H2 RECEPTOR antagonists uses

A

duodenal ulcer disease/GERD
Decreases gastric volume
increases pH

245
Q

H2 R antagonists MOA

A

Decreases hypersecretion of gastric fluid (h+)
From gastric parietal cells
decreased cAMP

246
Q

H2 receptor antagonists SE

A

Diarrhea
Headache
Skeletal muscle pain
Weakened gastric mucosa d/t bacteria (prolonged administration)
HA, confusion (CNS H2 receptors; more in elderly)
Bradycardia
Increase serum creatinine

247
Q

H2 receptor antagonists examples

A

Cimetidine (Tagamet)
Ranitidine (Zantac)
Famotidine (pepcid)

248
Q

Overgrowth of what gastric bacteria is most common with a weaken gastric mucosa

A

candida albicans

249
Q

Effect of H2 R antagonists on the kidneys

A

H2 compete for tubular secretion with creatinine.= increases serum creatinine by 15%

250
Q

Cimetidine (Tagamet) metabolized

A

CYP450, cleared in urine

251
Q

Cimetidine (Tagamet) inhibt CYP450 of these meds….

A

Warfarin, phenytoin, lidocaine, tricyclics, propranolol, nifedipine, meperidine, diazepam

252
Q

Cimetidine (Tagamet) Adverse effects:

A

Bradycardia, hypotension (cardiac H2 receptors)….rapid infusions
Increased plasma levels of prolactin
Inhibits dihydrotestosterone binding to androgen receptors (impotence)

253
Q

Cimetidine (Tagamet) Dose

A

150-300mg IV
½ dose in renal impairment

254
Q

Ranitidine (zantac) dose

A

50mg diluted to 20cc over 2 minutes
½ dose for renal impairment

255
Q

Famotidine (Pepcid) E1/2

A

Most potent, longest E ½ time (2.5-4 hrs)

256
Q

Famotidine (Pepcid) SE

A

Interferes with phosphate absorption
hypophosphatemia

257
Q

Famotidine (Pepcid) Dose

A

20mg IV
½ dose for renal impairment

258
Q

Proton (H+) pump inhibitors MOA

A

Irreversible binding to acid secretion “pumps”
Inhibit the movement of protons (H+) across the gastric parietal cells
Up to 5 days onset (3)

259
Q

Proton (H+) pump inhibitors use

A

Controlling gastric acidity
Decreasing volume
Healing esophagitis
Healing ulcers
Relieving symptoms of GERD
Best pharmacologic tx of Zollinger-Ellison syndrome

260
Q

PPI’s SE

A

bone fractures
SLE
acute interstitial nephritis
C-Diff diarrhea
Vitamin B12/Magnesium deficiency

Inhibits warfarin metabolism (work too well)
Blocks enzyme that activates clopidogrel (wont work as well)

261
Q

PPI’s Examples:

A

Omeprazole (Prilosec)
Pantoprazole (Protonix)
Lansoprazole (prevacid)
Dexlansoprazole (dexilent)

262
Q

Omeprazole (Prilosec)binding

A

prodrug
Protonates in PARIETAL CELLS to active form
Only inhibits pumps that are present
ACID-INHIBITION INCREASES WITH REPEATED DOSING
66% maximum inhibition

263
Q

Omeprazole (Prilosec) dose

A

Dose: 40 mg in 100cc NS over 30 minutes or
po > 3hrs prior (before OR)

264
Q

Omeprazole (prilosec) SE

A

Ha
Agitation
Confusion
Crosses bbb
Abdominal pain
n/v
Flatulence
Small bowel bacterial overgrowth

265
Q

Pantoprazole (Protonix)bioavailablility/ effect

A

Greater bioavailability and longer E ½ time compared to prilosec
Works as fast as ranitidine
1 hr prior to OR = decrease in gastric volume and ph

266
Q

Pantoprazole (Protonix)dose

A

40 mg in 100ml over 2-15 minutes

267
Q

PPI used for

A

Gerd
Gastroduodenal ulcers
Acute upper Gi hemm (infuse after egd)
NSAID ulcerations (ompeprazole)
schedule surgery

268
Q

H2 blockers are used for

A

Aspiration pneumonitis concerns (work faster than PPI)
Intermittent symptoms/cost effective

269
Q

antacids Particulate

A

Aluminum or magnesium based
Aspiration equals acid aspiration (dont give to full stomach)

270
Q

antacids Non-particulate

A

Sodium, carbonate, citrate, bicarbonate base
Neutralize acid (safer to aspirate)
Ex: sodium citrate (bicitra)

271
Q

Long term use of antacids

A

IF PH IS TOO HIGH- ACID BREAKDOWN OF FOOD INHIBITED and ACID REBOUND CAN OCCUR (when stop antacids)

MAGNESIUM BASED- COMMON OSMOTIC DIARRHEA and NEUROLOGIC AND NEUROMUSCULAR Impairment

CALCIUM BASED- HYPERCALCEMIA (concern for kidney stones)

SODIUM BASED- INCREASED SODIUM LOAD….HYPERTENSIVE PATIENTS (CHF)

272
Q

Sodium citrate (bicitra) MOA

A

non particulate
Neutralizes acid- (base + acid = SALT, CO2 AND WATER)

Protects against aspiration pneumonia-NOT against aspiration…

Increases intra-gastric volume (adding 15-30 ml)

273
Q

Sodium citrate (bicitra) length and start of effect

A

Work immediately…lose effectiveness 30-60 minutes

274
Q

Sodium citrate (bicitra) dose

A

15-30 ml po

275
Q

Dopamine blockers MOA

A

Stimulates gastric motility (prokinetic)
Increases lower esophageal sphincter tone
Stimulates peristalsis
Relaxes pylorus and duodenum- Gastric emptying and intestinal transit

276
Q

Dopamine blockers contraindications/ SE

A

Not administered to patients with dopamine depletion/inhibition
Extrapyramidal reactions (easily crosses BBB)
Orthostatic hypotension
Some effects on chemoreceptor trigger zone- Esp cinv and s/p csection but < 5-Ht3 drugs

277
Q

Dopamine blockers examples

A

Metoclopramide (reglan)
Domperidone
Droperidol (inapsine)

278
Q

Metoclopramide (reglan) SE

A

Abdominal cramping (if rapid Iv)
Muscle spasms
Hypotension
sedation
Increases prolactin release

Neuroleptic malignant syndrome; High temp, muscle rigidity, tachycardia, confusion

Decreases plasma cholinesterase levels; Slows metabolism of succinylcholine, mivacurium, ester LA

279
Q

Metoclopramide (reglan) dose

A

10-20 mg IV over 3-5 minutes (15-30 minutes prior to induction)

280
Q

domperidone compared to metoclopramide

A

Does not cross bbb
No anticholinergic activity

Also Increases prolactin secretion by pituitary- To greater degree

281
Q

domperidone SE

A

Dysrhythmias and sudden death
Available out of country

no FDA arrpoval

282
Q

Droperidol (inapsine) SE

A

Strong D2 antagonist
Extrapyramidal symptoms
Neuroleptic malignant syndrome
Avoid other cns depressants: barbiturates, opioids, general anesthetics

283
Q

Droperidol (inapsine) on N/v compared to other meds

A

More effective than metoclopramide/Equally effective to 4mg ondansetron (much cheaper)
For n/v

284
Q

Droperidol (inapsine) SE

A

2001 Black Box Warning…prolonged QT intervals/torsades with higher doses
Lots of serious drug interactions: amiodarone, diuretics, sotalol, mineralocorticoids, calcium channel blockers

285
Q

Droperidol (inapsine) dose

A

0.625-1.25mg IV

286
Q

Serotonin Release

A

Released from chromaffin cells of small intestine-> Vagal afferents through 5HT3 R -> vomiting

287
Q

5HT3 ANTAGONISTS Examples

A

Ondansetron (Zofran)
Granisetron (kytril)
dolasetron (anzemet)

288
Q

ondansetron 1/2 life

A

4 hours
give at end of procedure

289
Q

ondansetron SE

A

HA, diarrhea
Slight QT prolongation

290
Q

ondansetron dose

A

4-8 mg IV

291
Q

Corticosteroids MOA for CINV

A

centrally inhibit prostaglandin synthesis and control endorphin release
Increase effectiveness for 5HT3 antagonists and droperidol
Anti-inflammatory…less postop pain…less opioid

292
Q

Corticosteroids Example

A

Dexamethasone (decadron)

293
Q

Dexamethasone (decadron) onset / effect

A

Delay in onset of 2 hours
Efficacy persists for 24 hours

give at beginning of case

294
Q

Dexamethasone (decadron) Side effects

A

Diabetic Risk of perioperative hyperglycemia- Minimal side effects with 1 dose

Perineal burning/itching

295
Q

Dexamethasone (decadron) dose

A

4mg/8mg/

give more if airway trauma; 12, 16, 20 mg

296
Q

Scopalamine patch moa

A

Anticholinergics
muscarinic antagonist- Competitive antagonist of Ach

Central (Cross bbb) and peripheral effects

297
Q

Scopalamine patch peak concentration

A

concentration 8-24 hours
Apply 4 hours preop (onset)

298
Q

Scopalamine patch SE

A

dilated pupil- mydriasis/bright lights

299
Q

Scopalamine patch dose

A

1 patch for 24-72 hrs
Post-auricular
Priming dose (140 mcg)
1.5 mg over next 72 hours)

300
Q

Bronchodilators (B-receptor agonists) MOA

A

Structure similar to epinephrine-Stimulatory G proteins= activate camp +decrease ca +2 entry =
decrease contractile protein sensitivity to ca+2

Actions=
Reduce inflammatory cell activation
Directly relax smooth muscle….15% increase FEV1, 6 minutes (2 puffs)

301
Q

SABA repeat frequency

A

Q4 hr

302
Q

Side effects of Beta agonists

A

Tremor- B2 stimulation in skeletal muscle
Tachycardia
Transient decrease in arterial oxygenation
Hyperglycemia

Pharm Semester 2 (6 decks)

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