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Pharmacology 680 > Mostly Prop, some K, NSAIDS > Flashcards

Mostly Prop, some K, NSAIDS Flashcards

1
Q

What class is prop and why is it different from other IV sedatives?

A

: Sedative/hypnotic

because it is a hypnotic

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2
Q

Induction dose prop

A

1.5 – 2.5 mg/kg IV

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3
Q

how long does it take to become unconscious from prop?

A

about 30 seconds

[moves from stage 1 to stage 3 fast]

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4
Q

Major advantage of prop

A

Rapid awakening with minimal residual CNS effects
[patients can go home fast]

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5
Q

Chemistry of prop

A

1% solution in soybean oil, glycerol and egg lecithin (a long-chain triglyceride)

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6
Q

why is the chemistry important of prop?

A

Supports bacterial growth

Can increase plasma triglyceride levels

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7
Q

preservatives of diprivan

A

disodium edetate & NaOH

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8
Q

preservative of generic prop?

A

metabisulfite

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9
Q

Propofol known for pain at injection site, so it is common to mix with lidocaine. What is risk of this?

A

Propofol + lidocaine – coalesced oil – risk of pulmonary emboli

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10
Q

causes genital burning

A

aquavan due to formaldehyde

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11
Q

Brand of prop that causes increase injection site pain

A

ampofol

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12
Q

MOA of prop

A

GABAA receptor agonist (inhibitory neurotransmitter)

GABAA stimulation = hyperpolarization of cell membranes which causes receptor to not work

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13
Q

Uptake of prop

A

lungs and liver (cytochrome P-450)

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14
Q

Elimination ½ time prop

A

0.5 – 1.5 hrs

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15
Q

Context sensitive ½ time of prop

A

<3 hrs = 10 min
>3 hrs = 25 min
>8 hrs = 40 min

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16
Q

metabolism of prop?

A

Glucuronidation (liver) is major metabolic pathway

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17
Q

Excretion of prop?

A

excretion mostly through kidneys however Liver and/or renal disease does not impair elimination.

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18
Q

can you give prop to laboring moms?

A

YES! Crosses placenta but rapidly cleared from neonatal circulation so baby will be breathing, just make sure mom is stable

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19
Q

difference in peds dose of prop?

A

Require ↑ dosing d/t ↑ Vd and faster clearance (you can give like 4-5X dose)

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20
Q

difference in elderly dose of prop?

A

↓ dosing d/t ↓ Vd and slower clearance

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21
Q

sedation dose of prop?

A

25 – 100 mcg/kg/min

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22
Q

Agent of choice for short, endoscopic cases

A

prop

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23
Q

Maintenance dose prop?

A

100 – 300 mcg/kg/min (↓ with opioids and volatiles)

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24
Q

cool effect of prop that we like to use?

A

antiemetic! almost equal to zofran

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25
Q

how much prop to use as an antiemetic?

A

Small dose (10-15 mg) in PACU & with chemo induced N/V

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26
Q

Why is prop an antiemetic???

A

Possibly a direct depressant effect on vomiting center

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27
Q

5 non-anesthetic effects of prop

A
  1. antiemetic 10-15 mg
  2. antipruritic 10 mg
  3. anticonvulsant 1mg/kg
  4. bronchoconstriction
  5. Analgesia
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28
Q

dose of 1 mg/kg or greater of prop is useful as

A

↓ seizure duration during ECTs
anticonvulsant

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29
Q

what causes the bronchoconstriction seen with prop?

A

Metabisulfite (generic propofol) can cause bronchoconstriction (asthma, smokers)

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30
Q

what type of pain is prop decent for?

A

Not good for nociceptive pain (somatic, visceral); some analgesia for neuropathic pain (abnormal CNS processing of painful stimuli)

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31
Q

Neurologic effects prop

A

↓ CMRO2, ↓ cerebral blood flow, ↓ ICP

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32
Q

Cardiovascular effects prop?

A

↓ HR, ↓ SVR, ↓ cardiac output Commonly offset by laryngoscopy, intubation or LMA insertion

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33
Q

causes Extreme ↓ BP with prop admin

A

hypovolemia, LV dysfunction, elderly

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34
Q

why is prop good for ablations?

A

no SA or AV node effects or QTc prolongation

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35
Q

Profound bradycardia and/or asystole

A

Propofol Related Bradycardia

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36
Q

Increased incidence of Propofol Related Bradycardia

A

surgeries dealing with muscles of eyeball and oculocardiac reflex

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37
Q

treatment of prop brady?

A

glycopyrolate, epi

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38
Q

who is more prone to prop related brady?

A

younger more prone, remember they are HR dependant

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39
Q

oculocardiac reflex is

A

stimulation of cranial nerve V and X - vagal nerve

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40
Q

Dose-dependent Respiratory depression with prop causes

A

apnea, decrease RR and TV

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41
Q

what is prop enhanced and offset by?

A

Enhanced by opioids

Offset by surgical stimulation

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42
Q

what type of shift of hypoxic response curve will you see with prop?

A

downward (neg effect)

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43
Q

what is a positive effect of prop that we do not want to interfere with?

A

Hypoxic pulmonary vasoconstriction (HPV)

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44
Q

what causes benign green urine with no renal dysfunction with prop?

A

Phenol

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45
Q

Prolonged infusion of prop can lead to

A

liver injury and propofol infusion syndrome

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46
Q

benign cloudy urine with prop is caused by

A

uric acid

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47
Q

why is prop Good for lap trendelenburg procedures

A

↓ IOP after induction, sustained through intubation

48
Q

what does prop do to coags??

A

No change in coag factor or platelet function

Inhibits platelet aggregation

49
Q

4 lipid related effects prop?

A

Risk of infection
injection site pain
hypertriglyceridemia
pulmonary embolus

50
Q

Allergic Reaction of prop related to

A

Phenol related anaphylaxis (often after 1st exposure with neuromuscular blockers)

51
Q

Is Propofol Safe for Patients with Egg Allergies

A

We found no evidence of a relationship between foodallergyhistory and perioperativepropofolreaction.”

52
Q

Seen after >75 mcg/kg/min for >24 hours (ICUs)

A

Propofol Infusion Syndrome

53
Q

how to spot prop infusion syndrome?

A

Tachycardia during propofol anesthesia is sign of lactic acidosis, then profound bradycardia

54
Q

Mechanism of prop infusion syndrome?

A

Mimics mitochondrial myopathy (abnormal lipid metabolism in smooth and cardiac muscle)

55
Q

Hyperchloremic metabolic acidosis (NS) and ↑ organic acids (DM ketoacidosis, tourniquet release)

A

differential diagnoses of prop infusion syndrome

56
Q

tell me About Seizure Activity with prop?

A

Can cause seizure-like myoclonus after injection
Not cortical epileptic in origin
During EEG, does NOT induce seizures in epileptic patients
No contraindications with epileptic patients

57
Q

Accounts for 40% of KNOWN substance abuse in anesthesia practitioners

A

prop, it is a problem

58
Q

PCP derivative – dissociative anesthesia (thalamocortical and limbic systems)

A

Ketamine

59
Q

what will you see when you give K to patients?

A

Amnesia, analgesia, eyes open, spontaneous ventilation

60
Q

Major disadvantage of K

A

Emergence delirium (ED)

61
Q

what isomer is most commonly used of K and why

A

Racemic (R) most commonly used d/t more intense analgesia with fewer side effects.

62
Q

MOA of K?

A 
Non-competitive binding to N-methyl-D-aspartate (NMDA) receptors (antagonist)
Inhibits glutamate (excitatory transmitter) binding to glycine (required for NMDA receptor activation)
Inhibits catecholamine uptake into post-ganglion                                             nerves (like cocaine)
63
Q

5 other receptors K effects?

A

Opioid, monoaminergic, muscarinic, Na+ and Ca++ channels, nicotinic acetylcholines

64
Q

K Interacts with all opioid receptors and is
Synergistic with

A

opioid, dopamine and serotonin agonists to promote dissociation

65
Q

Anti-muscarinic properties of K include

A

bronchodilation, sympathomimetic, anti-erectile dysfunction

66
Q

Anti-nicotinic properties

A

may play role in analgesia

67
Q

onset and duration k

A

rapid 30 seconds onset and short duration of 5-15 mins dd

68
Q

what causes psych effects after emergence from ketamine

A

Redistributes from ↑ to ↓ perfusion tissue r/t high lipid solubility

69
Q

elimination ½ time K

A

2 – 3 hours

70
Q

Metabolism K and excretion

A

Hepatic (cyto P-450) and kidneys

71
Q

byproduct of K that we like?

A

norketamine bc it contributes to prolonged anesthesia

72
Q

what will you see with repeated doses of K?

A

Repeated doses - enzyme induction - analgesic tolerance - dependence

73
Q

Clinical uses of K?

A 
analgesia
chronic pain syndrome
OB bc no neonatal depression
psych
induction
74
Q

what meds are good for chronic pain syndromes

A

Ketamine. Mg++ and dextromethorphan

75
Q

Ketamine useful specifically for these types of pts with psych?

A

PTSD, also good for depression

76
Q

induction dose K

A

1-2 mg/kg IV; 4-8 mg/kg IM

77
Q

onset K

A

LOC in 30-60 sec IV, 2-5 mins IM

78
Q

how long does it take to Return to consciousness

A

approx. 15 minutes; full orientation in 60-90 minutes

79
Q

Major indication of k

A

burns

80
Q

caution k admin with these patients

A

CAD, pulm hypertension, high icp, critically ill

81
Q

↑ dose of k causes

A

burst suppression; anticonvulsant (does not alter seizure threshold)

82
Q

how does k effect Hemodynamics

A

↑ everything (BP, HR, CO, myocardial work and O2 demand)

Can be offset with benzos and volatiles

83
Q

ventilation reflixes mainly stay in tact, but important to consider what

A

aspiration risks should be intubated and give an antisialagogue

84
Q

Psychedelic Effects K

A

Visual (including transient blindness), auditory, vivid (full color) dreams, “floating”, hallucinations, delirium: some up to 24 hrs

85
Q

↑ risk factors for psych effects

A

> 15 years, female, >2 mg/kg/IV, personality disorders

86
Q

how do you prevent emergence delirium with k

A

Benzodiazepines most effective (midazolam better than diazepam)
Common “cocktail”: IV midazolam and glycopyrrolate before or with ketamine

87
Q

NSAIDS are

A

Analgesic, Anti-inflammatory, Antipyretic

88
Q

COX-1 Non-selective inhibitors advantage

A

↓ platelet aggregation

89
Q

COX-1 Non-selective inhibitors disadvantage

A

↓ renal function,
↑GI toxicity,
↓ platelet aggregation*

90
Q

cox 2 selective advantages

A

↓ pain, inflammation, fever
↓ GI toxicity
no platelet effects

91
Q

cox 2 selective disadvantages

A

↑ CV risk

92
Q

where do the unwanted side effects from nsaids come from

A

cox 1 receptor

93
Q

what does it mean when nsaids are highly protein bound?

A

means drug cant reach receptor because it is bound to the protein so you will see greater effects in ppl with low protein syndromes

94
Q

metabolism and excretion of nsaids

A

Liver metabolism, renal excretion

95
Q

↑ GI risks with nsaids seen with

A 
High dose, 
older age, 
H. pylori or ulcer history; 
combined with ASA, anticoagulants, 
corticosteroids
96
Q

CV risks when taking nsaids

A

MI, heart failure, HTN

97
Q

Naproxen appears to have ↓ risk with what major side effect nsaids

A

cv

98
Q

what can nsaids do to the kidneys and liver

A

NSAIDs can ↓ GFR

↑ LFTs and liver failure

99
Q

patients with cards issues should be on what nsaid

A

naproxen according to aha

100
Q

What patients have an increase of anaphylaxis with nsaids?

A

Pts with allergic rhinitis, nasal polyps, asthma r/t prostaglandins

101
Q

Potent analgesic, moderate anti-inflammatory, anti-pyretic

A

Ketorolac (Toradol)

102
Q

30 mg IM/IV of toradol is equal to

A

analgesia of MSO4 10 mg or meperidine 100 mg without CV or respiratory depression, minimal N/V but watch out with kidney patients

103
Q

onset and peak effect

A

onset dd 30-1 hr

peak 2-3 hrs [give faster acting until this kicks in]

104
Q

A OK protocol

A

atropine 1 mg for vagolysis
ondansetron 8 mg to block serotonin/vagolysis
ketorolac 30 mg block thromboxane

105
Q

Analgesic, antipyretic, insignificant anti-inflammatory action

A

Acetaminophen

106
Q

Leading cause of acute liver failure in U.S?

A

Acetaminophen r/t Metabolite: NAPQI (depletes antioxidant glutathione, directly damages liver cells)

107
Q

To ↓ liver toxicity risk, FDA recommends

A

≤ 2600 mg/day, ≤ 650 mg single dose.

108
Q

dose of iv acetamet

A

> 13 yo: 1 gm/15 minutes;

2-13 yo: 15 mg/kg

109
Q

Oldest, most widely used medicine in the world.
“Separated” from other NSAIDs because of its cardiovascular and cerebrovascular benefits.

A

Aspirin (ASA)

110
Q

what causes prolonged platelet aggregate inhibition with asa

A

Irreversibly inactivates COX-1

111
Q

Toxicity (all NSAIDs): 8

A 
N/V, 
abd pain, 
tinnitus, 
CNS depression, 
metabolic acidosis, 
renal failure, 
agitation, coma,
 hyperventilation (compensation)
112
Q

treatment for nsaid tox even though there is no antidote

A

Treat symptoms, hydrate, alkalinize urine, consider charcoal, hemodialysis

113
Q

Key point of eras

A

Multimodal analgesia = concurrent use of non-opioid analgesics and opioid sparing techniques to minimize opioid related adverse effects.

114
Q

Pre-op eras?

A

Combo of acetaminophen, NSAID and gabapentanoid

115
Q

intraop eras

A

Regional anesthesia or non-opioid analgesic technique

116
Q

post op eras

A

Continuation of 1) regional analgesia, especially if NPO; 2) acetaminophen; 3) NSAID; 4) gabapentanoid on scheduled (not PRN) basis

Pharmacology 680 (19 decks)

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