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Fall 20' Pharm. III > NCE Pharm review 1 and 2 power points > Flashcards

NCE Pharm review 1 and 2 power points Flashcards

1
Q

The two volatile agents that decrease Systemic Vascular Resistance more than the others?

A

Iso

Des

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2
Q

Which VA causes hypothermia because it suppresses the hypothalamic temperature regulators?

A

Isoflurane

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3
Q

What four things do VA change in relation to blood flow and the brain?

A

Dilate cerebral vessels

Increase cerebral blood flow

Increase cerebral blood flow and ICP

Decreases neuronal function and cerebral metabolism

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4
Q

The increase in ICP by Iso can be negated by what?

A

hyperventilation

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5
Q

Which VA is the least likely to dangerously increase ICP if keep the patient moderately hypocapnic?

A

Iso

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6
Q

Which VA has a slightly higher incidence of causing a cough reflex during maintenance when used with a LMA?

A

Isoflurane

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7
Q

How much MAC of a VA will completely block the ventilatory response to hypoxemia. Therefore, hypoxemia will not stimulate ventilation when using a volatile agent?

A

0.1 MAC

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8
Q

Hypoxic Pulmonary Vasoconstriction HPV is inhibited by a high concentration of volatile, what is the concentration?

A

1-1.5 or higher MAC

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9
Q

What volatile is considered completely halogenated with fluorine?

A

Des

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10
Q

Volatile agents that suppress ventilation the most?

The least?

A

Most: Des, Enflurane

Least: Halothane

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11
Q

What volatile agents most depresses the baroreceptor reflex?

Which one does it the least?

A

Most depress : Halothane and Sevo: No increase in HR even with decreases in blood pressure

Least depress: Iso and Des: HR increases as a reflex to decrease in blood pressure

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12
Q

Acute ETOH intoxication effect on MAC ?

A

decreases

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13
Q

Rank opioids most lipid soluble to least lipid soluble

Meperidine
Remifentanil
Morphine
Fentanyl 
Sufentanil
alfentanil
A

Sufentanil &raquo_space; fentanyl&raquo_space;> alfentanil&raquo_space;> meperidine > remifentanil > morphine

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14
Q

What receptors do spinal opioids work on?

A

Primarily Mu-2 but work on mu-1, kappa, and delta to produce supraspinal analgesia

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15
Q

Stimulation of mu-1 receptors cause what response?

A 
Spinal and supraspinal analagesia
Euphoria
Miosis
Bradycardia
Hypothermia
Urinary retention
pruritus
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16
Q

Mu-1 have a high or low abuse potential?

A

Low abuse potential

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17
Q

Opioid can cause nausea and vomiting by?

A

Stimulation of CTZ of the forth ventricle (floor). The triggered CTZ activates vomiting center near the brain stem.

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18
Q

Which opioid is not metabolized by the liver?

A

Remifentanil and is metabolized by nonspecific esterases in the blood stream.

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19
Q

Agonist/antagonist opioids work on what receptor(s) for therapeutic effect?

A

Primarily Kappa and also on delta

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20
Q

Naloxone reverses what actions of opioids?

A

Pruritus
Urinary retention
N/V

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21
Q

Higher doses of naloxone are required to reverse what opioid issue?

A

Reverse profound sedation and respiratory depression

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22
Q

Does morphine produce arterial or venous dilation?

A

Both due to histamine release

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23
Q

What two opioids cause histamine release?

A

Morphine and Meperidine

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24
Q

There are 3 CV actions that may cause a decrease in BP in an anesthetized patient given a high dose of fentanyl?

A

Decrease SVR (dilate arterial vessels)

Decrease venous return (dilate venous capacitance vessels)

Decrease in HR

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25
Q

How are ester locals “metabolized”?

A

Hydrolyzed by plasma and tissue cholinesterase

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26
Q

PABA is excreted where?

A

PABA is excreted unchanged in the urine

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27
Q

True or False?

Cross reactions between esters and amides?

A

No cross reactions

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28
Q

How could an ester be prolonged?

A

Prolonged in plasma cholinesterase deficiency

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29
Q

What does the PKa of a LA mean?

A

when 50% is ionized and 50% is unionized

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30
Q

lipid solubility of a LA parallels what?

A

potency of the LA

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31
Q

Protein binding of a LA parallels what?

A

duration of action of the LA

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32
Q

What is the short acting LA and what is the long acting LA?

A

Short : procaine

Long: bupivacaine and tetracaine

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33
Q

What is the progression of LA blockade? (what do you lose first to last)

A 
Autonomic
Temperature
Pain
Touch
Pressure
Motor
Vibrate/Proprioception
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34
Q

Treatment of LA toxicity?

A

20% Intralipid:

1.5 mL/kg over 1 minute

Continuous infusion of 0.25 mL/Kg until hemodynamically stable

Limit: 10 mL/Kg over 30 minutes

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35
Q

When administered alone does Nitrous cause hypotension?

A

No, but instead causes cutaneous vasoconstriction and increased SVR.

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36
Q

When administered alone what will Nitrous cause?

A

Nitrous will cause an increase in cardiac output when administered alone.

(also cutaneous vasoconstriction and increased SVR)

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37
Q

What is the dose limit of exogenous EPI if using Iso, Des, or Sevo?

A

5-6 mcg/kg

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38
Q

Fluid replacement for surgical trauma?

A

Minimal – 5 ml/kg/hour

Moderate - 6 ml/kg/hour

Extensive – 8 ml/kg/hour

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39
Q

Goal directed fluid therapy is guided by UOP, what is the amount of UOP you want per hour?

A

0.5ml/kg/hour

hemodynamically stable

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40
Q

Nerve fibers, tell me about type A, B, and C in relation to myelination?

A

Type A = Heavy myelination

Type B = Light myelination

Type C = No myelination

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41
Q

Type A nerve fibers have alpha, beta, gamma, and delta fiber subtypes, what are the reactions associated with each subtype?

A

Alpha: Proprioception, motor

Beta: Touch, pressure

Gamma: Muscles spindles

Delta: Pain, temperature

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42
Q

Type B nerve fibers, are they pre or post ganglionic autonomic?

A

preganglionic autonomic

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43
Q

Type C nerve fibers details?

A

Dorsal Root: Pain

Sympathetic: Postganglionic

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44
Q

Which ester local anesthetic is the #1 cause of methemoglobinemia?

A

Benzocaine

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45
Q

explain zero order pharmacokinetics?

What drugs follow this order?

A

Constant amount of drug is eliminated per unit of time

Metabolic pathways are considered saturated

Drug Examples: salicylates, theophylline, phenytoin, and ethanol

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46
Q

First order pharmacokinetics explain what you know?

A

Constant fraction of drug is eliminate per unit of time

Elimination rate is proportionated to the amount of drug in the body

Most drugs are eliminated in this manner

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47
Q

What is volume of distribution?

A

Amount of the drug in body divided by the amount in the blood

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48
Q

Small volume of distribution would tell you what about a drug?

A

lipid insolubility

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49
Q

Large Vd would tell you what about a drug?

A

lipid solubility (soluble)

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50
Q

Clearance is defined as?

A

Complete drug removal from a volume of plasma per unit of time

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51
Q

elimination half time is defined as?

A

Time to eliminate 50% of drug from the PLASMA

4 half lives = 94% complete

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52
Q

define context sensitive half time?

A

Describes the time necessary for the plasma drug concentration to decreases by 50% (or any other percentage) after discontinuing a continuous infusion of a specific duration (context refers to infusion duration). It considers the combined effect of distribution and metabolism as well as duration of continuous IV administration on drug pharmacokinetics

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53
Q

The relationship between Volume of Distribution, Clearance, and Half-Life?

A

T1/2 = 0.693 x Vd/CL

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54
Q

The relationship between Volume of Distribution, Clearance, and Half-Life?

A

T1/2 = 0.693 x Vd/CL

what is under the division sign is opposite to what is on the other side of the = sign

55
Q

when half life is increased what else increases?

A

volume of distribution is increased

56
Q

A drug follows first order kinetics and has a half life elimination of 6 hours. How much drug remains after 18 hours if 10mg was administered?

A

1.25mg after 18 hours.

(10mg to start, after 6 hours you have half which is 5mg, then after 6 more hours you have 2.5mg left, then after 6 more hours which = 18 total hours you have 1.25mg left)

57
Q

most drugs are eliminated by what order of kinetics?

A

first order kinetics

58
Q

major negative effects of mu-2 receptor?

A

Analgesia (Spinal)

Respiratory depression(decreased sensitivity of resp. center to CO2)

Addiction

Constipation (marked) decreased motility and tone of GI muscles

increased CSF pressure (cerebral edema) C/I in head injury

59
Q

In the resting state is the acetylcholine receptor open or closed?

A

closed

60
Q

In the resting state are the acetylcholine receptors open or closed?

A

closed

61
Q

what will open the channel at the neuromuscular junction?

A

Simultaneous binding of 2 acetylcholine molecules to the alpha subunits initiates conformational changes that open the channel

62
Q

if a single molecule of a non-depolarizing neuromuscular blocker (a competitive antagonist) binds to one alpha subunit at the neuromuscular channel what happens?

A

produces neuromuscular block

63
Q

how does Sch work?

A

Sch produces a prolonged depolarization of the endplate region that results in desensitization of nicotinic acetylcholine receptors; inactivation of voltage gated sodium channels at the neuromuscular junction and increase in potassium permeability in the surrounding membrane. Thus producing the failure of the action potential generation due to membrane hyperpolarization and a block ensues.

64
Q

what is true cholinesterase?

A

Acetylcholinesterase

65
Q

what is responsible for the rapid hydrolysis of released acetylcholine to acetic acid and choline?

A

acetylcholinesterase

66
Q

other names for plasma cholinesterase?
where is it synthesized?
what is it’s function?

A

Butyrylcholinesterase (plasma cholinesterase or pseudocholinesterase) is synthesized in the liver. It catalyzes (causes or accelerates) the hydrolysis of succinylcholine which occurs mainly in the plasma.

67
Q

all NMB are what type of compounds and structurally related to what

A

All neuromuscular blockers are QUATERNARY AMMONIUM compounds and are structurally related to acetylcholine.

68
Q

Majority of NMB are synthetic alkaloids, what is the exception?

A

Exception is tubocurarine which is extracted from and Amazonian vine. It is cheaper to isolate from this plant than to synthesized.

69
Q

what are the two classes of NMBD?

A

Benzylisoquinolinium

Steroidals

70
Q

list the benzyl lisoquinoliniums

A

Cisatracurium
atracurium
Tubocurarine
Mivacurium

71
Q 
Tell me everything you know about Nimbex?
isomer of?
what does it metabolize to?
what % is cleared renally?
potency compared to atricurium?
does it cause histamine release?
A

Isomer of atracurium

Hoffman elimination to laudanosine and a monoquaternary alcohol metabolite

No ester hydrolysis of parent molecule

Hoffman is ~ 77% of clearance

23% is cleared by other organs with 16% being renal

4-5 times as potent as atricurium

5 times less laudanosine is produced than atricurium and is thought to be of no clinical consequence

Does not cause histamine release like atracurium if given in clinical dose range

72
Q

The only currently available short acting NMBD that is not available in the US?

A

Mivacurium

73
Q

Significant details about Pancuronium (steroidal compound)

A

potent long acting

at room temp. remains stable for 6 months.

Vagolytic and butyrylcholinesterase inhibiting properties

~40-60% eliminated by kidneys and 11% in bile

74
Q

Vecuronium:

duration of action?

elimination?

liver or renal function more relied on?

metabolites and prolonged blockade?

A

intermediate duration of action

Principle elimination is liver with renal accounting for about 30%

30-40% cleared in bile

Duration relies on liver function more so than renal function

3-OH has 80% the neuromuscular blocking potency of Vecuronium and with prolonged administration this metabolite may contribute to prolonged neuromuscular blockade.

75
Q

Rocuronium:

onset/ duration of action?

more or less potent than vecuronium?

eliminated by?

stable for how long at room temp?

A

onset is fast, duration is intermediate acting.

6 times less potent than Vec

Primarily eliminated by liver and excreted in bile

stable for 60 days at room temperature

76
Q

what does ED50 or ED95 mean in relation to NMBD?

A

Expressed in terms of dose response relationship

50% depression of twitch height ED50 and 95% would be ED95

77
Q

Inhalation anesthetics potentiate the neuromuscular blocking effect of NMBD, what is the order from most to least?

A

DES > SEVO > ISO > Halothane > Nitrous Oxide, barbiturate, or propofol

78
Q

What is the mechanism for potentiation of NMBD by VA?

A

Central effect on alpha motoneurons and interneruonal synapses

Inhibition of postsynaptic nicotinic acetylcholine receptors

Augmentation of antagonist’s affinity at the receptor site

79
Q

Certain antibiotics can potentiate NMB…. name some?

A

Aminoglycoside
Polymyxins
Lincomycine
Clindamycin

80
Q

Which antibiotic exhibits post junctional activity only on the NMJ? (potentiates NMB)

A

Tetracycline

81
Q

how do antibiotics that potentiate NMB do so?

A

All inhibit the prejunctional release of acetylcholine and also depress postjunctional nicotinic acetylcholine receptor sensitivity to acetylcholine.

82
Q

what does hypothermia or magnesium sulfate do to NMBD?

A

Potentiates blockade

83
Q

How does magnesium potentiate NMBD?

A

High magnesium concentrations inhibit calcium channels at the presynaptic nerve terminals that trigger the release of acetylcholine

84
Q

Can LA potentiate NMBD?

A

ONLY in large doses, at clinical amounts it is not significant

85
Q

Which antidysrhythmic potentiates NMBD?

A

quinidine

86
Q

factors decreasing potency of NMBD?

A

hyperparathyroidism (atracurium)

Hypercalcemia for tubocuraine and pancuronium

87
Q

potency of NMBD… is inversely proportional to what?

A

Onset of action is inversely proportional to potency of NMBD

Low potency = rapid onset

High potency = slow onset

88
Q

Molar potency is highly predictive of a dugs time to onset of effect. Which NMB is the exception to the rule?

A

Atracurium

89
Q

potency of NMBD is expressed in what unit?

A

(micro)moles per kilogram and NOT mg/kg

90
Q

How do we compare the potency of NMBD?

A

ED50 and ED95

Measured by the amount of drug necessary to decrease the height of the baseline twitch by 50% and 95%

91
Q

ALL NMBD are competitive with Ach except for?

A

Sch

92
Q

why does Sch need 2 x the ED95 for dosing?

A

because of its rapid hydrolysis by plasma cholinesterase.

93
Q

Conditions that interfere with Plasma Cholinesterase?

A

Liver disease (severe)

Chronic renal failure

Starvation

Dialysis (soon after)

Infants (50%) by age 6 (70%), puberty (100%)

94
Q

Drugs that interfere with Plasma Cholinesterase?

A

Organophosphate exposure

Anticholinesterase meds

Metoclopramide

MAOI

Oral contraceptives used long-term

95
Q

Succinylcholine Disadvantages?

A

Myalgia

Hyperkalemia

Cardiac dysrhythmias

MH

Phase II Block: Resembles NMDR (>4 mg/kg)

Second Dose Effect: Brady after a 2nd dose within 5 min. can also cause asystole

96
Q

explain dibucaine number and what a dibucaine number of 80, 40-60, and 20 means?

A

Plasma cholinesterase production is the work of 2 genes

DN = 80 = present on both genes = homozygous (plasma cholinesterase)= Normal

DN = 40-60 = only present on one gene = heterozygous (1 in 480) produce 50% of enzyme

DN = 20 = missing on both genes = homozygous (atypical plasma cholinesterase) (1in 3200).

97
Q

where do osmotic diuretics work? (4 locations)

A

Proximal convoluted tubule

Descending limb of loop of Henle

Distal part of distal convoluted tubule

Collecting ducts/tubules

98
Q

where do loop diuretics work?

A

loop of henle

99
Q

where do thiazide diuretics work?

A

Proximal Part of distal convoluted tubule

100
Q

where do potassium sparing diuretics work?

A

Distal part of distal convoluted tubule

Collecting ducts/tubules

101
Q

where do carbonic anhydrase inhibitors work?

A

Brush border of proximal tubule

102
Q

How many mg are there in 10 mL of a 4% solution of cocaine?

A

400mg

4% is 40mg (0.4% would be 4mg) move the decimal place once to the right.
Thus 40mg per cc, and it is 10 cc so that would be 40mg x 10 = 400mg

103
Q 
Build up of inhalational anesthetic in the brain is fastest for an agent that has:
A.) low blood solubility
B.) High blood solubility
C.) Low lipid solubility
D.) High lipid solubility
A

A) low blood solubility

104
Q 
The most potent inhalational anesthetics have
A.) low blood solubility
B.) High blood solubility
C.) Low lipid solubility
D.) High lipid solubility
A

D) high lipid solubility

105
Q 
Intravascular infusion of which of the following substances would be most effective in promoting the osmotic movement of water into the circulation from the extracellular space
A.)  NaCl
B.)  Mannitol
C.)  Dextrose
D.)  Albumin
A

D) Albumin

106
Q

what type of nerve injury will cause wrist drop?

A

radial nerve injury

107
Q

what type of nerve injury will cause ape hand?

A

median nerve injury

108
Q

what type of nerve injury will cause claw hand?

A

ulnar nerve injury

109
Q

what type of nerve injury will cause inability to flex the forearm?

A

musculocutaneous nerve injury

110
Q

what type of nerve injury will cause an inability to ABDuct the arm?

A

axillary nerve injury

111
Q

Calcium Channel Blockers are particularly successful in treating hypertension in what three populations?

A

elderly

African Americans

salt sensitive patients

112
Q

what type of drug is milrinone?

A

an adenosine-3’, 5’- cAMP-selective phosphodiesterase enzyme (PDE) inhibitor

113
Q

which drug is described: selectively dilates the pulmonary vasculature without systemic effects.

A

milrinone

114
Q

what does nebulized milrinone reduce?

A

PVR compared to SVR

115
Q

How do phosphodiesterase inhibitors work?

A

prevent the degradation of cGMP and cAMP which are activated by NO and are intermediaries in a pathway that leads to vasodilation.

116
Q

the vasodilation caused by PDE inhibitors is via what?

A

via the activation of protein kinases, and reduction in cytosolic calcium.

117
Q

where do PDE5 inhibitors work?

A

higher expression in pulmonary circulation versus the systemic circulation. Thus PDE5 inhibitors have a relative selective effect on PVR as opposed to SVR.

118
Q

what two drugs have shown benefits in chronic Pulmonary Arterial Hptn (PAH) in prospective controlled trials (but most studies have been case studies and small cohort studies). These drugs have not been approved for these acute settings?

A

Sildenafil and Tadalafil

119
Q

which drug has been demonstrated to enhance effects of NO and may blunt rebound pulmonary pressure that occur during weaning off of inhaled NO?

A

sildenafil

120
Q

Explain Hypoxic Pulmonary Vasoconstriction (HPV)?

A

an increase in pulmonary vascular resistance in atelectatic lung areas. HPV optimizes overall gas exchange by shifting blood flow to better ventilated areas of the lung.

121
Q

True or False:

IV anesthetic agents have significant effect on HPV?

A

False, they have little effect.

122
Q

What drugs DO inhibit HPV in a dose dependent fashion?

and what would be the order from greatest to lest?

A

VA

halothane>enflurane>isoflurane/desflurane/sevoflurane

123
Q

What is avoided during thoracic anesthesia bc it inhibits HPV?

A

Nitrous

124
Q

what vasodilators decrease the action of HPV?

A

NTG and Nitroprusside

125
Q

What are the the three VA that at 1 MAC are weak HPV inhibitors and pretty equal?

A

ISO, SEVO, DES

126
Q

Receptors located in the 4th ventricle of the brain (floor) that cause N/V?

A 
Dopaminergic
Serotonergic
Histaminic
Muscarinic
Substance P
127
Q

Anti- dopaminergic drugs would be? (3)

A

Butyrophenones: Droperidol

Phenothiazines: Prochlorperazine

Benzamines: Metoclopramide

128
Q

Serotonin antagonist is?

A

zofran (5HT3)

129
Q

Anti-Histaminergic drug would be?

A

Diphenhydramine: Both antihistamine and anticholinergic effects (Benadryl)

130
Q

Anti- cholinergic drug would be?

A

Glycopyrrolate may be useful in neuraxial induced N/V

131
Q

name three H-2 Blockers

also tell me the function

A

Blocks acid stimulating effects of histamine and ACh

Cimetidine
Ranitidine
Famotidine

132
Q

Anti - Muscarininc drug would be?

A

Scopolamine is a high affinity muscarinic antagonist

133
Q

Substance P drug would be?

A

Neurokinin 1 Antagonists

Aprepitant: Only PO

Fosprepitant: IV is available

Comparable to ondansetron but lasts longer and is synergistic with other PONV medications

Fall 20' Pharm. III (5 decks)

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